2024-03-29T13:47:57Z
https://revistabiomedica.org/index.php/biomedica/oai
oai:oai.revistabiomedica.org:article/1
2016-11-22T10:32:54Z
biomedica:EDIT
Avances en visibilidad, acceso y reconocimiento internacional de la revista Biomédica
Gómez, Luis Alberto
Nicholls, Rubén Santiago
Instituto Nacional de Salud
2008-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/1
10.7705/biomedica.v28i1.1
Biomedica; Vol. 28 No. 1 (2008); 5-6
Biomédica; Vol. 28 Núm. 1 (2008); 5-6
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/1/1
https://revistabiomedica.org/index.php/biomedica/article/view/1/487
oai:oai.revistabiomedica.org:article/2
2009-12-17T12:36:55Z
biomedica:ARTI
Survival analysis of cervical cancer patients
Supervivencia de pacientes con cáncer de cuello uterino tratadas en el Instituto Nacional de Cancerología
Pardo, Constanza
Cendales, Ricardo
análisis de supervivencia
neoplasias del cuello uterino
registros de mortalidad
mortalidad hospitalaria
vigilancia epidemiológica
Colombia.
survival analysis
uterine cervical neoplasms
mortality registries
hospital mortality
epidemiologic surveillance
Colombia
Introduction. Uterine cervical cancer is the first cause of incidence and mortality in Colombian women. Nearly 10% of all the cases in the country are treated at the Instituto Nacional de Cancerología. Evaluation of the institutional success rates is suggested.Objective. Patient survival over a 5 year period was summarized for those admitted for treatment of cervical cancer at the Institute in the year 2000.Materials and methods. All patients with cervical cancer at the Institute in 2000 were included in the survival analysis. Frequencies, central tendencies and dispersion measures were used to describe categorical and numerical variables. Survival analysis was performed by using Kaplan Meier and the multivariate Cox regression model.Results. During the study period, 651 patients with cervical cancer were treated. Among the 455 eligible patients, 303 (66%) were alive at the end of the study period. Mean survival time for patients who did not die was 3.69 years, with a standard deviation of 2.58 years. Cumulated five year overall survival probability was 58.8% and mean survival was 4.53 years. The only variable that significantly affected the survival function was the clinical stage at the time of the diagnosis.Conclusions. Overall survival results are similar to those described in other international institutions. If larger cohort studies were used, the power of the study can be increased in order to identify other factors associated with the prognosis.
Introducción. El cáncer de cuello uterino es el de mayor incidencia y la primera causa de mortalidad en las mujeres colombianas. Cerca de 10% de todos los casos del país son tratados en el Instituto Nacional de Cancerología. Se requiere evaluar la experiencia institucional.Objetivo. Describir la supervivencia global a cinco años de las pacientes con cáncer de cuello uterino tratadas en el Instituto Nacional de Cancerología durante el 2000.Materiales y métodos. Análisis de supervivencia que incluyó todas las pacientes con cáncer de cuello uterino que fueron tratadas en el Instituto Nacional de Cancerología en el 2000. Se emplearon frecuencias y medidas de tendencia central y de dispersión, para resumir las variables categóricas y numéricas, respectivamente. El análisis de supervivencia se realizó mediante el método de Kaplan-Meier y la regresión de Cox.Resultados. Se trataron 651 pacientes en el 2000. Entre las 455 pacientes elegibles, 303 (66%) estaban vivas al finalizar el período. El tiempo medio de seguimiento para las pacientes que no murieron fue de 3,69 años, con una desviación estándar de 2,58 años. La probabilidad acumulada de supervivencia global a 5 años fue de 58,8% y el tiempo medio de supervivencia fue de 4,53 años. La única variable que afectó significativamente la función de supervivencia en el análisis multivariado de Cox fue el estadio clínico al momento del diagnóstico.Conclusiones. Los resultados de supervivencia global son similares a los reportados en la literatura. Se recomienda desarrollar estudios en cohortes más grandes para aumentar la potencia del estudio e identificar otros factores de pronóstico.
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/2
10.7705/biomedica.v29i3.2
Biomedica; Vol. 29 No. 3 (2009); 437-447
Biomédica; Vol. 29 Núm. 3 (2009); 437-447
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/2/2
https://revistabiomedica.org/index.php/biomedica/article/view/2/290
/*ref*/<p>1. Ferlay J, Bray F, Pisani P, Parkin DM. Globocan 2002 cancer incidence, mortality and prevalence worldwide. IARC CancerBase No. 5, version 2.0. Lyon: IARC Press; 2004.</p> <p>2. República de Colombia, Sistema Nacional de Salud, Instituto Nacional de Cancerología. Normas técnicas y administrativas. Guía de implantación, detección y control de cáncer de cuello uterino. Bogotá: Imprenta Nacional; 1994.</p> <p>3. República de Colombia, Ministerio de Salud. Resolución 00412 de 2000 (25 de febrero), por la cual se establecen las actividades, procedimientos e intervenciones de demanda inducida y obligatorio cumplimiento y se adoptan las normas técnicas y guías de atención para el desarrollo de las acciones de protección específica y detección temprana y la atención de enfermedades de interés en salud pública. Diario oficial No. 49.956, 31 de marzo de 2000. Bogotá D.C.: Ministerio de Salud; 2000.</p> <p>4. República de Colombia, Ministerio de la Protección Social. Política nacional de salud sexual y reproductiva. Bogotá: Ministerio de la Protección Social; 2000. Fecha de consulta: 23 de octubre de 2008. Disponible en: http://www.minproteccionsocial.gov.co/vbecontent/library/documents/DocNewsNo15132DocumentNo1893.PDF.</p> <p>5. Eifel P, Berek J, Markman M. Cancer of the cervix, vagina, and vulva. In: DeVita V, Hellman S, Rosenberg S, editors. Cancer principles and practice of oncology. 8th edition. Philadelphia: Lippincott Williams & Wilkins; 2008. p. 1496-543.</p> <p>6. Pérez C, Kavanagh B. Uterine cervix. In: Halperin E, Pérez C, Brady L, editors. Pérez and Brady's principles and practice of radiation oncology. 5th edition. Philadelphia: Lippincott Williams & Wilkins; 2008. p. 1533-609.</p> <p>7. Sankaranarayanan R, Madhukar-Budukh A, Rajkumar R. Effective screening programs for cervical cancer in low- and middle-income developing countries. Bull World Health Organ. 2001;79:954-62.</p> <p>8. Instituto Nacional de Cancerología. Anuario estadístico 2004. Bogotá, D.C.: Instituto Nacional de Cancerología; 2005. Fecha de consulta: 23 de octubre de 2008. Disponible en: http://www.incancerologia.gov.co/documentos/2_9_2006_2_56_34_PM_Páginas%20interiores_total.pdf</p> <p>9. Dos Santos I. Introducción al análisis de la supervivencia. En: Agencia Internacional de Investigación sobre el Cáncer. Epidemiología del cáncer: principios y métodos. Lyon, Francia: Agencia Internacional de Investigación sobre el Cáncer (IARC); 1999. p. 279-93.</p> <p>10. Jensen OM, Parkin DM, Mac Lennan R, Muir CS, Skeet RG. Análisis de supervivencia. En: Registros de cáncer: principios y métodos. Publicación científica No. 95. Lyon, Francia: Agencia Internacional de Investigación sobre el Cáncer (IARC); 1995. p. 153-72.</p> <p>11. Lea JS, Sheets EE, Wenham RM, Duska LR, Coleman RL, Miller DS, et al. Stage IIB-IVB cervical adenocarcinoma: prognostic factors and survival. Gynecol Oncol. 2002;84:115-9.</p> <p>12. Farley JH, Hickey KW, Carlson JW, Rose GS, Kost ER, Harrison TA. Adenosquamous histology predicts a poor outcome for patients with advanced-stage, but not early-stage, cervical carcinoma.Cancer. 2003;97:2196-202.</p> <p>13. Quinn MA, Benedet JL, Odicino F, Maisonneuve P, Beller U, Creasman WT, et al. Carcinoma of the cervix uteri. FIGO 6th Annual report on the results of treatment in gynecological cancer. Int J Gynaecol Obstet. 2006;95(Suppl.1):S43-103.</p> <p>14. Céspedes JE, Jaramillo I, Martínez R, Olaya S, Reynales J, Uribe C, et al. Efectos de la reforma de la seguridad social en salud en Colombia sobre la equidad en el acceso y la utilización de servicios de salud. Rev Salud Pública. 2000;2:145-64.</p> <p>15. Rubin P, Williams J. Carcinoma de cérvix uterino. En: Rubin P, editor. Oncología clínica: Enfoque multi-disciplinario para médicos y estudiantes. Octava edición. Madrid: Elsevier Science; 2003. p. 463-77.</p> <p>16. Murphy G, Lawrencw W, Lenhard R. Oncología clínica. Manual de la American Cancer Society. Publicación científica No. 559. Washington, D.C.: Organización Panamericana de la Salud; 1996.</p> <p>17. Green J, Kirwan J, Tierney J, Vale C, Symonds P, Fresco L, et al. Concomitant chemotherapy and radiation therapy for cancer of the uterine cervix. Cochrane Database Syst Rev. 2005;CD002225.</p> <p>18. Reed N. The management of uterine sarcomas. Clin Oncol. 2008;20:470-78.</p>
oai:oai.revistabiomedica.org:article/3
2009-12-17T12:36:52Z
biomedica:EDIT
Influenza pandémica 2009-2010, ¿en qué podemos mejorar la respuesta?
De la Hoz, Fernando
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/3
10.7705/biomedica.v29i3.3
Biomedica; Vol. 29 No. 3 (2009); 337-338
Biomédica; Vol. 29 Núm. 3 (2009); 337-338
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/3/3
https://revistabiomedica.org/index.php/biomedica/article/view/3/270
/*ref*/Novel Swine-Origin Influenza A (H1N1) Virus Investigation Team, Dawood FS, Jain S, Finelli L, Shaw MW, Lindstrom S, et al. Emergence of a novel swine origin influenza A H1N1 virus in Humans. N Engl J Med. 2009;360:2605-15.<br />2. Trifonov V, Khiabanian H, Rabadan R. Geographic dependence, surveillance and origins of the 2009 influenza A H1N1 virus. N Engl J Med. 2009;361:115-9.<br />3. World Health Organization. Pandemic influenza A H1N1. Update 61. Fecha de consulta: 17 de agosto de 2009. Disponible en: http://www.who.int/csr/don/2009_08_12/en/index.html.<br />4. Panamerican Health Organization. Actualización regional. Pandemia H1N1 2009. Fecha de consulta: 14 de agosto de 2009. Disponible en: http://new.paho.org/hq/index.php?option=com_content&task=view&id=1702&Itemid=1167.<br />5. Ministerio de la Protección Social. Informe de prensa 103 de 2009. Fecha de consulta: 17 de agosto de 2009. Disponible en: http://www.minproteccionsocial.gov.co/VBeContent/NewsDetail.asp?ID=18841&IDCompany=3.<br />6. Miller M, Viboud C, Balinska M, Simonsen L. The signature features of influenza pandemics. Implications for policy. N Engl J Med. 2009;360:2595-8.<br />7. Centers for Disease Control and Prevention. Novel H1N1 vaccination recommendations. Fecha de consulta: 17 de agosto de 2009. Disponible en: http://www.cdc.gov/h1n1flu/vaccination/acip.htm.<br />8. Yamada T. Poverty, Wealth, and access to pandemic influenza vaccines. N Engl J Med. 2009. Fecha de consulta: 17 de agosto de 2009. Disponible en: http://content.nejm.org/cgi/content/full/NEJMp0906972
oai:oai.revistabiomedica.org:article/4
2009-12-17T12:36:52Z
biomedica:CASO
Acute intermittent porphyria presenting as spontaneous hemothorax
Hemotórax espontáneo: una forma inusual de presentación de la porfiria intermitente aguda
Buitrago, Juliana
Santa, Sandra Viviana
hemothorax
porphyria
acute intermittent
abdomen
acute
abdominal pain
porphobilinogen
hydroxymethylbilane synthase
hemotórax
porfiria intermitente aguda
abdomen agudo
dolor abdominal
porfobilinógeno
sintasa de hidroximetilbilano
The porphyrias are inherited disorders of the heme biosynthetic pathway. They are relatively rare and often misdiagnosed; however, acute episodes can be curtailed by early administration of heme arginate. Acute intermittent porphyria is the commonest of acute forms of porphyria. Here, a case is presented of a 23-year-old male with acute intermittent porphyria who came to the emergency clinic with an unexplained abdominal pain. In addition, he exhibited spontaneous hemothorax (two liters of blood accumulated in the chest) as an unusual manifestation of the disease. The most relevant aspects of acute intermittent porphyria are discussed, along with its epidemiology, diagnosis, clinical presentation and treatment. Complexities and diagnostic requirements in making a diagnosis of porphyria are described.
Las porfirias son un grupo de alteraciones metabólicas de la síntesis del hem, de carácter hereditario. Son condiciones relativamente raras, de difícil diagnóstico, pero con una respuesta impresionante al tratamiento y con buen pronóstico, si se identifican y tratan a tiempo. La más común de las formas agudas es la porfiria intermitente aguda.Se presenta el caso de un hombre de 23 años que consultó por dolor abdominal y que, concomitantemente presentaba un hemotórax espontáneo de dos litros, presentación inusual nunca antes descrita para la porfiria intermitente aguda.Se incluye una breve revisión de los aspectos más relevantes de la porfiria intermitente aguda, epidemiología, diagnóstico, clínica y manejo, además de una serie de reflexiones sobre cómo sospechar tempranamente el diagnóstico.
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/4
10.7705/biomedica.v29i3.4
Biomedica; Vol. 29 No. 3 (2009); 339-347
Biomédica; Vol. 29 Núm. 3 (2009); 339-347
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/4/4
https://revistabiomedica.org/index.php/biomedica/article/view/4/271
/*ref*/DeLoughery TG. Porphyria, acute intermittent. Fecha de consulta: marzo del 2008. Disponible en:http://www.emedicine.com/med/topic1880.htm<br />2. De Siervi A, Méndez M, Varela L, Rossetti MV, Parera V, Batlle A. Estudios genéticos de las porfirias agudas en Argentina. Acta Bioquím Clin Latinoam. 2002;36:505-13.<br />3. Thadani H, Deacon A, Peters T. Diagnosis and management of porphyria. BMJ. 2000;320:1647-51.<br />4. Kappas A, Sassa S, Galbraith RA, Nardaman Y. The porphyries. In: Scriver CR, Beaudet AL, Sly WS, Valle D, editors. The metabolic basis of inherited diseases. 6th edition. New York: McGraw- Hill; 1989. p. 1305-66.<br />5. McColl KE, Dover S, Fitzsimons E, Moore MR. Porphyrin metabolism and the porphyries. In: Weatherall DJ, Ledingham JC, Warrell DA, editors. Oxford Textbook of Medicine. Oxford: Oxford University Press; 1996. p. 1388-99.<br />6. Monterio H, Bechara EJH, Abdalla DS. Free radicals involvement in neurological porphyrias and lead poisoning. Mol Cell Biochem. 1991;103:73-84.<br />7. Bonkovsky HL. Advances in understanding and treating “the little imitador”, acute porphyria. Gastroenterology.1993;105:590-4.<br />8. Lindberg RL, Parcher C, Grandchamp B. Porphobilinogen deaminase deficiency in mice causes a neuropathy resembling that of human hepatic porphyria. Nat Genet.1996;12:195-9.<br />9. Hahn M, Gildemeister OS, Krauss GL, Pepe JA, Lambrecht RW, Donohue S, et al. Effects of new anticonvulsants medications on porphyrin in cultured liver cells: potential implications for patients with acute porphyria. Neurology.1997;49:97-106.<br />10. Sassa S. Understanding the porphyries. Fecha de consulta: 10 de noviembre de 2008. Disponible en: http://www.uptodate.com/patients/content/topic.do?topicKey=~E4oMR6..hWichZE
oai:oai.revistabiomedica.org:article/5
2009-12-17T12:36:53Z
biomedica:CASO
Middle ear adenoma
Adenoma del oído medio
Medina, Edwin Abraham
adenoma/patología
oído medio
inmunohistoquímica
diagnóstico diferencial
tumor carcinoide
Adenoma/pathology
ear
middle
immunohistochemistry
differential
diagnosis
carcinoid tumor
Middle ear neoplasms are rare lesions and difficult to diagnose due to limited information about their biology and the lack of standard criteria for their analysis. Herein, a middle ear neoplasm is described that became apparent because of its appearance in the external ear duct as it protruded from the middle ear through the eardrum. Following resection, the specimen was determined to be a benign epithelial tumor. Absence of adequate clinical information complicated the diagnosis; therefore,histochemistry and immunohistochemistry analyses were necessary to reach the final diagnosis of middle ear adenoma. Diagnostic criteria are proposed to properly diagnose these types of lesions.
Las neoplasias del oído medio son lesiones raras que, generalmente, plantean retos diagnósticos por la escasa información existente sobre su biología y la carencia de uniformidad de criterios para su análisis.Se presenta el caso de un tumor de oído observado clínicamente en el canal auditivo externo, el cual protruía del oído medio a través del tímpano, y en cuyo espécimen de resección se encontró un tumor epitelial benigno con una de sus superficies revestida por epitelio escamoso. La escasa información clínica inicial incrementó la dificultad diagnóstica y para su diagnóstico se requirió apoyo en técnicas de histoquímica e inmunohistoquímica. El diagnóstico definitivo fue adenoma del oído medio. Además, se hace una revisión del tema y se plantean algunas claves diagnósticas sobre este tipo de lesiones.
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/5
10.7705/biomedica.v29i3.5
Biomedica; Vol. 29 No. 3 (2009); 348-353
Biomédica; Vol. 29 Núm. 3 (2009); 348-353
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/5/5
https://revistabiomedica.org/index.php/biomedica/article/view/5/273
/*ref*/Stanley MW, Horwitz CA, Levinson RM, Sibley RK. Carcinoid tumors of the middle ear. Am J Clin Pathol. 1987;87:592-600.<br />2. Berns S, Pearl G. Middle ear adenoma. Arch Pathol Lab Med. 2006;130:1067-9.<br />3. Wassef M, Kanavaros P, Polivka M, Nemeth J, Monteil JP, Frachet B, et al. Middle ear adenoma. A tumor displaying mucinous and neuroendocrine differentiation. Am J Surg Pathol. 1989;13:838-47.<br />4. Orendorz-FrÄ
czkowska K, Jaworska M, Gawron W, Badowski R. Middle ear ceruminous adenoma as a rare cause of hearing loss and vertigo: Case reports. Auris Nasux Larinx. 2005;32:393-7.<br />5. Gunduz M, Yamanaka N, Saito T, Kuki K, Yokoyama M, Nakamine H. Middle ear adenoma with neuroendocrine differentiation. Auris Nasus Larynx. 2000;27:73-6.<br />6. Hale RJ, McMahon RFT, Whittaker JS. Middle ear adenoma: Tumour of mixed mucinous and neuroendocrine differentiation. J Clin Pathol. 1991;44:652-4.<br />7. Ribé A, Fernández PL, Ostertarg H, Clarós P, Bombí JA, Palacín A, et al. Middle ear adenoma (MEA): A report of two cases, one with predominant “plasmocitoid” features. Histopathology. 1997;30:359-64.<br />8. Mills SE, Fechner RE. Middle ear adenoma: A cytologically uniform neoplasm displaying a variety of architectural patterns. Am J Surg Pathol. 1984;8:677-85.<br />9. Torske KR, Thompson LD. Adenoma versus carcinoid tumor of the middle ear: a study of 48 cases and review of the literature. Mod Pathol. 2002;15:543-55.<br />10. Prophet EB, Mills B, Arrington JB, Sobin LH. Laboratory methods in histotechnology. Washington DC: Armed Forces Institute of Pathology/American Registry of Pathology; 1992. p. 151, 156-60, 219-20.<br />11. Rosai J. Rosai and Ackerman’s surgical pathology. 9th edition. Philadelphia: Mosby-Elsevier Inc.; 2004. p. 2774, 2776-7.<br />12. Wenig BM. The ear. En: Weidner N, editor. Modern surgical pathology. 1st edition. New York: Saunders-Elsevier Science; 2003. p. 285-6.<br />13. Mills SE. Tumors of the upper aerodigestive tract and ear. Atlas of tumor pathology. 3rd series. Fascicle 26. Washington D.C.: Armed Forces Institute of Pathology; 2000. p. 401-6, 431-4.<br />14. Wenig BM. The ear. In: Mills SE, editor. Sternberg’s diagnostic surgical pathology. 4th edition. Philadelphia: Lippincott Williams & Wilkins; 2004. p. 1053-4, 1058-60.<br />15. Gaffey MJ, Mills SE, Fechner RE, Intemann SR, Wick MR. Aggressive Papillary middle-ear tumor. A clinicopathologic entity distinct from middle-ear adenoma. Am J Surg Pathol. 1988;12: 790-7.<br />16. Lassaletta L, Patrón M, Olóriz J, Pérez R, Gavilán J. Avoiding misdiagnosis in ceruminous gland tumours. Auris Nasux Larinx. 2003;30:287-90.<br />17. Iqbal A, Newman P. Ceruminous gland neoplasia. Br J Plast Surg. 1998;51:317-20.<br />18. Thompson LD, Nelson BL, Barnes EL. Cerominous adenomas. A clinicopathologic study of 41 cases with a review of literature. Am J Surg Pathol. 2004;28:308-18.<br />19. Kuwabara H, Haginomori SI, Takamaki A, Ito K, Takenaka H, Kurisu Y, et al. Lipomatous pleomorphic adenoma of the cerominous gland. Pathol Int. 2006;56:51-3.<br />20. Conlin PA, Mira JL, Graham SC, Kaye KS, Cordero J. Ceruminous gland adenoid cystic carcinoma with contralateral metastasis and the brain. Arch Pathol Lab Med. 2002;126:87-9.
oai:oai.revistabiomedica.org:article/6
2009-12-17T12:36:55Z
biomedica:TEMA
Metacaspases and their role in the life cycle of human protozoan parasites
Las metacaspasas y su rol en la vida y muerte de los parásitos protozoarios humanos
González, Iveth J.
caspasa
apoptosis
Plasmodium
Leishmania
Trypanosoma
malaria
caspases
apoptosis
Plasmodium
Leishmania
Trypanosoma
malaria
Metacaspases are caspase-related cysteine-proteases that are present in organisms devoid of caspases such as plants, yeast, and protozoan parasites. Since caspases are important effector molecules in mammalian apoptosis, the possible role of metacaspases in programmed cell death has been evaluated in the organisms where they are expressed. In some species of the human protozoan parasites Trypanosoma spp. and Leishmania spp., metacaspases have been involved in programmed cell death, although a role of metacaspases in recycling processes in T. brucei has also been suggested. Metacaspases are also expressed in Plasmodium spp., however their role in these organisms is still unknown. More than one metacaspase gene is present in some of these parasites, which suggests that these proteins are physiologically redundant or have different functions depending on their localization and protein interactions. The catalytic activity of metacaspases is different from that of caspases—again noting that metacaspase genes are absent in mammals. These characteristics make metacaspases and their activating mechanisms interesting subjects of research in the development of new drug targets for the treatment of trypanosomiasis, leishmaniasis, and malaria. A summary of the literature on metacaspases is provided, and Latin American researchers are encouraged to more actively explore the metacaspase potential.
Las metacaspasas son proteasas de cisteína similares estructuralmente a las caspasas y cuyos genes están presentes en organismos carentes de caspasas, tales como plantas, levaduras y parásitos protozoarios.El bien conocido papel de varias caspasas en la apoptosis de células de mamíferos, ha motivado el estudio del posible rol de las metacaspasas en la muerte celular programada de los organismos en los cuales se expresan. Así, por ejemplo, las metacaspasas de los parásitos protozoarios humanos de los géneros Trypanosoma y Leishmania han sido implicadas en muerte celular programada. Sin embargo, algunos estudios en T. brucei señalan que estas proteínas podrían estar involucradas en otras funciones biológicas tales como procesos de reciclaje. Los parásitos del género Plasmodium también expresan metacaspasas, pero aún se sabe poco sobre su función.La presencia de más de una metacaspasa en algunos de estos microorganismos, ha llevado a especular que estas proteínas podrían tener funciones fisiológicamente redundantes o diferentes de acuerdo con su localización e interacción con otras moléculas. Los estudios recientes han demostrado que la especificidad catalítica de las metacaspasas difiere de aquélla de las caspasas. Esta característica, sumada a la ausencia de sus genes codificadores en el genoma de mamíferos, hace de las metacaspasas y de sus mecanismos de activación un área interesante de investigación en la identificación de nuevos blancos terapéuticos en los parásitos causantes de tripanosomiasis, leishmaniasis y malaria.La presente revisión resume la información disponible sobre las metacaspasas y busca motivar la generación de masa crítica en este tema en los países hispanohablantes.
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/6
10.7705/biomedica.v29i3.6
Biomedica; Vol. 29 No. 3 (2009); 485-493
Biomédica; Vol. 29 Núm. 3 (2009); 485-493
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/6/6
https://revistabiomedica.org/index.php/biomedica/article/view/6/297
/*ref*/Uren AG, O’Rourke K, Aravind LA, Pisabarro MT, Seshagiri S, Koonin EV, et al. Identification of paracaspases and metacaspases: two ancient families of caspase-like proteins, one of which plays a key role in MALT lymphoma. Mol Cell. 2000;6:961-7.<br />2. Lavrik IN, Golks A, Krammer PH. Caspases: pharmacological manipulation of cell death. J Clin Invest. 2005;115:2665-72.<br />3. Riedl SJ, Shi Y. Molecular mechanisms of caspase regulation during apoptosis. Nat Rev Mol Cell Biol. 2004;5:897-907.<br />4. MacFarlane M, Williams AC. Apoptosis and disease: a life or death decision. EMBO Rep. 2004;5:674-8.<br />5. Yuan J, Shaham S, Ledoux S, Ellis HM, Horvitz HR. The C. elegans cell death gene Ced-3 encodes a protein similar to mammalian interleukin-1β-converting enzyme. Cell. 1993;75:641-52.<br />6. Kumar S, Doumanis J. The fly caspases. Cell Death Differ. 2000;7:1039-44.<br />7. Debrabant A, Lee N, Bertholet S, Duncan R, Nakhasi HL. Programmed cell death in trypanosomatids and other unicellular organisms. Int J Parasitol. 2003;33:257-67.<br />8. Koonin EV, Aravind L. Origin and evolution of eukaryotic apoptosis: the bacterial connection. Cell Death Differ. 2002;9:394-404.<br />9. Vercammen D, Declercq W, Vandenabeele P, van Breusegem F. Are metacaspases caspases? J Cell Biol. 2007;179:375-80.<br />10. Vercammen D, van de Cotte B, De Jaeger G, Eeckhout D, Casteels P, Vandepoele K, et al. Type II metacaspases Atmc4 and Atmc9 of Arabidopsis thaliana cleave substrates after arginine and lysine. J Biol Chem. 2004;279:45329-36.<br />11. Madeo F, Herker E, Maldener C, Wissing S, Lachelt S, Herlan M, et al. A caspase-related protease regulates apoptosis in yeast. Mol Cell. 2002;9:911-7.<br />12. González IJ, Desponds C, Schaff C, Mottram JC, Fasel N. Leishmania major metacaspase can replace yeast metacaspase in programmed cell death and has arginine-specific cysteine peptidase activity. Int J Parasitol. 2007;37:161-72.<br />13. Lee N, Gannavaram S, Selvapandiyan A, Debrabant A. Characterization of metacaspases with trypsin-like activity and their putative role in the programmed cell death in the protozoan parasite Leishmania. Eukaryot Cell. 2007;6:1745-57.<br />14. Trzyna WC, Legras XD, Cordingley JS. A type-1 metacaspase from Acanthamoeba castellanii. Microbiol Res. 2008;163:414-23.<br />15. Bidle KD, Haramaty L, Barcelos E Ramos J, Falkowski P. Viral activation and recruitment of metacaspases in the unicellular coccolithophore, Emiliania huxleyi. Proc Natl Acad Sci USA. 2007;104:6049-54.<br />16. Okamoto OK, Hastings JW. Genome-wide analysis of redox-regulated genes in a dinoflagellate. Gene. 2003;321:73-81.<br />17. Herker E, Jungwirth H, Lehmann KA, Maldener C, Frohlich KU, Wissing S, et al. Chronological aging leads to apoptosis in yeast. J Cell Biol. 2004;164:501-7.<br />18. Bettiga M, Calzari L, Orlandi I, Alberghina L, Vai M. Involvement of the yeast metacaspase Yca1 in ubp10Delta-programmed cell death. FEMS Yeast Res. 2004;5:141-7.<br />19. Mazzoni C, Herker E, Palermo V, Jungwirth H, Eisenberg T, Madeo F, et al. Yeast caspase 1 links messenger RNA stability to apoptosis in yeast. EMBO Rep. 2005;6:1076-81.<br />20. Weinberger M, Ramachandran L, Feng L, Sharma K, Sun X, Marchetti M, et al. Apoptosis in budding yeast caused by defects in initiation of DNA replication. J Cell Sci. 2005;118:3543-53.<br />21. Mitsui K, Nakagawa D, Nakamura M, Okamoto T, Tsurugi K. Valproic acid induces apoptosis dependent of Yca1p at concentrations that mildly affect the proliferation of yeast. FEBS Lett. 2005;579:723-7.<br />22. Khan MA, Chock PB, Stadtman ER. Knockout of caspase-like gene, YCA1, abrogates apoptosis and elevates oxidized proteins in Saccharomyces cerevisiae. Proc Natl Acad Sci USA. 2005;102:17326-31.<br />23. Wadskog I, Maldener C, Proksch A, Madeo F, Adler L. Yeast lacking the SRO7/SOP1-encoded tumor suppressor homologue show increased susceptibility to apoptosis-like cell death on exposure to NaCl stress. Mol Biol Cell. 2004;15:1436-44.<br />24. Flower TR, Chesnokova LS, Froelich CA, Dixon C, Witt SN. Heat shock prevents alpha-synuclein-induced apoptosis in a yeast model of Parkinson’s disease. J Mol Biol. 2005;351:1081-100.<br />25. Silva RD, Sotoca R, Johansson B, Ludovico P, Sansonetty F, Silva MT, et al. Hyperosmotic stress induces metacaspase- and mitochondria-dependent apoptosis in Saccharomyces cerevisiae. Mol Microbiol. 2005;58:824-34.<br />26. Ivanovska I, Hardwick JM. Viruses activate a genetically conserved cell death pathway in a unicellular organism. J Cell Biol. 2005;170:391-9.<br />27. Suarez MF, Filonova LH, Smertenko A, Savenkov EI, Clapham DH, von Arnold S, et al. Metacaspase-dependent programmed cell death is essential for plant embryogenesis. Curr Biol. 2004;14:R339-40.<br />28. Hoeberichts FA, ten Have A, Woltering EJ. A tomato metacaspase gene is upregulated during programmed cell death in Botrytis cinerea-infected leaves. Planta. 2003;217:517-22.<br />29. Watanabe N, Lam E. Two Arabidopsis metacaspases AtMCP1b and AtMCP2b are arginine/lysine-specific cysteine proteases and activate apoptosis-like cell death in yeast. J Biol Chem. 2005;280:14691-9.<br />30. Richie DL, Miley MD, Bhabhra R, Robson GD, Rhodes JC, Askew DS. The Aspergillus fumigatus metacaspases CasA and CasB facilitate growth under conditions of endoplasmic reticulum stress. Mol Microbiol. 2007;63:591-604.<br />31. Meslin B, Barnadas C, Boni V, Latour C, De Monbrison F, Kaiser K, et al. Features of apoptosis in Plasmodium falciparum erythrocytic stage through a putative role of PfMCA1 metacaspase-like protein. J Infect Dis. 2007;195:1852-9.<br />32. Le Chat L, Sinden RE, Dessens JT. The role of metacaspase 1 in Plasmodium berghei development and apoptosis. Mol Biochem Parasitol. 2007;153:41-7.<br />33. Ambit A, Fasel N, Coombs GH, Mottram JC. An essential role for the Leishmania major metacaspase in cell cycle progression. Cell Death Differ. 2008;15:113-22.<br />34. Kosec G, Álvarez VE, Aguero F, Sánchez D, Dolinar M, Turk V, et al. Metacaspases of Trypanosoma cruzi: possible candidates for programmed cell death mediators. Mol Biochem Parasitol. 2006;145:18-28.<br />35. Mottram JC, Helms MJ, Coombs GH, Sajid M. Clan CD cysteine peptidases of parasitic protozoa. Trends Parasitol. 2003;19:182-7.<br />36. Szallies A, Kubata BK, Duszenko M. A metacaspase of Trypanosoma brucei causes loss of respiration competence and clonal death in the yeast Saccharomyces cerevisiae. FEBS Lett. 2002;517:144-50.<br />37. Helms MJ, Ambit A, Appleton P, Tetley L, Coombs GH, Mottram JC. Bloodstream form Trypanosoma brucei depend upon multiple metacaspases associated with RAB11-positive endosomes. J Cell Sci. 2006;119:1105-17.<br />38. Figarella K, Rawer M, Uzcategui N L, Kubata BK, Lauber K, Madeo F, et al. Prostaglandin D2 induces programmed cell death in Trypanosoma brucei bloodstream form. Cell Death Differ. 2005;12:335-46.<br />39. Belenghi B, Romero-Puertas MC, Vercammen D, Brackenier A, Inze D, Delledonne M, et al. Metacaspase activity of Arabidopsis thaliana is regulated by S-nitrosylation of a critical cysteine residue. J Biol Chem. 2007;282:1352-8.<br />40. Moss CX, Westrop GD, Juliano L, Coombs GH, Mottram JC. Metacaspase 2 of Trypanosoma brucei is a calcium-dependent cysteine peptidase active without processing. FEBS Lett. 2007;581:5635-9.<br />41. Jäättelä M. Programmed cell death: many ways for cells to die decently. Ann Med. 2002;34:480-8.<br />42. Bursch W. Multiple cell death programs: Charon’s lifts to Hades. FEMS Yeast Res. 2004;5:101-10.<br />43. Vaux DL, Strasser A. The molecular biology of apoptosis. Proc Natl Acad Sci USA. 1996;93:2239-44.<br />44. Lee N, Bertholet S, Debrabant A, Muller J, Duncan R, Nakhasi HL. Programmed cell death in the unicellular protozoan parasite Leishmania. Cell Death Differ. 2002;9:53-64.<br />45. Lindoso JA, Cotrim PC, Goto H. Apoptosis of Leishmania (Leishmania) chagasi amastigotes in hamsters infected with visceral leishmaniasis. Int J Parasitol. 2004;34:1-4.<br />46. Wanderley JL, Benjamin A, Real F, Bonomo A, Moreira ME, Barcinski MA. Apoptotic mimicry: an altruistic behavior in host/Leishmania interplay. Braz J Med Biol Res. 2005;38:807-12.<br />47. van Zandbergen G, Bollinger A, Wenzel A, Kamhawi S, Voll R, Klinger M, et al. Leishmania disease development depends on the presence of apoptotic promastigotes in the virulent inoculum. Proc Natl Acad Sci USA. 2006;103:13837-42.<br />48. Vercammen D, Belenghi B, van de Cotte B, Beunens T, Gavigan JA, De Rycke R, et al. Serpin1 of Arabidopsis thaliana is a suicide inhibitor for metacaspase 9. J Mol Biol. 2006;364:625-36.
oai:oai.revistabiomedica.org:article/7
2009-12-17T12:36:53Z
biomedica:ARTI
Effectiveness of cytology-based cervical cancer screening in the Colombian health system
Efectividad de la citología cérvico-uterina para la detección temprana de cáncer de cuello uterino en el marco del sistema de salud de Colombia
Murillo, Raúl
Cendales, Ricardo
Wiesner, Carolina
Piñeros, Marion
Tovar, Sandra
neoplasias del cuello uterino
tamización masiva
evaluación de programas y proyectos de salud
citología
Colombia
Uterine cervical neoplasms
mass screening
program evaluation
cytology
Colombia
Introduction. Despite the implementation of cytological screening since 1991, cervical cancer continuous to be the leading cause of cancer mortality among Colombian women.Objectives. The effectiveness of cytology-based cervical cancer screening was subjected to review in the context of the Colombian health system.Materials and methods. A case-control study was done. Invasive cervical cancer cases between 25-69 years were recruited and histopathological confirmation was required. Controls without invasive cancer were matched by age and neighborhood. Cases and controls were recruited in four Colombian provinces representing different settings for cervical cancer control with respect to program performance and mortality rates. The cases were randomly selected from the pathology in each province (year 2005). A survey of risk factors and cytology history in the previous 72 months was conducted.Results. Fifty cases and 50 controls in each department were enrolled for a total of 400 subjects. The average age was 48.4 years, illiteracy 12.5%, and persons without health insurance 13.8%.The average number of Pap-smears was higher among controls (p<0.01). Cases with a Pap-smear in the previous 36 months was nearly half (49.5%). Oral contraceptives and the lack of cytology were associated with invasive cervical cancer.Conclusions. Cytology-based screening continued to be effective for early detection of cervical cancer in Colombia but its effectiveness was determined by quality of Pap-smears rather than by screening coverage. Governmental guidelines need to be revisited. Case-control studies provided a useful tool for evaluation of the screening program.
Introducción. El cáncer de cuello uterino continúa siendo la primera causa de muerte por cáncer en mujeres colombianas, a pesar de la implementación desde 1991 de la detección temprana basada en la citología.Objetivos. Evaluar la efectividad de la citología cérvico-uterina en Colombia.Materiales y métodos. Se realizó un estudio de casos y controles (de población), equiparado por edad y entorno social. Los casos fueron mujeres de 25 a 69 años con cáncer invasor y los controles, mujeres sin cáncer invasor. Se trabajó en cuatro departamentos como escenarios diferenciales según el nivel de organización de la detección temprana y la mortalidad por esta causa. Los casos se seleccionaron aleatoriamente de los registros de patología en cada departamento (2005). Se aplicó una encuesta sobre los factores de riesgo y la historia de las citologías en los 72 meses previos.Resultados. Se incluyeron 50 casos y 50 controles por departamento (400 sujetos). El promedio de edad fue de 48,4 años, el analfabetismo de 12,5% y las personas sin aseguramiento de 13,8%. El promedio de citologías fue más alto en los controles que en los casos (p<0,01). El porcentaje de casos con antecedente de citología fue de 49,5%. El uso de anticonceptivos y la falta de práctica de la citología estuvieron asociados con cáncer invasor (OR=2,53 y 3,54, respectivamente).Conclusiones. La citología sigue siendo efectiva en la detección temprana del cáncer de cuello uterino. La efectividad está determinada más por la calidad de la prueba que por las coberturas de población. Es necesario revisar la normatividad del país. Los estudios de casos y controles son una herramienta útil en la evaluación de programas.
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/7
10.7705/biomedica.v29i3.7
Biomedica; Vol. 29 No. 3 (2009); 354-361
Biomédica; Vol. 29 Núm. 3 (2009); 354-361
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/7/7
https://revistabiomedica.org/index.php/biomedica/article/view/7/277
/*ref*/Kitchener H, Castle P, Cox J. Achievements and limitation of cervical cytology screening. Vaccine. 2006;24:63-70.<br />2. Ferlay J, Bray F, Pisani P, Parkin DM. Cancer incidence, mortality and prevalence worldwide. Lyon: IARC Press; 2002.<br />3. Sankaranarayanan R, Madhukar-Budukh A, Rajkumar R. Effective screening programmes for cervical cancer in low- and middle-income developing countries. Bull World Health Organ. 2001;79:954-62.<br />4. Murillo R, Almonte M, Pereira A, Ferrer E, Gamboa O, Jerónimo J, et al. Cervical cancer screening programs in Latin America and the Caribbean. Vaccine. 2008;26:L37-48.<br />5. Aristizábal N, Cuello C, Correa P, Collazos T, Haenszel W. The impact of vaginal cytology on cervical cancer risks in Cali, Colombia. Int J Cancer. 1984;34:5-9.<br />6. Liu S, Semenciw R, Probert A, Mao Y. Cervical cancer in Canada: changing patterns in incidence and mortality. Int J Gynecol Cancer. 2001;11:24-31.<br />7. Murillo R. Control del cáncer de cuello uterino en Colombia: triunfos y desafíos de la tamización basada en la citología cérvico-uterina. Biomédica. 2008;28:468-70.<br />8. Piñeros M, Hernández G, Bray F. Increasing mortality rates of common malignancies in Colombia: an emerging problem. Cancer. 2004;101:2285-92.<br />9. Murillo R, Piñeros M, Hernández G. Atlas de mortalidad por cáncer en Colombia. Bogotá: Instituto Nacional de Cancerología, Instituto Geográfico Agustín Codazzi; 2004.<br />10. Wiesner C, Murillo R, Piñeros M, Tovar S, Cendales R, Gutiérrez MC. El control del cáncer cervicouterino en Colombia: percepción de los actores del sistema de salud. Rev Panam Salud Pública. 2008; en imprenta.<br />11. Herrero R, Brinton LA, Reeves WC, Brenes MM, de Britton RC, Gaitan E, et al. Screening for cervical cancer in Latin America: a case-control study. Int J Epidemiol. 1992;21:1050-6.<br />12. Hernández-Ávila M, Lazcano-Ponce EC, de Ruiz PA, Romieu I. Evaluation of the cervical cancer screening programme in Mexico: a population-based case-control study. Int J Epidemiol. 1998;27:370-6.<br />13. Zappa M, Visioli CB, Ciatto S, Iossa A, Paci E, Sasieni P. Lower protection of cytological screening for adenocarcinomas and shorter protection for younger women: the results of a case-control study in Florence. BJC. 2004;90:1784-6.<br />14. Sasieni P, Adams J, Cuzick J. Benefit of cervical screening at different ages: evidence from the UK audit. Of screening histories. BJC. 2003;89:88-93.<br />15. Andrae B, Kemetli L, Sparén P, Silfverdal L, Strander B, Ryd W, et al. Screening-preventable cervical cancer risks: evidence from a nationwide audit in Sweden. J Natl Cancer Inst. 2008;100:622-9.<br />16. Piñeros M, Cendales R, Murillo R, Wiesner C, Tovar S. Cobertura de la citología de cuello uterino y factores relacionados en Colombia, 2005. Rev Salud Pública (Bogotá). 2007;9:327-41.<br />17. Lazcano-Ponce EC, Moss S, Alonso P, Salmerón J, Hernández M. Cervical cancer screening in developing countries: why is it ineffective? The case of Mexico. Arch Med Res. 1999;30:240-50.<br />18. Lewis MJ. A situational analysis of cervical cancer in Latin America and the Caribbean. Washington D.C.: Pan American Health Organization; 2004.<br />19. Gamboa OA, Chicaíza L, García-Molina M, Díaz J, González M, Murillo R, et al. Cost-effectiveness of conventional cytology and HPV-DNA testing for cervical-cancer screening in Colombia. Salud Pub Mex. 2008;50:276-85.
oai:oai.revistabiomedica.org:article/8
2009-12-17T12:36:54Z
biomedica:ARTI
Efficacy of Orbscan II® and Pentacam® topographers by a repeatability analysis when assessing elevation maps in candidates to refractive surgery
Eficacia del Orbscan II y Pentacam en la evaluación de los mapas de elevación en candidatos a cirugía refractiva mediante un análisis de repetibilidad
Blanco, Claudia
Núñez, María Ximena
córnea
topografía de la córnea
queratocono
reproducibilidad de resultados
sesgo de selección
eficacia
cornea
corneal topography
keratoconus
reproducibility of results
selection bias
efficacy
Introduction: Anterior and posterior corneal elevations are measurements used to detect keratoconus suspects.Purpose: To determine the efficacy of Orbscan II® and Pentacam® when assessing their elevation maps.Materials and methods: The efficacy of the Orbscan II and Pentacam measuring the anterior and posterior corneal elevations were evaluated in a sample of 68 eyes. The concordance between the two devices and the coefficient of repeatability were measured following the parameters of the British Standard Institution by the Bland-Altman concordance analysis and the Lin concordance correlation coefficient.Results: The coefficient of repeatability at the point of maximum anterior elevation was 68.29% with the Orbscan and 24.20% with the Pentacam. The concordance correlation coefficient was 0.64 (CI 95%: 0.48-0.76) with the Orbscan and 0.94 with the Pentacam (CI 95%: 0.91-0.96). The coefficient of repeatability at the point of maximum posterior elevation was 38.7% with the Orbscan and 68.0% with the Pentacam. The concordance correlation coefficient was 0.69 with the Orbscan (CI 95%: 0.55-0.80) with a precision of 0.71 and an accuracy of 0.97, and 0.24 with the Pentacam (CI 95%: 0.00-0.45) with a precision of 0.24 and an accuracy of 0.99.Conclusions: Measurement of the point of maximum posterior elevation is better with the Orbscan II and less precise with the Pentacam. The random error can be reduced by using the mean of three assessments and can serve as a guide in the search of diagnostic devices with minimum absolute relative error in all measurements.
Introducción. La elevación posterior es una de las medidas usadas para detectar pacientes con sospecha de queratocono.Objetivo. Determinar la eficacia del Orbscan II y Pentacam en la evaluación de los mapas de elevación.Materiales y métodos. Se evaluaron 68 ojos con Orbscan II y Pentacam. Con parámetros del British Standard Institution, se midieron el coeficiente de repetibilidad mediante un análisis de concordancia con el método de Bland-Altman y el coeficiente de correlación de concordancia de Lin. Se midió la concordancia entre ambos equipos.Resultados. El coeficiente de repetibilidad del punto de máxima elevación anterior en Orbscan fue de 68,29% y de 24,20% en Pentacam. El coeficiente de correlación de concordancia fue de 0,64 (IC95% 0,48-0,76) en Orbscan y en Pentacam fue de 0,94 (IC95% 0,91-0,96). El coeficiente de repetibilidad del punto de máxima elevación posterior en Orbscan fue de 38,69% y en Pentacam fue 68,03%. El coeficiente de correlación de concordancia en Orbscan fue de 0,69 (IC95% 0,55-0,80) con una precisión de 0,71 y una exactitud de 0,97, y en Pentacam fue de 0,24 (IC95% 0,00-0,45) con una precisión de 0,24 y una exactitud de 0,99.Conclusiones. La eficacia de Orbscan II y Pentacam en la evaluación del punto de máxima elevación posterior resulta afectada por la imprecisión de la medida y es peor en el Pentacam. Este error aleatorio se puede manejar usando la media de tres mediciones y nos orienta a la búsqueda de equipos en los que el error relativo absoluto sea el menor posible en todas las medidas que ofrezca.
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/8
10.7705/biomedica.v29i3.8
Biomedica; Vol. 29 No. 3 (2009); 362-368
Biomédica; Vol. 29 Núm. 3 (2009); 362-368
2590-7379
0120-4157
eng
spa
https://revistabiomedica.org/index.php/biomedica/article/view/8/8
https://revistabiomedica.org/index.php/biomedica/article/view/8/9
https://revistabiomedica.org/index.php/biomedica/article/view/8/278
/*ref*/Rao S, Raviv T, Majmudar PA, Epstein RJ. Role of Orbscan II in screening keratoconus suspects before refractive corneal surgery. Ophthalmology. 2002;109:1642-6.<br />2. Turner T. What corneal topography can tell you about corneal shape. In: Drummond AE, editor. Customized corneal ablation: The quest for supervision.1st edition. Grove Road: Slack Inc; 2001. p. 11-32.<br />3. Jain R, Dilraj G, Grewal SP. Repeatability of corneal parameters with Pentacam after laser in situ keratomileusis. Indian J Ophthalmol. 2007;55:341-7.<br />4. Shankar H, Taranath D, Santhirathelagan CT, Pesudovs K. Anterior segment biometry with Pentacam: comprehensive assessment of repeatability of automated measurements. J Cataract Refract Surg. 2008; 34: 103-13.<br />5. Lackner B, Schmidinger G, Pieh S, Funovics MA, Skorpik C. Repeatability and reproducibility of central corneal thickness measurement with Pentacam, Orbscan, and Ultrasound. Optom Vis Sci. 2005;82:892-9.<br />6. Chen D, Lam AK. Intrasession and intersession repeatability of the Pentacam system on posterior corneal assessment in the normal human eye. J Cataract Refract Surg. 2007;33:448-54.<br />7. Carvajal R. Medición. En: Carvajal A, Torres C, Pubiano J, editores. Estadística para análisis epidemiológico.1 edición. Cali: Catorse; 2004. p. 18-32.<br />8. British Standards Institution. Accuracy (trueness and precision) of measurement methods and results: general principles and definitions. BS ISO 5725 part 1. London; HMO; 1994.<br />9. British Standards Institution. Accuracy (trueness and precision) of measurement methods and results: basic methods for the determination of repeatability and reproducibility of a standard measurement method. BS ISO 5725 part 2. London: HMO; 1994.<br />10. Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet. 1986;8:307-10.<br />11. Lin LI. A concordance correlation coefficient to evaluate reproducibility. Biometrics. 1989;45:255-68.<br />12. Lin LI. A note on the concordance correlation coefficient. Biometrics. 2000;56:324-5.<br />13. Fam HB, Lim KL. Corneal elevation indices in normal and keratoconic eyes. J Cataract Refract Surg. 2006;32:1281-7.<br />14. Hashemi H, Mehravaran S. Corneal changes after laser refractive surgery for myopia: comparison of Orbscan II and Pentacam findings. J Cataract Refract Surg. 2007;33:841-7.<br />15. Quisling S, Sjoberg S, Zimmerman B, Goins K, Sutphin J. Comparison of Pentacam and Orbscan IIz on posterior curvature topography measurements in keratoconus eyes. Ophthalmology. 2006;113:1629-32.
oai:oai.revistabiomedica.org:article/9
2009-12-17T12:36:54Z
biomedica:ARTI
Adverse events associated with tramadol and dipirona administration in a level III hospital
Detección de efectos secundarios asociados a la administración de tramadol y dipirona en un hospital de alta complejidad
Montoya, Giovanny
Vaca, Claudia
Parra, María Fernanda
dipirona/efectos secundarios
tramadol/efectos secundarios
costos en medicamentos
farmacoepidemiología
Dipyrone/adverse effects
tramadol/adverse effects
drug costs pharmaco-epidemiology
Introduction. The efficacy and safety of pharmaceutical drugs such as dipirone and tramadol must be a primary objective in the post-marketing period and as they are used in specific population groups.Objectives. The frequency of adverse effects (including therapeutic failure) with the medications tramadol and dipirona were described and estimated.Material and methods. At the Hospital Universitario de la Samaritana, Bogotá, D.C., Colombia, adverse events associated with dipirone and tramadol were rigorously tracked in patients hospitalized in the internal medicine, as well as the orthopedics and surgery departments. For a period of six months, data were collected by means of the Instituto Nacional de Vigilancia Médica y Alimentos (INVIMA) standard report form. Direct costs of adverse event treatment to the patient were calculated.Results. Adverse reactions were detected 213 times in 171 (8.4%) of the 2,547 patients admitted to the services (incidence rate. Of these instances, 53.4% were rated as possible for dipirone and 46.82% for tramadol. Of the total, 0.6% (16 cases) were classes as serious adverse events. The gastrointestinal system was the most affected, with the incidences of adverse events for dipirone of 27%) and tramadol of 42.9%. The total cost generated by the medical response to the 213 adverse events was estimated to be US$14,346.53.Conclusions. An unacceptable level of preventable adverse events was described that impacted the well-being of patients, as well as the costs associated with remedial treatment. These data recommend that institutional pharmacovigilance programs be required.
Introducción. Un objetivo prioritario después de la comercialización de medicamentos, como la dipirona y el tramadol, en grupos particulares de población, como el colombiano, es garantizar la eficacia y la seguridad.Objetivo. Describir y estimar la frecuencia de efectos secundarios, incluida la falla terapéutica, asociados al uso de tramadol y a la dipirona en el Hospital Universitario de La Samaritana (III nivel).Materiales y métodos. Se hizo seguimiento intensivo de los efectos secundarios asociados a la dipirona y al tramadol en los pacientes hospitalizados en los Servicios de Medicina Interna, Ortopedia y Cirugía, durante un período de seis meses como parte de un proyecto a un año. La información se recolectó mediante el formato para reporte al Instituto Nacional de Vigilancia Médica y Alimentos, INVIMA. La probabilidad de causalidad se estableció mediante el algoritmo de la Organización Mundial de la Salud. Se calcularon los costos directos desde la perspectiva del pagador.Resultados. Se detectaron 213 efectos secundarios en 171 de los 2.547 pacientes que ingresaron a los servicios (proporción de incidencia, 8,4%). El 53,4% se clasificó como posible para la dipirona y 46,82% para el tramadol; el 0,62%, (16 casos) correspondió a efectos secundarios serios. El sistema más frecuentemente afectado fue el gastrointestinal: dipirona, 27%, y tramadol, 42,9%. El costo generado por la atención de los efectos secundarios a los medicamentos del estudio fue de US$ 14.346,53.Conclusiones. El impacto negativo de los efectos secundarios de los medicamentos, los recursos que se emplean en su atención y la capacidad de prevenirlos, demuestran que se requieren programas institucionales de farmacovigilancia.
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/9
10.7705/biomedica.v29i3.9
Biomedica; Vol. 29 No. 3 (2009); 369-381
Biomédica; Vol. 29 Núm. 3 (2009); 369-381
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/9/10
https://revistabiomedica.org/index.php/biomedica/article/view/9/280
/*ref*/Hamerschlak N, Cavalcanti A. Neutropenia, agranulocytosis and dipyrone. Sao Paulo Med J. 2005;123:247-9.<br />2. Schönhöfer P, Offerhaus L, Herxheimer A. Dipyrone and agranulocytosis: what is the risk? Lancet. 2003; 361:968-9.<br />3. Plager M. Las preguntas más frecuentes acerca de Novalgina®. Sanofi-Aventis. Fecha de consulta: 5 de noviembre de 2006. Disponible en: http://en.sanofi-aventis.com/publications/publications.asp<br />4. Edwards JE, McQuay HJ. Dipyrone and agranulocytosis: what is the risk? Lancet. 2002:360:1438.<br />5. Sollero L. Incidence of agranulocytosis and the use of dipyrone in Brazil. Rev Bras Pesquisas Med Biol. 1976;9:79-86.<br />6. Hamerschlak N, Maluf E, Pasquini R, Eluf-Neto J, Moreira FR, Cavalcanti AB, et al. Incidence of aplastic anemia and agranulocytosis in Latin America: the LATIN study. Sao Paulo Med J. 2005;123:101-4.<br />7. Grond S, Sablotzki A. Clinical pharmacology of tramadol. Clin Pharmacokinet. 2004;43:879-923.<br />8. Tribiño G, Maldonado C, Segura O, Díaz J. Costos directos y aspectos clínicos de las reacciones adversas a medicamentos en pacientes hospitalizados en el servicio de medicina interna de una institución de tercer nivel de Bogotá. Biomédica. 2006;26:31-41.<br />9. Grupo de Farmacovigilancia INVIMA/UN. Boletín de Farmacovigilancia. No. 11. Fecha de consulta: 28 de septiembre 28 de 2006. Disponible en http://web.invima.gov.co/Invima//farmacovigilancia/docs_boletines/BOLETIN%2011.pdf<br />10. Segura O, Maldonado C. Las reacciones adversas a medicamentos: una aproximación desde el punto de vista económico. Biomédica. 2003;23:401-7.<br />11. Hunziker T, Bruppacher R, Kuenzi U, Maibach R, Braunschweig S, Halter F, et al. Classification of ADRs: a proposal for harmonization and differentiation based on the experience of the Comprehensive Hospital Drug Monitoring Bern/St. Gallen, 1974-1993. Pharmacoepidemiol Drug Saf. 2002;11:159-63.<br />12. Londoño A. PR Vademecum 2008. 7ª edición. Bogotá: Licitelco S.A.; 2007.<br />13. Dólar HOY. Cotización del dólar en Colombia. Fecha de consulta: 24 de marzo de 2008. Disponible en: http://www.wilkinsonpc.com.co/free/dolar-hoy.html.<br />14. Pucino F, Beck CL, Seifert RL, Strommen GL, Sheldon PA, Silbergleit IL. Pharmacogeriatrics. Pharmacotherapy. 1985;5:314-26<br />15. Dennis R, Gutiérrez JM, Rodríguez MN. Creación de un programa piloto de farmacovigilancia en el Hospital Universitario San Ignacio. Acta Médica Colombiana. 1998;23:15-22.<br />16. Katzung BG, Bertram G. Farmacología básica y clínica. 10ª edition. East Norwalk: Mc Graw Hill/Appleton & Lange; 1996.<br />17. Cadieux RJ. Drug interactions in the elderly. How multiple drug use increases risk exponentially. Postgrad Med. 1989;86:179-86.<br />18. Schneider JK, Mion LC, Frengley JD. Adverse drug reactions in an elderly outpatient population. Am J Hosp Pharm. 1992;49:90-6.<br />19. Carty MA, Everitt DE. Basic principles of prescribing for geriatric outpatients. Geriatrics. 1989;44:85-98.<br />20. Carnevali DL, Patrick M. Nursing management for the elderly. 2ª edition. Philadelphia: JB Lippincott Co; 1986.<br />21. García-Martínez JM, Fresno JA, Lastres P, Bernabéu C, Betés PO, Martín-Pérez J. Effect of metamizol on promyelocytic and terminally differentiated granulocytic cells. Comparative analysis with acetylsalicylic acid and diclofenac. Biochem Pharmacol. 2003;65:209-17.<br />22. Laporte JR, Capella D. Métodos aplicados en estudios descriptivos de utilización de medicamentos. En: Laporte JR, Tognoni G, editores. Principios de epidemiología del medicamento. 2ª edición. Barcelona: Ediciones Técnicas y Científicas S.A; 1993. p. 68-9.<br />23. Carbonin P, Pahor M, Bernabei R, Sgadari A. Is age an independent risk factor of adverse drug reactions in hospitalized medical patients? J Am Geriatr Soc. 1991;39:1093-9.<br />24. Nolan L, O’Malley K. Prescribing for the elderly. Part I: Sensitivity of the elderly to adverse drug reactions. J Am Geriatr Soc. 1988;36:142-9.<br />25. Leape LL, Brennan TA, Laird N, Lawthers AG, Localio AR, Barnes BA, et al. The nature of adverse events in hospitalized patients. Results of the Harvard Medical Practice Study II. N Engl J Med. 1991;324:377-84.
oai:oai.revistabiomedica.org:article/10
2009-12-17T12:36:54Z
biomedica:ARTI
Gender, age and plasma lipids differences associated with apolipoprotein E polymorphism in school children
Diferencias de sexo, edad y lípidos plasmáticos asociadas al polimorfismo de la apolipoproteína E en un grupo de escolares de Quindío, Colombia
Loango, Nelsy
Gallego, Martha Lucía
Restrepo, Beatriz
Landázuri, Patricia
polimorfismo genético
apolipoproteínas E
lípidos
colesterol
triglicéridos
polimorfismo
hormonas
niño
adolescente
Polymorphism
genetic
apolipoproteins E
lipids
cholesterol
triglycerides
hormones
child
adolescent
Introduction. Apolipoprotein E (apoE) polymorphism is a genetic determinant of total cholesterol and LDL-c levels. Several studies have examined the relationship between variations at the APO E and cardiovascular disease. It is important to determine this relationship in the Colombian population.Objectives. The relationship of apoE polymorphisms was associated with lipid profile by age and sex.Materials and methods. A sample of 500 children aged 8 to 18 years, were selected from school populations in Quindio Province, Colombia. ApoE genotypes were determined by polymerase chain reaction and restriction enzyme. Lipid profiles were obtained by commercial kits.Results. The apoE allele frequencies were as follows: E3 - 91.6%, E2 - 5.3, and E4 - 3.1%. Genotypic frequencies were as follows: E3/E3 - 90.8%, E2/E3 - 5.6%, and E3/E4 - 3.2%. No homozygotes for E2/E2 and E4/E4 were recovered. Similar genotypic and allelic distribution was found for each gender. ApoE genotype and gender had a significant effect on total serum cholesterol (CT) and low density lipoprotein cholesterol (c-LDL). In boys these variables were related as follows: E4>E3>E2 (p<0.05); in girls the relationships were somewhat changed Polimorfismos apoE y lípidos en escolares(E3>E4>E2). High density lipoprotein cholesterol (c-HDL) levels in boys were related as follows: E2>E4>E3; for girls, E4>E2>E3. In boys, for all variables, the protector effect was in E2; but in girls this allele was only a protector for CT and c-LDL, For triacylglycerol (TAG), very low density lipoprotein cholesterol (c-VLDL) and c-HDL, this the protector effect was associated with the E4 allele, (p<0.05).Conclusion. The results suggested that modulation of apoE genotype on plasma lipids was influenced by gender and age, especially in girls older than 10 years.
Introducción. El polimorfismo de la apolipoproteína E (apoE) es un factor determinante genético de los niveles de colesterol total y colesterol LDL.Objetivo. Evaluar la relación del polimorfismo apoE con el perfil lipídico por edad y sexo en escolares quindianos de 8 a18 años.Materiales y métodos. Se utilizó la reacción en cadena de la polimerasa y enzimas de restricción para la genotipificación de apoE en 500 escolares de 8 a 18 años. Los lípidos sanguíneos se determinaron con estuches comerciales.Resultados. La frecuencia alélica fue: E3 (91,6%), E2 (5,3%) y E4 (3,1%); y la frecuencia genotípica: E3/E3 (90,8%), E2/E3 (5,6%) y E3/E4 (3,2%). No se encontraron homocigotos para E2/E2 y E4/E4. Se encontraron distribución genotípica y alélica similares para cada sexo.El genotipo apoE y el sexo tuvieron un efecto significativo sobre el colesterol total y el colesterol LDL. En niños, ambas variables se distribuyeron así: E4>E3>E2 (p<0,05); en niñas: E3>E4>E2; el colesterol LDL en niños fue: E2>E4>E3; y, en niñas: E4>E2>E3.En niños, el alelo con efecto protector fue el E2, en todas las variables; mientras que, en las niñas, este alelo fue protector sólo para el colesterol total y colesterol LDL; para triacilglicéridos y colesterol VLDL y altos niveles de colesterol LDL, el efecto protector estuvo en el E4 (p<0,05).Conclusión. Estos resultados sugieren una asociación entre el genotipo apoE y los lípidos plasmáticos de la población estudiada, influenciada por sexo y edad, especialmente, en niñas mayores de 10 años. Sin embargo, se necesita ampliar la población.
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/10
10.7705/biomedica.v29i3.10
Biomedica; Vol. 29 No. 3 (2009); 382-391
Biomédica; Vol. 29 Núm. 3 (2009); 382-391
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/10/11
https://revistabiomedica.org/index.php/biomedica/article/view/10/282
/*ref*/Hixson JE. Apolipoprotein E polymorphism affect athero-esclerosis en young males. Pathobiological determinants of atheroesclerosis in Youth (PDAY) Research Group. Arterioescler Thromb. 1991;11:1237-44.<br />2. Heeren J, Beisiegel U, Grewal T. Apolipoprotein E recycling: Implications for dyslipidemia and atherosclerosis. Arterioscler Thromb Vasc Biol. 2006;26;442-8.<br />3. Bennet AM, Di Angelantonio E, Ye Z, Wensley F, Dahlin A, Ahlbom A, et al. Association of apolipoprotein E genotypes with lipid levels and coronary risk. JAMA. 2007;298:1300-11.<br />4. Dong LM, Wilson C, Wardell MR, Simmons T, Mahley R, Weisgraber KH, et al. Human apolipoprotein E: Role of arginine 61 in mediating the lipoprotein preferences of the E3 and E4 isoforms. J Biol Chem. 1994;269:22358-65.<br />5. Ministerio de la Protección Social, Organización Panamericana de la Salud. Situación de Salud Colombia. Indicadores básicos 2007. p. 24. Fecha de consulta: 13 de septiembre de 2008. Disponible en: http://www.minproteccionsocial.gov.co/vBecontent/NewsDetail.asp?ID=15895&IDCompany=3<br />6. Instituto Seccional de Salud del Quindío. Indicadores básicos en salud. SIVIGILA. Bogotá D.C.: INS; 2005.<br />7. Uscátegui RM, Álvares MC, Leguado I, Soler W, Martínez I, Arias R, et al. Factores de riesgo cardiovascular en niños de 6 a 18 años de Medellín, Colombia. An Pediat (Barc). 2004:58:411-7.<br />8. Gracia B, de Plata C. Pradilla A, Leiva J. Factores de riesgo para enfermedades de mayor prevalencia en el Valle del Cauca útiles para el desarrollo de estrategias de prevención. Colomb Med. 2003;34:47-55.<br />9. Poveda E, Callas N, Baracaldo C, Castillo C, Hernández P, Guerra M. Evaluación de las concentraciones de lípidos y apoproteínas A-I y B-100 en un grupo de escolares de cinco departamentos del centro-oriente de Colombia. Biomédica. 2007;27:385-99.<br />10. Song Y, Stampfer MJ, Liu S. Meta-analysis: apolipoprotein E genotypes and risk for coronary heart disease. Ann Intern Med. 2004;141:137-47.<br />11. Friedewald WT, Levy RI, Fredickson DS. Estimation of the concentration of c-LDL in plasma without use of the preparative ultracentrifuge. Clin Chem. 1972;18:499-502.<br />12. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the Third Report of National Cholesterol Education Program (NCEP). Expert Panel on Detection. Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult treatment Panel III). JAMA. 2001;285:2486-96.<br />13. Scherr C, Magalhães CK, Malheiros W. Lipid profile analysis in school children. Arq Bras Cardiol. 2007;89: 65-70.<br />14. Castelli W, Fernández-Cruz A. Recomendaciones de ILIB para el diagnóstico de las dislipidemias en Latinoamérica. Cardiovas Risk Fact (edición en español). 1994;3(Suppl.1):10-27.<br />15. Kavey RE, Daniels SR, Lauer RM, Atkins DL, Hayman LL, Tauber K. American Heart Association guidelines for primary prevention of atherosclerotic cardiovascular disease beginning in childhood. J Pediatr. 2003; 142: 368-72.<br />16. Ford ES, Mokdad AH, Ajani UA. Trends in risk factors for cardiovascular disease among children and adolescents in the United States. Pediatrics. 2004;114:1534-44.<br />17. Kavey RE, Daniels SR, Lauer RM, Atkins DL, Hayman LL, Taubert K. American Heart Association guidelines for primary prevention of atherosclerotic cardiovascular disease beginning in childhood. Circulation. 2003;107:1562-6.<br />18. Moreno A, Torres AL, Cartagena AE, Herrera MH. Determinación de la asociación del polimorfismo de la apolipoproteína E (Apo E) relacionada con la presencia de placa aterosclerótica coronaria. NOVA. 2006;4.1-116.<br />19. Torres AL, Guerra-Muñoz M, Segrera A, Wagner J, Alvarado M. Modulación de los niveles de lípidos y lipoproteínas por el polimorfismo de la apolipoproteína E en individuos sanos de Bogotá D.C. NOVA. 2005; 3:1-120.<br />20. Callas N, Poveda E, Baracaldo C, Hernández P, Castillo C, Guerra M. Polimorfismo genético de la apolipoproteína E en un grupo de escolares del centro-oriente colombiano: comparación con las concentraciones plasmáticas de lípidos y apolipoproteínas. Biomédica. 2007;27:526-36<br />21. Celaya J, Rodríguez A, Michelle P, Arends A. Estudios de polimorfismos del gen (APOE) de la apolipoproteína-E (Apo E) y su relación con niveles elevados de colesterol total, lipoproteínas y triglicéridos séricos en niños de edad escolar. Rev Soc Med Quir Hosp Emerg Perez de León. 2007;38(Suppl.1):19-26.<br />22. Shin MH, Kim HN, Cui LH, Kweon SS, Park KS, Heo H, et al. The effect of apolipoprotein E polymorphism on lipid levels in Korean adults. J Korean Med Sci. 2005;20:361-6.<br />23. Liberopoulos E, Miltiadous G, Hatzivassiliou M, Ayrton N, Bairaktari E, Cariolou M, et al. Apolipoprotein E polymorphism in northwestern Greece: Frequency and effect on lipid parameters. Ann Clin Lab Sci. 2004; 34:347-54.<br />24. Medina-Urrutia AX, Cardoso-Saldana GC, Zamora-González J, Liria YK, Posadas-Romero C. Apolipo-protein E polymorphism is related to plasma lipids and apolipoprotein in Mexican adolescents. Hum Biol. 2004;76:605-14.<br />25. Gamboa R, Hernández-Pacheco G, Hesiquio R, Zúniga J, Masso F, Montano LF, et al. Apolipoprotein E polymorphism in the Indian and Mestizo populations of Mexico. Hum Biol. 2000;72:975-81.<br />26. Lehtimaki T, Moilanen T, Viikari J, Herblom HK, Ehnholm C, Riinnemaa T, et al. Apolipoprotein E phenotypes in Finnish youths: a cross-sectional and 6-year follow-up study. J Lipid Res. 1990;31:487-95.<br />27. Parson JJ. Antioqueño colonization in western Colombia. Berkeley: University of California Press; 1949.<br />28. Jiménez I, Mora O, López G, Jiménez ME, Zuluaga L, Isaza R, et al. Idiopathic epilepsy with generalized tonic clonic seizures in Antioquia, Colombia: Is the joint Amerindian and Negroid racial admixture the cause of its high prevalence? Biol Res. 1996;29:297-304.<br />29. Schaefer EJ, Lamon-Fava S, Johnson S, Ordovas JM, Schaefer MM, Castelli WP, et al. Effects of gender and menopausal status on the association of apolipoprotein E phenotype with plasma lipoprotein levels. Results from the Framingham Offspring Study. Arterioscler Thromb. 1994;14:1105-13,<br />30. Ortega H, Castilla P, Gómez-Coronado D, Garcés C, Benavente M, Rodríguez-Artalejo F, et al. Influence of apolipoprotein E genotype on fat-soluble plasma antioxidants in Spanish children1. Am J Clin Nutr. 2005;81:624-32.<br />31. Zofkova I, Zajickova K, Hill M, Horinek A. Apolipoprotein E gene determines serum testosterone and dehydroepiandrosterone levels in postmenopausal women. Eur J Endocrinol. 2002;147:503-6.<br />32. Garcés C, Benavente M, Cano B, Viturro E, Ortega H, Horcajada C, et al. Effects of dehidroepiandrosterone-sulfate on the Apo E genotype influence on plasma lipid levels in prepuberal children. J Clin Endocrinol Metab. 2003;88:3997-4000.<br />33. Vermeulen A. Dehydroepiandrosterone sulfate and ageing. Ann NY Acad Sci. 1995;774:121-7.<br />34. Thorngate FE, Strockbine PA, Erickson SK. Williams DL. Altered adrenal gland cholesterol metabolism in the apoE-deficient Mouse. J Lipid Res. 2002;43:1920-6.<br />35. Agirbasli M, Ciliv G, Cakir S, Srinivasan S, Berenson GS, Ozme S. Body mass index and lipid levels in children from Ankara, Turkey versus Bogalusa, Louisiana. Prev Med. 2005;41:843-5.
oai:oai.revistabiomedica.org:article/11
2009-12-17T12:36:54Z
biomedica:ARTI
Impact of an open waste disposal site on the occurrence of respiratory symptoms and on health care costs of children
Impacto de un botadero a cielo abierto en el desarrollo de síntomas respiratorios y en costos familiares de atención en salud de niños entre 1 y 5 años en Cali, Colombia
Girón, Sandra Lorena
Mateus, Julio César
Méndez, Fabián
disposición de residuos sólidos
salud del niño
costos de la atención en salud
evaluación en salud
estudios de cohortes
Colombia
refuse disposal
child health (public health)
health care costs
health evaluation
cohort studies
Colombia
Introduction. Exposure to contaminants of waste disposal sites potentially has negative health effects on population living in close vicinity. However, the impact to the community in terms of illness and health care costs have not been documented in Colombia.Objective. To determine the effects of an open waste disposal site on the occurrence of respiratory symptoms in children 1-5 year old and on associated household care costs in Cali, Colombia.Material and methods. A cohort of 863 1-5 year old children was assembled—409 exposed to the site and 454 living more distant. Over a 6-month period, measurement of respiratory symptoms and estimates of associated costs were undertaken once a month by interviewing the mother or another adult responsible of child health. A longitudinal logistical analysis was used to determine the independent effect of the disposal site on the occurrence of respiratory symptoms. Differences in average costs between families of exposed and unexposed children were estimated by non-parametric bootstrap techniques.Results. Exposure to the disposal site was associated with a larger probability of respiratory symptoms (odds ratio=1.37, 95%CI 1.17-1.60) and with higher household medical costs due to respiratory symptoms were on the average US$ 10.19 higher (95% US$ 2.63 - 16,82).Conclusion. Living in neighborhoods close to garbage disposal sites has negative effects on the respiratory health of children and results in increased family costs related to treatment of associated respiratory symptoms.
Introducción. La exposición a agentes contaminantes provenientes de los sitios de disposición final de residuos sólidos, tiene efectos potencialmente negativos en la salud de la población que vive en su área de influencia.Objetivos. Determinar los efectos del botadero municipal a cielo abierto en Cali, conocido como el botadero de Navarro, en el desarrollo de síntomas respiratorios en niños entre 1 y 5 años de edad y en los costos familiares relacionados con la atención de estos síntomas.Materiales y métodos. Se ensambló una cohorte de niños expuestos y no expuestos al botadero y se les hizo seguimiento durante 6 meses. El desarrollo de síntomas respiratorios y los costos relacionados con la atención en salud se evaluaron mensualmente con entrevistas al adulto responsable del cuidado del niño. Se hizo un análisis logístico longitudinal para determinar el efecto independiente del botadero en el desarrollo de síntomas respiratorios. Mediante técnicas estadísticas no paramétricas de bootstrap, se determinaron las diferencias promedio de costos entre las familias de los niños expuestos y no expuestos.Resultados. La exposición al botadero se asoció a una probabilidad más alta de desarrollar síntomas respiratorios (OR=1,37, IC95% 1,17-1,60) y a mayores costos familiares relacionados con el desarrollo de esos síntomas en niños (diferencia promedio: Col$ 24.038,5; IC95% 6.211,0-39.650,4).Conclusiones. La exposición al botadero tiene efectos negativos sobre la salud respiratoria infantil y sobre los costos familiares relacionados con la atención de los síntomas.
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/11
10.7705/biomedica.v29i3.11
Biomedica; Vol. 29 No. 3 (2009); 392-402
Biomédica; Vol. 29 Núm. 3 (2009); 392-402
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/11/12
https://revistabiomedica.org/index.php/biomedica/article/view/11/284
/*ref*/Fielder HM, Poon-King CM, Palmer SR, Moss N, Coleman G. Assessment of impact on health of residents living near the Nant-y-Gwyddon landfill site: retrospective analysis. BMJ. 2000;320:19-22.<br />2. Vrijheid M. Health effects of residence near hazardous waste landfill sites: a review of epidemiologic literature. Environ Health Perspect. 2000;108 (Suppl.1):101-12.<br />3. Elliott P, Briggs D, Morris S, de Hoogh C, Hurt C, Jensen TK, et al. Risk of adverse birth outcomes in populations living near landfill sites. BMJ. 2001;323:363-8.<br />4. Paigen B, Goldman LR, Highland JH, Magnant MM, Steegman AT. Prevalence of health problems in children living near Love Canal. Haz Waste Haz Mat. 1985;2: 23-43.<br />5. Carabin H, Gyorkos TW, Soto JC, Penrod J, Joseph L, Collet JP. Estimation of direct and indirect costs because of common infections in toddlers attending day care centers. Pediatrics. 1999;103:556-64.<br />6. Elden LM, Coyte PC. Socioeconomic impact of otitis media in North America. J Otolaryngol. 1998;27 (Suppl. 2): 9-16.<br />7. Frank TL, Cropper JA, Hazell ML, Frank PI, Hannaford PC. Childhood asthma: healthcare resource utilization in those with and without a diagnosis of the condition. Respir Med. 2004;98:454-63.<br />8. Anand VK. Epidemiology and economic impact of rhinosinusitis. Ann Otol Rhinol Laryngol 2004;193 (Suppl.):3-5.<br />9. Austin JB, Selvaraj S, Russell G. Childhood asthma in the Highlands of Scotland - morbidity and school absence. Scott Med J. 2004;49:18-21.<br />10. Crystal-Peters J, Neslusan CA, Smith MW, Togias A. Health care costs of allergic rhinitis-associated conditions vary with allergy season. Ann Allergy Asthma Immunol. 2002;89:457-62.<br />11. Stevens CA, Turner D, Kuehni CE, Couriel JM, Silverman M. The economic impact of preschool asthma and wheeze. Eur Respir J. 2003;21:1000-6.<br />12. Hosmer DW, Lemeshow S. Applied logistic regression. New York, NY: John Wiley & Sons; 1989.<br />13. Diggle P, Heagerty P, Liang K-Y, Zeger S. Analysis of longitudinal data. 2nd edition. New York, NY: Oxford University Press; 2002.<br />14. Barber JA, Thompson SG. Analysis of cost data in randomized trials: an application of the non-parametric bootstrap. Stat Med. 2000;19:3219-36.<br />15. Thompson SG, Barber JA. How should cost data in pragmatic randomized trials be analyzed? BMJ. 2000;320:1197-200.<br />16. Wong TW, Wun YT, Yu TS, Tam W, Wong CM, Wong AH. Air pollution and general practice consultations for respiratory illnesses. J Epidemiol Community Health. 2002;56:949-50.<br />17. Hernández-Cadena L, Téllez-Rojo MM, Sanín-Aguirre LH, Lacasaña-Navarro M, Campos A, Romieu I. Relación entre consultas a urgencias por enfermedad respiratoria y contaminación atmosférica en Ciudad Juárez, Chihuahua. Salud Pública Mex. 2000;42:288-97.<br />18. Maître A, Collot-Fertey D, Anzivino L, Marques M, Hours M, Stoklov M. Municipal waste incinerators: air and biological monitoring of workers for exposure to particles, metals, and organic compounds. Occup Environ Med. 2003;60:563-9.<br />19. Delfino RJ, Gong H, Linn WS, Hu Y, Pellizzari ED. Respiratory symptoms and peak expiratory flow in children with asthma in relation to volatile organic compounds in exhaled breath and ambient air. J Expo Anal Environ Epidemiol. 2003;13:348-63.<br />20. Ballester Díez F, Tenías JM, Pérez-Hoyos S. Efectos de la contaminación atmosférica sobre la salud una introducción. Rev Esp Salud Pública. 1999;73:109-21.<br />21. Simoni M, Lombardi E, Berti G, Rusconi F, La Grutta S, Piffer S, et al. Mould/dampness exposure at home is associated with respiratory disorders in Italian children and adolescents: the SIDRIA-2 Study. Occup Environ Med. 2005;62:616-22.<br />22. Simoni M, Lombardi E, Berti G, Rusconi F, La Grutta S, Piffer S, et al. Effects of indoor exposures on respiratory and allergic disorders. Epidemiol Prev. 2005;29(Suppl.2):57-61.<br />23. Skorge TD, Eagan TM, Eide GE, Gulsvik A, Bakke PS. Indoor exposures and respiratory symptoms in a Norwegian community sample. Thorax. 2005;60:937-42.<br />24. Basu AM, Stephenson R. Low levels of maternal education and the proximate determinants of childhood mortality: a little learning is not a dangerous thing. Soc Sci Med. 2005;60:2011-23.<br />25. Valadez JJ, Hage J, Vargas W. Understanding the relationship of maternal health behavior change and intervention strategies in a Nicaraguan NGO network. Soc Sci Med. 2005;61:1356-68.<br />26. Zmirou D, Gauvin S, Pin I, Momas I, Sahraoui F, Just J, et al. Traffic related air pollution and incidence of childhood asthma: results of the Vesta case-control study. J Epidemiol Community Health. 2004;58:18-23.<br />27. Peden DB. Development of atopy and asthma: candidate environmental influences and important periods of exposure. Environ Health Perspect. 2000;108(Suppl.3):475-82.<br />28. Pino P, Walter T, Oyarzun M, Villegas R, Romieu I. Fine particulate matter and wheezing illnesses in the first year of life. Epidemiology. 2004;15:702-8.<br />29. Sreeramareddy CT, Shankar RP, Sreekumaran BV, Subba SH, Joshi HS, Ramachandran U. Care seeking behaviour for childhood illness- a questionnaire survey in western Nepal. BMC Int Health Hum Rights. 2006;6:7.<br />30. Ozonoff D, Colten ME, Cupples A, Heeren T, Schatzkin A, Mangione T, et al. Health problems reported by residents of a neighborhood contaminated by a hazardous waste facility. Am J Ind Med. 1987;11:581-97.<br />31. Dunne MP, Burnett P, Lawton J, Raphael B. The health effects of chemical waste in an urban community. Med J Aust. 1990;152:592-7.<br />32. Miller MS, McGeehin MA. Reported health outcomes among residents living adjacent to a hazardous waste site, Harris County, Texas, 1992. Toxicol Ind Health. 1997;13:311-9.<br />33. Lipscomb JA, Goldman LR, Satin KP, Smith DF, Vance WA, Neutra RR. A follow-up study of the community near the McColl waste disposal site. Environ Health Perspect. 1991;94:15-24.<br />34. Hertzman C, Hayes M, Singer J, Highland J. Upper Ottawa street landfill site health study. Environ Health Perspect. 1987;75:173-95.<br />35. Wheeler BW, Ben-Shlomo Y. Environmental equity, air quality, socioeconomic status, and respiratory health: a linkage analysis of routine data from the Health Survey for England. J Epidemiol Community Health. 2005; 59:948-54.<br />36. Rushton L. Health hazards and waste management. Br Med Bull. 2003;68:183-97.<br />37. Lanata CF, Rudan I, Boschi-Pinto C, Tomaskovic L, Cherian T, Weber M, et al. Methodological and quality issues in epidemiological studies of acute lower respiratory infections in children in developing countries. Int J Epidemiol. 2004;33:1362-72.
oai:oai.revistabiomedica.org:article/12
2010-01-08T02:02:51Z
biomedica:ARTI
Identification of genes associated with germination of conidia to form mycelia in the fungus Paracoccidioides brasiliensis
Identificación de algunos genes asociados al proceso de germinación de la conidia al micelio en Paracoccidioides brasiliensis
García, Ana María
Hernández, Orville
Aristizábal, Beatriz H.
Cano, Luz Elena
McEwen, Juan G.
Restrepo, Ángela
Paracoccidioides
esporas fúngicas
micelio
germinación
Paracoccidioides
spores
fungal
mycelium
germination
Introduction. Paracoccidioides brasiliensis is a thermo-dimorphic fungus. At room temperature it grows as a mold that produces conidia, whereas in the vertebrate host it grows as a multiple-budding yeast. The molecular mechanisms involved in the germination from the conidia to the mycelia process remain unknown.Objective. The kinetics of conidia to mycelia germination process were studied in the dimorphic fungus P. brasiliensis. Gene expression during this process was evaluated by construction and analysis of an EST library.Materials and methods. For the germination kinetics study, P. brasiliensis conidia were isolated as single cell units. Then, they were cultured at 18° C in BHI (brain-heart infusion) broth for 24, 48, 72 and 96 hr. After each perion, they were examined by light microscopy. From conidia harvested at 96 hr, an EST library was constructed; at this stage the gene expression was presumed to be maximal for the germination process.Results. During the conidia to the mycelia developmental process, the following germination rates were observed: at 24 hr, 11.7±1.2%; at 48 hr, 30±0.6%; at 72 hr, 43±1.3%; and at 96 hr, 66±2.4%. At the 96 hour stage, an EST library was constructed. It consisted of 129 sequences grouped in 4 contigs and 7 singlets for a total of 11 possible genes. Eight of the sequences had not been described previously in other EST libraries of this fungus.Conclusions. New genes were identified that were expressed during the conidia to the mycelia germination process and may represent genes specific to the germination process.
Introducción. Paracoccidioides brasiliensis es un hongo dimórfico térmico, que a temperatura ambiente se presenta como un moho productor de conidias, mientras que en el huésped se comporta como una levadura de gemación múltiple. Los mecanismos moleculares que rigen la germinación de conidia a micelio aún se desconocen.Objetivo. Estudiar en P. brasiliensis la cinética del proceso de germinación de conidia a micelio y determinar los genes expresados durante este proceso mediante la construcción y el análisis de una librería EST (Expressed Sequence Tag).Materiales y métodos. Para el estudio de la cinética de germinación, se produjeron y aislaron conidias de P. brasiliensis. Estas fueron incubadas en cultivos líquidos a 18°C por 24, 48, 72 y 96 horas, y se examinaron por microscopía de luz. A partir de conidias cultivadas por 96 horas, se construyó y caracterizó una librería EST, la cual representaría los genes expresados durante el proceso de germinación.Resultados. Durante el proceso de germinación de conidia a micelio, se observó 11,7±1,2%, 30±0,6%, 43±1,3% y 66±2,4% de germinación a las 24, 48, 72 y 96 horas de incubación, respectivamente. Además, se obtuvo una librería del proceso de germinación consistente en 129 secuencias agrupadas en cuatro secuencias contiguas y siete secuencias únicas, para un total de 11 posibles genes. Ocho secuencias (72,7%) no habían sido descritas anteriormente en otras librerías informadas para este hongo y podrían representar genes específicos de la germinación de conidia a micelio.Conclusiones. Éste es el primer reporte en el que se identifican genes no descritos anteriormente, que son expresados durante la germinación de conidia a micelio, proceso de gran importancia en la biología de P. brasiliensis.
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/12
10.7705/biomedica.v29i3.12
Biomedica; Vol. 29 No. 3 (2009); 403-412
Biomédica; Vol. 29 Núm. 3 (2009); 403-412
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/12/13
https://revistabiomedica.org/index.php/biomedica/article/view/12/285
/*ref*/Brummer E, Castaneda E, Restrepo A. Paracoccidioido-mycosis: an update. Clin Microbiol Rev. 1993;6:89-117.<br />2. Restrepo A, Tobon AM. Chapter 266. Paracoccidioides brasiliensis. In: Mandell GL, Bennetts JE, Dollin, R, editors. Principles and practice of infectious diseases. 6th edition. Philadelphia, P.A: Elsevier; 2005. p. 3062-8.<br />3. Camilo J, Tabares AM, Gómez BL, Aristizábal BE, Cock AM, Restrepo A. The oral route in the pathogenesis of paracoccidioidomycosis: an experimental study in BALB/c mice infected with P. brasiliensis conidia. Mycopathologia. 2001;151:57-62.<br />4. McEwen JG, Brummer E, Stevens DA, Restrepo A. Effect of murine polymorphonuclear leukocytes on the yeast form of Paracoccidioides brasiliensis. Am J Trop Med Hyg. 1987;36:603-8.<br />5. Goldman GH, dos Reis E, Duarte DC, de Souza LA, Quiapin AC, Vitorelli PM, et al. Expressed sequence tag analysis of the human pathogen Paracoccidioides brasiliensis yeast phase: identification of putative homologues of Candida albicans virulence and pathogenicity genes. Eukaryot Cell. 2003;2:34-48.<br />6. Nunes LR, Costa de Oliveira R, Leite DB, da Silva VS, dos Reis E, da Silva ME, et al. Transcriptome analysis of Paracoccidioides brasiliensis cells undergoing mycelium-to-yeast transition. Eukaryot Cell. 2005;4:2115-28.<br />7. Queiroz-Telles F. Paracoccidioides brasiliensis: Ultra-structural findings. In: Franco LC, Restrepo A, Del Negro G, editors. Paracoccidioidomycosis. Boca Raton, FL: CRC Press; 1994. p. 27-48.<br />8. Salazar ME, Restrepo A. Morphogenesis of the mycelium-to-yeast transformation in Paracoccidioides brasiliensis. Sabouraudia. 1985;23:7-11.<br />9. Aristizábal BH, Clemons KV, Stevens DA, Restrepo A. Morphological transition of Paracoccidioides brasiliensis conidia to yeast cells: in vivo inhibition in females. Infect Immun. 1998;66:5587-91.<br />10. Cock AM, Cano LE, Vélez D, Aristizábal BH, Trujillo J, Restrepo A. Fibrotic sequelae in pulmonary paracocci-dioidomycosis: histopathological aspects in BALB/c mice infected with viable and non-viable Paracoccidioides brasiliensis propagules. Rev Inst Med Trop Sao Paulo. 2000;42:59-66.<br />11. McEwen JG, Bedoya V, Patino MM, Salazar ME, Restrepo A. Experimental murine paracoccidiodomycosis induced by the inhalation of conidia. J Med Vet Mycol. 1987;25:165-75.<br />12. Cano LE, Brummer E, Stevens DA, Restrepo A. An evaluation of the enzyme-linked immunoabsorbent assay (ELISA) for quantitation of antibodies to Paracoccidioides brasiliensis. J Med Vet Mycol. 1986;24:467-75.<br />13. Cano LE, Gómez B, Brummer E, Restrepo A, Stevens DA. Inhibitory effect of deferoxamine or macrophage activation on transformation of Paracoccidioides brasiliensis conidia ingested by macrophages: reversal by holotransferrin. Infect Immun. 1994;62:1494-6.<br />14. González A, Aristizábal BH, Gómez EC, Restrepo A, Cano LE. Short report: Inhibition by tumor necrosis factor-alpha-activated macrophages of the transition of Paracoccidioides brasiliensis conidia to yeast cells through a mechanism independent of nitric oxide. Am J Trop Med Hyg. 2004;71:828-30.<br />15. González A, de Gregori W, Vélez D, Restrepo A, Cano LE. Nitric oxide participation in the fungicidal mechanism of gamma interferon-activated murine macrophages against Paracoccidioides brasiliensis conidia. Infect Immun. 2000;68:2546-52.<br />16. Restrepo BI, McEwen JG, Salazar ME, Restrepo A. Morphological development of the conidia produced by Paracoccidioides brasiliensis mycelial form. J Med Vet Mycol. 1986;24:337-9. <br />17. Felipe MS, Andrade RV, Petrofeza SS, Maranhao AQ, Torres FA, Albuquerque P, et al. Transcriptome characterization of the dimorphic and pathogenic fungus Paracoccidioides brasiliensis by EST analysis. Yeast. 2003;20:263-71.<br />18. Felipe MS, Torres FA, Maranhao AQ, Silva-Pereira I, Pocas-Fonseca MJ, Campos EG, et al. Functional genome of the human pathogenic fungus Paracoccidioides brasiliensis. FEMS Immunol Med Microbiol. 2005;45:369-81.<br />19. Bastos KP, Bailao AM, Borges CL, Faria FP, Felipe MS, Silva MG, et al. The transcriptome analysis of early morphogenesis in Paracoccidioides brasiliensis mycelium reveals novel and induced genes potentially associated to the dimorphic process. BMC Microbiol. 007;7:29.<br />20. Restrepo A, Salazar ME, Cano LE, Patiño MM. A technique to collect and dislodge conidia produced by Paracoccidioides brasiliensis mycelial form. J Med Vet Mycol.1986;24:247-50.<br />21. Restrepo A, Jiménez BE. Growth of Paracoccidioides brasiliensis yeast phase in a chemically defined culture medium. J Clin Microbiol.1980;12:279-81.<br />22. Calich VL, Purchio A, Paula CR. A new fluorescent viability test for fungi cells. Mycopathologia.1979;66:175-7.<br />23. Marra MA, Kucaba TA, Hillier LW, Waterston RH. High-throughput plasmid DNA purification for 3 cents per sample. Nucleic Acids Res.1999;27:e37.<br />24. Ewing B, Green P. Base-calling of automated sequencer traces using phred. II. Error probabilities. Genome Res.1998;8:186-94.<br />25. Huang X, Madan A. CAP3: A DNA sequence assembly program. Genome Res.1999;9:868-77.<br />26. White O, Kerlavage AR. TDB: new databases for biological discovery. Methods Enzymol.1996;266:27-40.<br />27. Tavares AH, Silva SS, Dantas A, Campos EG, Andrade RV, Maranhao AQ, et al. Early transcriptional response of Paracoccidioides brasiliensis upon internalization by murine macrophages. Microbes Infect.2007;9:583-90.<br />28. Bailao AM, Shrank A, Borges CL, Parente JA, Dutra V, Felipe MS, et al. The transcriptional profile of Paracoccidioides brasiliensis yeast cells is influenced by human plasma. FEMS Immunol Med Microbiol. 2007;51:43-57.<br />29. Ramírez JR. Paracoccidioides brasiliensis: conversion of yeastlike forms into mycelia in submerged culture. J Bacteriol. 1971;105:523-6.<br />30. Fedorova ND, Khaldi N, Joardar VS, Maiti R, Amedeo P, Anderson MJ, et al. Genomic islands in the pathogenic filamentous fungus Aspergillus fumigatus. PLoS Genet. 2008;4:e1000046.<br />31. Hand RA, Jia N, Bard M, Craven RJ. Saccharomyces cerevisiae Dap1p, a novel DNA damage response protein related to the mammalian membrane-associated progesterone receptor. Eukaryot Cell. 2003;2:306-17.<br />32. Gant TM, Wilson KL. Nuclear assembly. Annu Rev Cell Dev Biol. 1997;13:669-95.<br />33. Tranque P, Hu MC, Edelman GM, Mauro VP. rRNA complementarity within mRNAs: a possible basis for mRNA-ribosome interactions and translational control. Proc Natl Acad Sci USA. 1998;95:12238-43.
oai:oai.revistabiomedica.org:article/13
2009-12-17T12:36:54Z
biomedica:ARTI
Characterization of Aedes albopictus (Skuse, 1894) (Diptera:Culicidae) larval habitats near the Amazon River in Colombia
Caracterización preliminar de los sitios de cría de Aedes (Stegomyia) albopictus (Skuse, 1894) (Diptera: Culicidae) en el municipio de Leticia, Amazonas, Colombia
Carvajal, José Joaquín
Moncada, Ligia Inés
Rodríguez, Mauricio Humberto
Pérez, Ligia del Pilar
Olano, Víctor Alberto
Aedes
vectores de enfermedades
control vectorial
plancton
Colombia
Aedes
disease vectors
vector control
plankton
Colombia
Introduction. Because the role of Aedes albopictus as an incriminated vector of several viral pathogens, its control is important to human health. To establish appropriate control methods, characterization of the larval habitats is a necessary first step.Objective. Habitats of the immature stages of Ae. albopictus were characterized with respect to physical-chemical parameters and by floral and faunal arrays present.Materials and methods. Leticia is located at the southernmost tip of Colombia on the banks of the Amazon River. In the urban area, 154 houses were inspected in December 2002 and January 2003. Physical-chemical data were collected, including exposure to sunlight, location, container size and material, water conductivity, and dissolved oxygen. Macroinvertebrates and plankton samples were taken at each positive larval site. The results were compared using descriptive analysis, principal component analysis, classification dendrograms, and diversity indexes.Results. Twenty-one habitats were found positive for Diptera, and 13 were positive for Ae. albopictus larvae. Most of the positive habitats (92%) were located near the houses--they were small or medium size receptacles located in the shade. This water generally had low conductivity and low turbidity, although high values of these parameters were also identified. The habitats had low diversity indexes for macroinvertebrates and high diversity indexes for plankton. In the principal component analysis, significant correlation was found with mites, oligochaetes and hemipterans (the macroinvertebrates) and with bacilarophyceaes, clorophyceaes and cianophyceas (the algal forms).Conclusion. In Leticia, females of Ae. albopictus were found in newly established habitats with sufficient availability of resources, low conductivity, and turbidity, lower intra-and interspecific competition.
Introducción. Dada la importancia de Aedes albopictus en la salud pública, es necesario caracterizar los criaderos para establecer medidas de control.Objetivo. Caracterizar en función de los parámetros físico-químicos y grupos de organismos presentes, los criaderos de los estadios inmaduros de Ae. albopictus en Leticia, Amazonas.Materiales y métodos. Se inspeccionaron 154 viviendas en el área urbana en diciembre 2002 y enero 2003, para buscar criaderos de Ae. albopictus y otros dípteros con estadios acuáticos inmaduros. En los criaderos con resultados positivos se tomaron datos físico-químicos cualitativos y cuantitativos: exposición al sol, ubicación, tamaño, material, conductividad, turbidez, oxígeno disuelto, temperatura y presencia de macroinvertebrados y plancton. Los resultados se compararon mediante análisis descriptivos, análisis de componentes principales, dendrogramas de clasificación e índices de diversidad.Resultados. Se encontraron 21 criaderos con larvas de dípteros, 13 con Ae. albopictus; 92% de ellos estaban ubicados en el peridomicilio, en recipientes pequeños o medianos, dispuestos en la sombra, con baja turbidez y conductividad, bajos índices de diversidad para macroinvertebrados y altos para organismos productores de plancton. En el análisis de componentes principales, se encontró correlación significativa con ácaros, oligoquetos y hemípteros (macroinvertebrados), y con bacilarofíceas, clorofíceas y cianofíceas (plancton). En presencia de otros culícidos, las larvas de Ae. albopictus fueron escasas.Conclusión. En este estudio se encontró que las hembras de Ae. albopictus depositan sus huevos en depósitos de agua recién establecidos con disponibilidad suficiente de recurso, baja conductividad y turbidez, y menor competencia intraespecífica e interespecífica.
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/13
10.7705/biomedica.v29i3.13
Biomedica; Vol. 29 No. 3 (2009); 413-423
Biomédica; Vol. 29 Núm. 3 (2009); 413-423
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/13/14
https://revistabiomedica.org/index.php/biomedica/article/view/13/286
/*ref*/Forattini OP. Identificão de Aedes (Stegomyia) albopictus no Brasil. Rev Saúde Pública. 1986;20:244-5.<br />2. Vélez ID, Quiñones M, Suárez M, Olano V, Murcia LM, Correa E, et al. Presencia de Aedes albopictus en Leticia, Amazonas, Colombia. Biomédica. 1998;18:192-8.<br />3. Suárez M. Aedes albopictus (Skuse) (Diptera, Culicidae) en Buenaventura, Colombia. Inf Quinc Epidemiol Nac. 2001;6:221-4.<br />4. Cuéllar-Jiménez ME, Velásquez-Escobar OL, González-Obando R, Morales-Reichman CA. Detección de Aedes albopictus (Skuse) (Diptera: Culicidae) en la ciudad de Cali, Valle del Cauca, Colombia. Biomédica. 2007;27:273-9.<br />5. Gratz NG. Critical review of the vector status of Aedes albopictus. Med Vet Entomol. 2004;18:215-27.<br />6. Serufo JC, Montes de Oca HM, Tavares VA, Souza AM, Rosa RV, Jamal MC, et al. Isolation of dengue virus type 1 from larvae of Aedes albopictus in Campos Altos City, State of Minas Gerais, Brazil. Mem Inst Oswaldo Cruz. 1993;83:503-4.<br />7. Ibañez-Bernal S, Briceño B, Mutebi SP, Argot E, Rodríguez G, Martínez-Campos C, et al. First record in America of Aedes albopictus naturally infected with dengue virus during the 1995 outbreak at Reynosa, México. Med Vet Entomol. 1997;11:305-9.<br />8. Holick J, Kile A, Ferraro W, Delaney R, Iwaseczko M. Discovery of Aedes albopictus infected with West Nile Virus in Southeastern Pennsylvania. J Am Mosq Control Assoc. 2002;18:131.<br />9. Méndez F, Barreto M, Arias JF, Rengifo G, Muñoz J, Burbano ME, et al. Human and mosquito infections by dengue viruses during and after epidemics in a dengue-endemic region of Colombia. Am J Trop Med Hyg. 2006;74:678-83.<br />10. Olano V. Vigilancia entomológica: un componente en salud pública. Inf Quinc Epidemiol Nac. 1999;4:273-4.<br />11. Instituto Geográfico Agustín Codazzi. Atlas Básico de Colombia. Bogotá, D.C.; División de Difusión Geográfica; 1989.<br />12. Secretaría de Salud Departamental. 2001–2003. Informes de levantamiento de índice aédico en el municipio de Leticia. Leticia: Gobernación del Amazonas; 2004.<br />13. Berríos V, Sielfeld W. Superclase crustácea, crustáceos continentales. Programa de Biodiversidad, Universidad Arturo Prat Iquique, Chile. Fecha de consulta: 12 de julio de 2005. Disponible en: http://www.insectos.cl/pdf/CRUSTACEA.pdf.<br />14. McAlpine J, Peterson B, Shewell G, Teskey H, Vockeroth J. Manual of Nearctic Diptera. Quebec: Canadian Government Publishing Centre; 1993.<br />15. Merritt RW, Cummins KW. An introduction to the aquatic insects of North America. Third edition. Dubuque, Iowa: Kendall/Hunt Publishing Company; 1996.<br />16. Milligan M. Identification manual for the aquatic Oligochaeta of Florida. Sarasota, Florida: Freshwater Oligochaetes; 1997.<br />17. Peckarsky BL, Fraissinet PR, Penton MA, Conklin DJ. Freshwater macroinvertebrates of northeastern North America. Ithaca, New York: Cornell University Press; 1990.<br />18. Thorp J, Covich A. Ecology and classification of North American Freshwater Invertebrates. 2nd edition. San Francisco: Academic Press; 2001.<br />19. La Casse WJ, Yamaguti S. Mosquito fauna of Japan and Korea. Washington, D.C.: USAF School of Aviation Medicine Air University; 1950.<br />20. Chareonviriyaphap T, Akratanakul P, Nettanomsak S, Huntamai S. Larval habitats and distribution patterns of Aedes aegypti (Linnaeus) and Aedes albopictus (Skuse), in Thailand. Southeast Asian J Trop Med Public Health. 2003;34:529-35.<br />21. Simard F, Nchoutpouen E, Toto JC, Fontenille D. Geographic distribution and breeding site preference of Aedes albopictus and Aedes aegypti (Diptera: Culicidae) in Cameroon, Central Africa. J Med Entomol. 2005;42:726-31.<br />22. Foratini OP, Kakitani I, Mureb MA, De Rezende L. Produtividade de criadouro de Aedes albopictus em ambiente urbano. Rev Saúde Pública. 1997;31:545-55.<br />23. Sehgal SS, Pillot MK. Preliminary studies on the chemical nature of mosquito-breeding waters in Dehli. Bull World Health Organ. 1970;42:647-50.<br />24. Carrieri M, Bacchi M, Bellini R, Maini S. On the competition occurring between Aedes albopictus and Culex pipiens (Diptera: Culicidae) in Italy. Environ Entomol. 2003;32:1313-21.<br />25. Devi NP, Janhari RH. Mosquito species associated within some western Himalayas phytogeographic zones in the Garhwal region of India. J Insect Sci. 2007;7:1-10.<br />26. Alto B, Juliano S. Precipitation and temperature effects on populations of Aedes albopictus (Diptera: Culicidae): implications for range expansion. J Med Entomol. 2001;38:646-56.<br />27. Sota T, Mogi M. Survival time and resistance to desiccation of diapauses and non-diapause eggs of temperate Aedes (Stegomyia) mosquitoes. Entomol Exp Appl. 1992;63:151-61.<br />28. Sunahara T, Mogi M. Variability of intra and interespecific competitions of bamboo stump mosquito larvae over small and large spatial scales. Oikos. 2002;97:87-96.<br />29. Calado D, Navarro MA. Avaliaçâo da influência da temperatura sobre o desenvolvimiento de Aedes albopictus. Rev Saúde Pública. 2002;36:173-9.<br />30. Estrada-Franco J, Craig G Jr. Biología, relaciones con enfermedades y control de Aedes albopictus (Cuaderno técnico No. 42). Washington D. C.: Organización Panamericana de la Salud; 1995.<br />31. Learner MA, Lockhead G, Hughes BD. A review of the biology of British Naididae (Oligochaeta) with emphasis on the lotic environment. Freshwater Biol. 1978;8:357-75.<br />32. Marten G. The potential of mosquito-indigestible phytoplankton for mosquito control. J Am Mosquito Control Assoc. 1987;3:105-6.<br />33. Sunahara T, Ishizaka K, Mogi M. Habitat size: determining the opportunity for encounters between mosquito larvae and aquatic predators. J Vector Ecol. 2002;27:8-20.<br />34. Roldán G. Fundamentos de limnología neotropical. Colección Ciencia y Tecnología Universidad de Antioquia. Medellín: Editorial Universidad de Antioquia; 1992.<br />35. Sunahara T, Mogi M. Priority effects of bamboo-stump mosquito larvae: Influences of water exchange and leaf litter input. Ecol Entomol. 2002;27:346-54.
oai:oai.revistabiomedica.org:article/14
2009-12-17T12:36:54Z
biomedica:ARTI
Outbreak of urban rabies transmitted by dogs in Santa Marta, northern Colombia
Brote de rabia urbana transmitida por perros en el distrito de Santa Marta, Colombia, 2006-2008
Páez, Andrés
Rey, Gloria
Agudelo, Carlos
Dulce, Alvaro
Parra, Edgar
Díaz-Granados, Hernando
Heredia, Damaris
Polo, Luis
rabies
rabies virus
Lyssavirus
zoonoses
epidemiologic surveillance
Colombia
rabia
virus de la rabia
Lyssavirus
zoonosis
vigilancia epidemiológica
Colombia
Introduction. An urban rabies outbreak occurred in the District of Santa Marta between April 2006 and January 2008, which resulted in the deaths of 4 humans and 28 dogs.Objectives. Three objectives were entertained—first, the diagnostic laboratory techniques were described as well as the rabies control actions taken; second, the impact of anti-rabies dog vaccination was assessed in terms of neutralizing antibody seroconversion; and third, the epidemiological significance and public health implications of the outbreak were examined.Materials and methods. Rabies diagnosis was achieved by direct immunofluorescence, inoculation of mice and immunohistochemistry. Typing of the virus was achieved by indirect immunofluorescence. Control activities included a dog population census, vaccination and treatments for persons exposed to rabies, mass vaccination of dogs and cats, and initiation of a community education program. Seroconversion was investigated by capture ELISA.Results. Antigenic variant 1 was detected in all cases. Of vaccinated dogs, 77% were seropositive,and 47% were seroprotected against rabies. No differences were found in the humoral response between dog gender; however significant differences in dog seroprotection were discovered between localized comunities in Santa Marta.Conclusions. The 2006-2008 urban rabies outbreak was the largest reported in a city in Colombia. It was caused by rabid dogs, and demonstrated that these animals are still a threat for human health despite the existence of efficient rabies vaccines. The control of the outbreak was achieved 20 months after the first rabies case in dogs, and 14 months after the initiation of the first mass vaccination of animals. The necessity of implementation and maintenance of rabies control strategies is underlined for minimizing human risk.
Introducción. En el distrito de Santa Marta ocurrió un brote de rabia urbana entre abril de 2006 y enero de 2008, con cuatro casos fatales en humanos y 28 en perros.Objetivos. Describir el brote, las técnicas de diagnóstico de laboratorio y las acciones de control de foco empleadas. Medir el impacto de la vacunación antirrábica canina en términos de seroconversión de anticuerpos neutralizantes. Discutir el significado epidemiológico y las implicaciones en salud pública.Materiales y métodos. Los casos se diagnosticaron por inmunofluorescencia directa, prueba biológica en ratón e inmunohistoquímica. La tipificación viral se hizo por inmunofluorescencia indirecta. Las acciones de control consistieron en un censo canino, vacunación y tratamientos antirrábicos a la población expuesta, vacunación canina y felina, y educación comunitaria. La seroconversión fue investigada por medio de la prueba ELISA de captura.Resultados. La variante antigénica 1 se caracterizó en todos los casos. Se observó seropositividad en 77% de los perros vacunados y protección serológica contra la rabia, en 47%. No se observaron diferencias de la respuesta humoral entre sexos de los perros, pero sí existieron diferencias de los porcentajes de perros protegidos entre las comunas del distrito.Conclusiones. Este brote de rabia ha sido el de mayor magnitud en una ciudad colombiana, según los datos oficiales. Fue causado por perros, lo cual reitera la amenaza que aún representa la rabia urbana para la salud pública, a pesar de la existencia de vacunas eficientes.El control del brote se logró 20 meses después del primer caso en perros y 14 meses después de haberse iniciado la primera vacunación masiva en animales. Es necesario implementar y mantener acciones para el control de la rabia urbana y evitar su impacto en los humanos.
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/14
10.7705/biomedica.v29i3.14
Biomedica; Vol. 29 No. 3 (2009); 424-436
Biomédica; Vol. 29 Núm. 3 (2009); 424-436
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/14/15
https://revistabiomedica.org/index.php/biomedica/article/view/14/288
/*ref*/Beran GW, Steele JH. Handbook of zoonoses. Section B: Boca Ratón, Fl: CRC Press; 1994. p. 307.<br />2. Wunner WH, Larson JK, Dietzchold B, Smith CL. The molecular biology of rabies virus. Rev Infect Dis. 1988;10(Suppl.4):771-84.<br />3. Tordo N, Kouknetzoff A. The rabies virus genome: an overview. Onderstepoort J Vet Res. 1993;60:263-9.<br />4. Bourhy H, Kissi B, Audry L, Smreczak M, Sadkowska-Todys M, Kulonen K, et al. Ecology and evolution of rabies virus in Europe. J Gen Virol. 1999;80:2545-57.<br />5. Guerra MA, Curns AT, Rupprecht CE, Hanlon CA, Krebs JW, Childs JE. Skunk and raccoon rabies in the eastern United States: temporal and spatial analysis. Emerg Infect Dis. 2003;9:1143-50.<br />6. Nel L, Jacobs J, Jaftha J, Meredith C. Natural spillover of a distinctly Canidae-associated biotype of rabies virus into an expanded wildlife host range in southern Africa. Virus Genes. 1997;15:79-82.<br />7. Sabeta CT, Bingham J, Nel LH. Molecular epidemiology of canid rabies in Zimbabwe and South Africa. Virus Res. 2003;91:203-11.<br />8. Johnson N, Black C, Smith J, Un H, McElhinney LM, Aylan O, et al. Rabies emergence among foxes in Turkey. J Wildl Dis. 2003;39:262-70.<br />9. Krebs JW, Williams SM, Smith JS, Rupprecht CE, Childs JE. Rabies among infrequently reported mammalian carnivores in United States, 1960-2000. J Wildl Dis. 2003;39:253-61.<br />10. Stankov S. Typing of field rabies virus strains in FR Yugoslavia by limited sequence analysis and monoclonal antibodies. Med Pregl. 2001;54:446-52.<br />11. Páez A, Saad C, Núñez C, Boshell J. Molecular epidemiology of rabies in northern Colombia 1994-2003:Evidence for human and fox rabies associated with dogs. Epidemiol Infect. 2005;133:529-36.<br />12. Ministerio de Salud, Instituto Nacional de Salud. Rabia. Serie de notas e informes técnicos. Quinta edición. Bogotá, D.C.: Minsalud-INS: 1995.<br />13. Rico A, Díaz A, Rico E. Informe de la rabia urbana en Colombia, 1996-2001. Programa de Zoonosis. Bogotá D.C.: Ministerio de Salud: 2001.<br />14. Páez A, Núñez C, García C, Boshell J. Molecular epidemiology of rabies epizootics in Colombia: evidence for human and dog rabies associated with bats. J Gen Virol. 2003;84:795-802.<br />15. Páez A, Núñez C, García C, Boshell J. Epidemiología molecular de epizootias de rabia en Colombia 1994-2002. Evidencia de rabia humana y canina asociada a quirópteros. Biomédica. 2003;23:19-30.<br />16. Hughes GJ, Páez A, Boshell J, Rupprecht CE. A phylogenetic reconstruction of the epidemiological history of canine rabies virus variants in Colombia. Infect Gen Evol. 2004;4:45-51.<br />17. Páez A, Velasco-Villa A, Rey G, Rupprecht C. Molecular epidemiology of rabies in Colombia 1994-2005 based on partial nucleoprotein gene sequences. Virus Res. 2007;130:172-81.<br />18. Ministerio de la Protección Social. Resolución 002921 de junio 25 de 2007. Declaración de emergencia sanitaria por brote de rabia humana transmitida por caninos y desabastecimiento de vacunas y sueros anti-rábicos en el Distrito de Santa Marta, Colombia. Bogotá, D.C.: Ministerio de la Protección Social; 2007.<br />19. McQueen JL, Lewis AL, Schneider NJ. Rabies diagnosis by fluorescent antibody. Its evaluation in a public health laboratory. Am J Public Health. 1960;50:1743-52.<br />20. Meslin FX, Kaplan MM, Koprowski H. The mouse inoculation test (Chapter 6), and The fluorescent antibody test (Chapter 7). In: World Health Organization. Laboratory techniques in rabies. Fourth edition. Geneva: World Health Organization; 1996.<br />21. Rodríguez G. Diagnóstico inmunológico del virus de la rabia en tejido incluido en parafina. Inf Quinc Epidemiol Nac. 1997;16:235-6.<br />22. Koprowski H. Prueba de inoculación en ratones. En: Organización Mundial de la Salud. Técnicas de laboratorio aplicadas a la rabia. Washington D.C.: OPS/OMS; 1956. p. 57-69.<br />23. Dietzschold B, Rupprecht CE, Tollis M, Lafon M, Mattel J, Wiktor TJ, et al. Antigenic diversity of the glycoprotein and nucleocapsid proteins of rabies and rabies related viruses: implications for epidemiology and control of rabies. Rev Infect Dis. 1988;10(Suppl.4):785-98.<br />24. Ministerio de Salud, Instituto Nacional de Salud. Rabia. Guía práctica para la atención integral de personas agredidas por un animal potencialmente transmisor de rabia. Serie de notas e informes técnicos No. 4. Sexta edición. Bogotá, D.C.: Ministerio de Salud-INS: 2002.<br />25. Scheffé H. Statistical inference in the non-parametric case. Ann Math Statist. 1943;14:305-32.<br />26. Kolmogorov A. Confidence limits for an unknown distribution function. Ann Math Statist. 1941;12:461-3.<br />27. Smirnov NV. Table for estimating the goodness of fit of empirical distributions. Ann Math Statist. 1948;19:279-81.<br />28. Mann HB, Whitney DR. On a test of whether one or two random variables is stochastically larger than the other. Ann Math Statist. 1947;18:50-60.<br />29. Schneider MC. Estudo de avaliação sobre área de risco para a raiva no Brasil. Rio de Janeiro, 1990 (Dissertação de Mestrado). Rio de Janeiro: Escola Nacional de Saúde Pública da Fundação Oswaldo Cruz; 1990.<br />30. Valderrama J, García I, Figueroa G, Rico E, Sanabria J, Rocha N, et al. Brotes de rabia humana transmitida por vampiros en los municipios de Bajo y Alto Baudó, departamento del Chocó, Colombia 2004-2005. Biomédica. 2006;26:387-96.<br />31. Delgado S, Carmenes P. Immune response following a vaccination campaign against rabies in dogs from northwestern Spain. Rev Vet Med. 1997;31:257-61.<br />32. Shimazaki Y, Inoue S, Takahashi C, Gamoh K, Etoh M, Kamiyama T, et al. Immune response to Japanese rabies vaccine in domestic dogs. J Vet Med B Infect Dis Vet Public Health. 2003;50:95-8.<br />33. Rigo L, Honer MR. Titulacao de anticorpo contra o virus de raiva em caes, em Campo Grande, MS na Campanha Anti-rábica de 2003. Rev Soc Bras Med Trop. 2006;39:553-5.<br />34. López R, Díaz A, Condori E. Susceptibilidad canina a rabia después de una campaña de vacunación en zonas endémicas del Perú. Revista Peruana de Medicina Experimental y Salud Pública. 2007;24:13-9.<br />35. Chomel B, Chappuis G, Bullón F, Cárdenas E, de Beublain TD, Lombard M, et al. Mass vaccination campaign against rabies: are dogs correctly protected? The Peruvian experience. Rev Infect Dis. 1988;10(Suppl.4):697-702.<br />36. Seghaier C, Cliquet F, Hammami S, Aouina T, Aubert M. Rabies mass vaccination campaigns in Tunisia: are vaccinated dogs correctly immunized? Am J Trop Med Hyg. 1999;61:879-84.
oai:oai.revistabiomedica.org:article/15
2009-12-17T12:36:55Z
biomedica:ARTI
In vitro susceptibility of Trypanosoma cruzi strains from Santander, Colombia, to hexadecylphosphocholine (miltefosine), nifurtimox and benznidazole
Susceptibilidad in vitro a hexadecilfosfocolina (miltefosina), nifurtimox y benznidazole de cepas de Trypanosoma cruzi aisladas en Santander, Colombia
Escobar, Patricia
Luna, Katherine Paola
Hernández, Indira Paola
Rueda, César Mauricio
Zorro, María Magdalena
Croft, Simon L.
Trypanosoma cruzi
Chagas disease
miltefosine benznidazole
nifurtimox
drug therapy
Colombia
Trypanosoma cruzi
enfermedad de Chagas
miltefosina
benznidazol
nifurtimox
quimioterapia
Colombia
Introduction. The current chemotherapy for Chagas disease is unsatisfactory with only two drugs available for treatment. Research to discover new drugs for Chagas disease is urgent. Hexadecyl-phosphocholine (HPC, miltefosine) has been demonstrated to have in vitro activity against Trypanosoma cruzi parasites, but its activity on different Colombian T. cruzi strains is not known.Objective. To evaluate the in vitro susceptibility of T. cruzi strains isolated from humans and vectors in Santander, Colombia. to miltefosine, nifurtimox and benznidazole.Materials and methods. Eight T. cruzi Colombian strains and three reference strains (Esmeraldo, SilvioX10 and Y) were studied. Drug activities against extracellular epimastigotes and intracellular amastigotes were determined by microscopic counting. The results were expressed as the concentrations that inhibited 50% and 90% growth (IC50 and IC90).Results. For miltefosine a similar range of drug activity was observed against all the Colombian strains, all parasites being more susceptible to miltefosine than to the reference drugs. The intracellular amastigotes were more susceptible to miltefosine (IC50 0.08 to 0.63 μM and IC90 0.21 to 2.21 μM) than extracellular forms (IC50 <0.92 to 2.29 μM and IC90 1.38 to 4.76 μM). For reference drugs, parasites were more susceptible to nifurtimox than to benznidazole and some differences in activity of benznidazole between T. cruzi strains was observed.Conclusions. The results showed the significant in vitro activity of miltefosine against T. cruzi stages, and the expected results for the reference drugs. Further in vivo studies with miltefosine are planned.
Introducción. Los tratamientos actuales para la enfermedad de Chagas son insatisfactorios y sólo existen dos medicamentos disponibles. La búsqueda de alternativas terapéuticas es prioritaria. La hexadecilfosfocolina (miltefosina) ha mostrado actividad in vitro contra Trypanosoma cruzi. Sin embargo, su actividad en aislamientos de T. cruzi obtenidos en Colombia aún no ha sido reportada.Objetivo. Evaluar la susceptibilidad in vitro a miltefosina, nifurtimox y benznidazole de cepas de T. cruzi aisladas de humanos y vectores en Santander, Colombia.Materiales y métodos. Se evaluó la susceptibilidad de los tres medicamentos en ocho cepas colombianas de T. cruzi y tres cepas de referencia: Esmeraldo, Silvio X10 y Y. La actividad de los compuestos fue determinada en epimastigotes extracelulares y amastigotes intracelulares, por conteo microscópico. Los resultados se expresaron en concentraciones inhibitorias 50 y 90 (CI50 y CI90).Resultados. Para la miltefosina, se observaron rangos similares en la actividad del medicamento entre las cepas colombianas; todos los parásitos fueron más susceptibles a la miltefosina que a los medicamentos de referencia. Los amastigotes intracelulares fueron más sensibles a la miltefosina (CI50, 0,08 a 0,63 μM y CI90, 0,21 a 2,21 μM) que las formas extracelulares (CI50, <0,92 a 2,29 μM y CI90, 1,38 a 4,76 μM). En los medicamentos de referencia, los parásitos fueron más susceptibles al nifurtimox que al benznidazole. Se observaron algunas diferencias en la actividad del benznidazole en las cepas estudiadas de T. cruzi.Conclusiones. Los resultados obtenidos de la actividad in vitro de miltefosina y de los medicamentos de referencia contra aislamientos de T. cruzi son satisfactorios y serán considerados en estudios posteriores in vivo.
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/15
10.7705/biomedica.v29i3.15
Biomedica; Vol. 29 No. 3 (2009); 448-455
Biomédica; Vol. 29 Núm. 3 (2009); 448-455
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/15/16
https://revistabiomedica.org/index.php/biomedica/article/view/15/292
/*ref*/World Health Organization. Tropical disease research, progress 2003-2004: 17th Programme Report of the UNICEF/UNDP/World Bank/WHO. Special Programme for Research and Training in Tropical Diseases. Report No. 17. Geneva: WHO; 2005.<br />2. Brisse S, Barnabe C, Tibayrenc M. Identification of six Trypanosoma cruzi phylogenetic lineages by random amplified polymorphic DNA and multilocus enzyme electrophoresis. Int J Parasitol. 2000;30:35-44.<br />3. Saravia NG, Holguin AF, Cibulskis RE, D’Alessandro A. Divergent isoenzyme profiles of sylvatic and domiciliary Trypanosoma cruzi in the eastern plains, piedmont, and highlands of Colombia. Am J Trop Med Hyg. 1987;36:59-69.<br />4. Ruiz-García M, Montilla M, Nicholls SO, Angarita L, Álvarez D. Genetic relationships and spatial genetic structure among clonal stocks of Trypanosoma cruzi in Colombia. Heredity. 2000;85:318-27.<br />5. Cuervo P, Cupolillo E, Segura I, Saravia N, Fernandes O. Genetic diversity of Colombian sylvatic Trypanosoma cruzi isolates revealed by the ribosomal DNA. Mem Inst Oswaldo Cruz. 2002;97:877-80.<br />6. Montilla MM, Guhl F, Jaramillo C, Nicholls S, Barnabe C, Bosseno MF, et al. Isoenzyme clustering of Trypanosomatidae Colombian populations. Am J Trop Med Hyg. 2002;66:394-400.<br />7. Salazar A, Schijman AG, Triana-Chávez O. High variability of Colombian Trypanosoma cruzi lineage I stocks as revealed by low-stringency single primer-PCR minicircle signatures. Acta Trop. 2006;100:110-8.<br />8. Moncayo A. Chagas disease: current epidemiological trends after the interruption of vectorial and transfusional transmission in the Southern Cone countries. Mem Inst Oswaldo Cruz. 2003;98:577-91.<br />9. Gutiérrez R, Angulo VM, Tarazona Z, Britto C, Fernandes O. Comparison of four serological tests for the diagnosis of Chagas disease in a Colombian endemic area. Parasitology. 2004;129:439-44.<br />10. Sosa S, Segura E. Tratamiento de la infección por Trypanosoma cruzi en fase indeterminada. Experiencia y normatización actual en la Argentina. Medicina. 1999;59(Suppl.2):166-70.<br />11. Lauria-Pires L, Braga MS, Vexenat AC, Nitz N, Simoes-Barbosa A, Tinoco DL, et al. Progressive chronic Chagas heart disease ten years after treatment with anti-Trypanosoma cruzi nitroderivatives. Am J Trop Med Hyg. 2000;63:111-8.<br />12. Urbina JA, Docampo R. Specific chemotherapy of Chagas disease: controversies and advances. Trends Parasitol. 2003;19:495-501.<br />13. Jannin J, Villa L. An overview of Chagas disease treat-ment. Mem Inst Oswaldo Cruz. 2007;102(Suppl.1):95-7.<br />14. Bhattacharya SK, Sinha PK, Sundar S, Thakur CP, Jha TK, Pandey K, et al. Phase 4 trial of miltefosine for the treatment of Indian visceral leishmaniasis. J Infect Dis. 2007;196:591-8.<br />15. Soto J, Soto P. Miltefosina oral para el tratamiento de la leishmaniasis. Biomédica. 2006;26(Suppl.1):207-17.<br />16. Croft SL, Seifert K, Duchene M. Antiprotozoal activities of phospholipid analogues. Mol Biochem Parasitol. 2003;126:165-72.<br />17. Saraiva VB, Gibaldi D, Previato JO, Mendonca-Previato L, Bozza MT, Freire-De-Lima CG, et al. Proinflammatory and cytotoxic effects of hexadecylphosphocholine (miltefosine) against drug-resistant strains of Trypanosoma cruzi. Antimicrob Agents Chemother. 2002;46:3472-7.<br />18. Lira R, Contreras LM, Rita RM, Urbina JA. Mechanism of action of anti-proliferative lysophospholipid analogues against the protozoan parasite Trypanosoma cruzi: potentiation of in vitro activity by the sterol biosynthesis inhibitor ketoconazole. J Antimicrob Chemother. 2001;47:537-46.<br />19. Santa-Rita RM, Santos H, Meirelles MN, de Castro SL. Effect of the alkyl-lysophospholipids on the proliferation and differentiation of Trypanosoma cruzi. Acta Trop. 2000;75:219-28.<br />20. Santa-Rita RM, Lira R, Barbosa HS, Urbina JA, de Castro SL. Anti-proliferative synergy of lysophospholipid analogues and ketoconazole against Trypanosoma cruzi (Kinetoplastida: Trypanosomatidae): cellular and ultrastructural analysis. J Antimicrob Chemother. 2005;55:780-4.<br />21. Andrade SG, Andrade V, Brodskyn C, Magalhaes JB, Netto MB. Immunological response of Swiss mice to infection with three different strains of Trypanosoma cruzi. Ann Trop Med Parasitol. 1985;79:397-407.<br />22. Filardi LS, Brener Z. Susceptibility and natural resistance of Trypanosoma cruzi strains to drugs used clinically in Chagas disease. Trans R Soc Trop Med Hyg. 1987;81:755-9.<br />23. Revollo S, Oury B, Laurent JP, Barnabe C, Quesney V, Carriere V, et al. Trypanosoma cruzi: impact of clonal evolution of the parasite on its biological and medical properties. Exp Parasitol. 1998;89:30-9.<br />24. Croft SL, Snowdon D, Yardley V. The activities of four anticancer alkyllysophospholipids against Leishmania donovani, Trypanosoma cruzi and Trypanosoma brucei. J Antimicrob Chemother. 1996;38:1041-7.<br />25. Klenner T, Beckers T, Nooter K, Holtmann H. Influence of hexadecylphosphocholine (miltefosine) on cytokine synthesis and biological responses. Adv Exp Med Biol. 1996;416:181-7.<br />26. Escobar P, Matu S, Marques C, Croft SL. Sensitivities of Leishmania species to hexadecylphosphocholine (miltefosine), ET-18-OCH(3) (edelfosine) and ampho-tericin B. Acta Trop. 2002;81:151-7.<br />27. Soto J, Arana BA, Toledo J, Rizzo N, Vega JC, Díaz A, et al. Miltefosine for new world cutaneous leishmaniasis. Clin Infect Dis. 2004;38:1266-72.<br />28. Escobar P, Yardley V, Croft SL. Activities of hexadecylphosphocholine (miltefosine), AmBisome, and sodium stibogluconate (Pentostam) against Leishmania donovani in immunodeficient scid mice. Antimicrob Agents Chemother. 2001;45:1872-5.<br />29. Murray HW, Delph-Etienne S. Visceral leishmanicidal activity of hexadecylphosphocholine (miltefosine) in mice deficient in T cells and activated macrophage microbicidal mechanisms. J Infect Dis. 2000;181:795-9.<br />30. Maya JD, Repetto Y, Agosin M, Ojeda JM, Téllez R, Gaule C, et al. Effects of nifurtimox and benznidazole upon glutathione and trypanothione content in epimastigote, trypomastigote and amastigote forms of Trypanosoma cruzi. Mol Biochem Parasitol. 1997;86:101-6.<br />31. de Castro SL. The challenge of Chagas’ disease chemotherapy: an update of drugs assayed against Trypanosoma cruzi. Acta Trop. 1993;53:83-98.<br />32. Andrade SG, Rassi A, Magalhaes JB, Ferriolli Filho F, Luquetti AO. Specific chemotherapy of Chagas disease: a comparison between the response in patients and experimental animals inoculated with the same strains. Trans R Soc Trop Med Hyg. 1992;86:624-6.<br />33. Toledo MJ, Guilherme AL, da Silva JC, de Gasperi MV, Mendes AP, Gomes ML, et al. Trypanosoma cruzi: chemotherapy with benznidazole in mice inoculated with strains from Parana state and from different endemic areas of Brazil. Rev Inst Med Trop Sao Paulo. 1997;39:283-90.<br />34. Murta SM, Gazzinelli RT, Brener Z, Romanha AJ. Molecular characterization of susceptible and naturally resistant strains of Trypanosoma cruzi to benznidazole and nifurtimox. Mol Biochem Parasitol. 1998;93:203-14.<br />35. Laurent JP, Barnabe C, Quesney V, Noel S, Tibayrenc M. Impact of clonal evolution on the biological diversity of Trypanosoma cruzi. Parasitology. 1997;114:213-8.<br />36. de Lana M, da Silveira A, Barnabe C, Quesney V, Noel S, Tibayrenc M. Trypanosoma cruzi: compared vectorial transmissibility of three major clonal genotypes by Triatoma infestans. Exp Parasitol. 1998;90:20-5.<br />37. Toledo MJ, de Lana M, Carneiro CM, Bahia MT, Machado-Coelho GL, Veloso VM, et al. Impact of Trypanosoma cruzi clonal evolution on its biological properties in mice. Exp Parasitol. 2002;100:161-72.<br />38. Toledo MJ, Bahia MT, Carneiro CM, Martins-Filho OA, Tibayrenc M, Barnabe C, et al. Chemotherapy with benznidazole and itraconazole for mice infected with different Trypanosoma cruzi clonal genotypes. Antimicrob Agents Chemother. 2003;47:223-30.<br />39. Villarreal D, Barnabe C, Sereno D, Tibayrenc M. Lack of correlation between in vitro susceptibility to benznidazole and phylogenetic diversity of Trypanosoma cruzi, the agent of Chagas disease. Exp Parasitol. 2004;108:24-31.
oai:oai.revistabiomedica.org:article/16
2009-12-17T12:36:55Z
biomedica:ARTI
Effects of aerial applications of the herbicide,glyphosate and insecticides on human health
Evaluación de los efectos del glifosato y otros plaguicidas en la salud humana en zonas objeto del programa de erradicación de cultivos ilícitos
Varona, Marcela
Henao, Gloria Lucía
Díaz, Sonia
Lancheros, Angélica
Murcia, Álix
Rodríguez, Nelcy
Álvarez, Víctor Hugo
plaguicidas
herbicidas
exposición a plaguicidas
exposición a riesgos ambientales
riesgo
toxicidad
pesticides
herbicide
pesticide exposure
environmental exposure
toxicity
Introduction. The herbicide glyphosate is administered aerially by the Program to Eradicate Illicit Crops Program and is undertaken in rigorous compliance with the Environmental Management Plan.Objective. The effects of the glyphosate herbicide and other aerially applied insecticides were measured to determine possible impact on human health.Materials and methods. In 2006-2006, a survey was taken of 112 individuals living in herbicide-treated areas of the Colombian provinces of Huila, Tolima, Putumayo, Guaviare, Santander, Antioquia, Magdalena and La Guajira. Samples of blood were examined for presence of acetylcholinesterase and organochlorine insecticides; urine was analyzed for glyphosate and its metabolites.Results. Fifty percent (50%) of the individuals sampled acknowledged the use of control chemicals as part of their work. The mean exposure time to the chemicals was 84.4 months, with a mean daily exposure of 5.6 hours. The most commonly used pesticides were of category I--extremely hazardous. In individuals sampled for glyphosate (39.6% of the total), 64.3% indicated the use of this herbicide at ground level in agricultural work. A statistically significative relationship was found between the use of glyphosate at ground level, and the concentration levels of glyphosate in the urine samples (odds ratio=2.54, 95% CI: 1.08 to 6.8).Conclusion. These data did not show a relationship between the aerial sprayings of glyphosate for illicit crops eradication and an impact on human health, nor with occupational exposure to this and other chemicals (insecticides) with a high levels of toxicity.
Introducción. El Programa de Erradicación de Cultivos Ilícitos con Glifosato se ejecuta dando cumplimiento a lo establecido en el Plan de Manejo Ambiental.Objetivo. Explorar los posibles efectos del glifosato y otros plaguicidas sobre la salud humana como resultado de las aspersiones aéreas.Materiales y métodos. Se realizó un estudio descriptivo en 112 individuos procedentes de las áreas asperjadas de los departamentos de Huila, Tolima, Putumayo, Guaviare, Santander, Antioquia, Magdalena y La Guajira, durante 2005 y 2006. Se aplicó una encuesta y se recolectaron muestras de orina para la determinación de glifosato, y de sangre, para la determinación de acetilcolinesterasa y organoclorados. Se llevó a cabo un análisis simple y se exploraron las posibles asociaciones.Resultados. El 50,0% (56 individuos) de la población manifestó el uso de plaguicidas en su trabajo. El tiempo que llevaban utilizando los plaguicidas fue de 84,8 meses y refirieron aplicar plaguicidas 5,6 horas al día. El predominio de los plaguicidas usados fue extremadamente tóxico. De 39,6% de los individuos a quienes se les cuantificó glifosato, 64,3% reportaron su uso en actividades agrícolas. Se encontró una relación estadísticamente significativa entre el uso de glifosato terrestre (manual) y los niveles de este herbicida en orina (OR=2,54; IC95% 1,08-6,08).Conclusión. No hubo hallazgos concluyentes entre la exposición a glifosato empleado en la erradicación de cultivos ilícitos y los efectos en la salud, debido a que se halló exposición ocupacional concomitante por la misma sustancia y por otras de mayor toxicidad que el glifosato.
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/16
10.7705/biomedica.v29i3.16
Biomedica; Vol. 29 No. 3 (2009); 456-475
Biomédica; Vol. 29 Núm. 3 (2009); 456-475
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/16/17
https://revistabiomedica.org/index.php/biomedica/article/view/16/294
/*ref*/Internacional Programme on Chemical Safety (IPCS). The WHO recommended classification of pesticides by hazard and guidelines to classifictation. Geneva: World Health Organization; 2004.<br />2. Salazar C, González G, Arcila O. Guaviare. Población y territorio. Instituto Amazónico de Investigaciones Científicas, SINCHI, Ministerio del Medio Ambiente. Bogotá D.C.: TM Editores; 1999. p. 1-193.<br />3. Grupo Factores de Riesgo Ambiental, Subdirección de Vigilancia y Control. Intoxicaciones por sustancias químicas en Colombia notificadas al SIVIGILA. Bogotá D.C.: Instituto Nacional de Salud; 2007.<br />4. Bernal HH, Paredes M. Impacto ambiental ocasionado por las sustancias químicas, los cultivos ilícitos y actividades conexas. Santa Fe de Bogotá: Dirección Nacional de Estupefacientes; 2001. p. 42. Fecha de consulta: 21 de octubre de 2003. Disponible en: http://www.dne.gov.co/?idcategoria=790<br />5. Ministerio de Salud. Decreto 1843 del 22 de julio de 1991. Disposiciones sanitarias sobre uso y manejo de plaguicidas. Bogotá: Ministerio de Salud; 1991. p. 1-69.<br />6. Dirección Nacional de Estupefacientes. La lucha de Colombia contra las drogas ilícitas: acciones y Resultados. Bogotá D.C.: DNE; 2002.<br />7. Solomon K, Anedón A, Cerdeira A, Marshall J, Sanín L. Estudio de los efectos del programa de erradicación de cultivos ilícitos mediante la aspersión aérea con el herbicida glifosato (PECIG) y de los cultivos ilícitos en la salud humana y en el medio ambiente. Bogotá, D.C.: CICAD; 2005. Fecha de consulta: 22 de febrero de 2008. Disponible en: http://www.dne.gov.co/index.php?idcategoria=792<br />8. Burger M, Fernández S. Exposición al herbicida glifosato: aspectos clínicos toxicológicos. Rev Med Uruguay. 2004;20:202-7.<br />9. Williams GM, Kroes R, Munro IC. Safety evaluation and risk assessment of the herbicide Roundup and its active ingredient, glyphosate for humans. Regul Toxicol Pharmacol. 2000;31:117-65.<br />10. Devine MD, Duke SO, Fedtke C. Physiology of herbicide action. Englewood Cliffs, NJ: PTR Prentice Hall; 1993.<br />11. Ministerio de Salud, Instituto Nacional de Salud. Información sobre glifosato. Uso y toxicología. Santa Fé de Bogotá: Ministerio de Salud, INS; 1992.<br />12. United States Environmental Protection Agency (EPA). Registration eligibility decision facts. Glyphosate. Publication No. EPA-738-F-93-011. Washington D.C.: EPA; 1993.<br />13. Worthing CR, Hance RJ. The pesticide manual. 9th edition. Surrey, Great Britain: The British Crop Protection Council; 1991. p. 459-60.<br />14. Chang CY, Peng YC, Hung DZ, Hu WH, Yang DY, Lin TJ. Clinical impact of upper gastrointestinal tract injuries in glyphosate-surfactant oral intoxication. Hum Exp Toxicol. 1999;18:475-8.<br />15. Lee HL, Chen KW, Chi CH, Huang JJ, Tsai LM. Clinical presentations and prognostic factors of a glyphosate - surfactant herbicide intoxication: a review of 131 cases. Acad Emerg Med. 2000;7:906-10.<br />16. Monroy CM, Cortés AC, Sicard DM, Groot H. Cito-toxicidad y genotoxicidad en células humanas expuestas in vitro a glifosato. Biomédica. 2005;25:335-45.<br />17. Ministerio de Defensa. Identificación del herbicida glifosato, propiedades y toxicidad. 2002. Fecha de consulta: 22 de febrero de 2008. Disponible en: http://www.dne.gov.co/recursos_user/documentos/Doc_tecnicos/glifosato.pdf.<br />18. Unidad Administrativa Especial, Dirección Nacional de Estupefacientes, Ministerio de Justicia y del Derecho. Identificación del herbicida a aplicar, propiedades y toxicidad. Plan de manejo ambiental para la aplicación del herbicida glifosato en la erradicación de cultivos ilícitos. Documento técnico. Santa Fe de Bogotá: Ministerio de Justicia y del Derecho; 1998.<br />19. Environmental Protection Agency (EPA). Consumer factsheet on: Glyphosate. Ground water and drinking water, 1995. Fecha de consulta: 22 de febrero de 2008. Disponible en: http://www.epa.gov/ogwdw000/contaminants/dw_contamfs/glyphosa.html<br />20. Jauhiainen A, Räsänen K, Sarantila R, Nuutinen J, Kangas J. Occupational exposure of forest workers to glyphosate during brush saw spraying work. Am Ind Hyg Assoc J. 1991;52:61-4.<br />21. Cox C. Herbicide factsheet: Glyphosate (Roundup). Journal of Pesticide Reform. 1998;18:3-17.<br />22. University of Idaho, University of California at Davis, Institute for Environmental Toxicology, Michigan State University, National Agricultural. Extension toxicology network. Pesticide information profiles. Glyphosate. 1996. Fecha de consulta: 22 de febrero de 2008. Disponible en: http://extoxnet.orst.edu/pips/glyphosa.htm<br />23. De Ross A, Blair A, Rusiecki J, Hoppin J, Svec M, Dosemeci M, et al. Cancer incidence among glyphosate–exposed pesticide applicators in the agricultural health study. Environ Health Perspect. 2005;113:49-54.<br />24. Revelo D. Efectos de la fumigación aérea con glifosato. Valle del Guamuez-San Miguel-Orito. Mocoa: Dasalud Putumayo, Oficina de Planeación, Sección Epidemiología; 2001. p. 24.<br />25. Uribe C. Supuestos efectos del glifosato en la salud humana. Clínica de Toxicología Uribe Cualla. Informe técnico. 2001. Fecha de consulta: 22 de febrero de 2008. Disponible en: http://www.ciponline.org/colombia/wwwfuc1s.pdf<br />26. Limperos G, Ranta KE. A rapid screening test for the determination of the approximate cholinesterase activity of human blood. Science. 1953;117:453-5.<br />27. United States Environmental Protection Agency (EPA). Manual of analytical methods for pesticides in humans and environmental samples. A compilation of methods selected for use in pesticide monitoring programs. Analysis of human blood or serum. Publication No. EPA–600/8-80-038. Section 5, A(3),(a). Atlanta, USA: U.S Government Printing Office; 1980. p. 1-7<br />28. Córdoba D. Toxicología. Cuarta Edición. Bogotá: Editorial Manual Moderno; 2000. p. 121-6.<br />29. Organización Panamericana de la Salud. Vigilancia sanitaria de plaguicidas: experiencia de Plagsalud en Centroamérica. Washington D.C: OPS; 2004.<br />30. Grupo Regulación y Control de Plaguicidas Químicos de Uso Agrícola, Instituto Colombiano Agropecuario. Comercialización de plaguicidas. Producción-ventas-importación-exportación. Bogotá: Editorial Produmedios; 2002.<br />31. Acquavella J, Alexander B, Mandel J, Gustin C, Baker B, Chapman P, et al. Glyphosate biomonitoring for farmers and their families: results from the Farm Family Exposure Study. Environ Health Perspect. 2004;112:321-6.<br />32. Idrovo A. Plaguicidas usados en la fumigación de cultivos ilícitos y salud humana: ¿una cuestión de ciencia o política? Rev Salud Pública. 2004;6:199-211.<br />33. Nagami H, Nishigaki Y, Matsushima S, Matsushita T, Asanuma S, Yajima N, et al. Hospital-based survey of pesticide poisoning in Japan, 1998-2002. Int J Occup Environ Health. 2005;11:180-4.<br />34. Williams G, Kroes R, Munro I. Safety evaluation and risk assessment of the herbicide Roundup and its active ingredient, glyphosate, for humans. Regul Toxicol Pharmacol. 2000;31:117-65.
oai:oai.revistabiomedica.org:article/17
2009-12-17T12:36:55Z
biomedica:BREV
Presence of antibodies to cardiac neuroreceptors in patients with Chagas disease
Presencia de anticuerpos contra neurorreceptores cardiacos de acetilcolina muscarínicos tipo II en pacientes con enfermedad de Chagas e implantación de marcapasos
Echeverry, María Clara
Tovar, Nubia Catalina
Mora, Guillermo
enfermedad de Chagas
Trypanosoma cruzi
receptores muscarínicos
marcapaso artificial
anticuerpos
corazón
Chagas disease
Trypanosoma cruzi
receptors
muscarinic
pacemaker
artificial
antibodies
heart
Introduction. The presence of antibodies against cardiac neuroreceptors has been established in several kinds of heart diseases as well as in Chagas disease. The antibody type most frequently identified is that which recognizes the muscarinic acetyl choline receptor type II (anti-m2MAChR).Objective. The frequency of the anti-m2MAChR was determined in a group of Colombian patients with permanent pacemaker implantation and Chagas disease.Materials and methods. Fifty-two patients with Chagas disease and permanent heart pacemaker implantation were matched by implantation diagnosis with 52 individuals that required pacemaker, but without Chagas disease. The presence of antibodies that recognized the m2MACh was assessed in the two groups by ELISA and Western blot by using two peptide sequences of the (m2MAChR), the second extracellular domain (2e) and the third intracellular domain (3i).Results. Serological response frequency against 2e-m2MAChR in Chagas patients was 32.7% compared with 3.8% (p<0.01) in the controls; response against 3i-m2MAChR was 51.9% compared with 19.2% (p<0.01) for the controls. No clinical differences were observed between individuals that presented anti-m2MAChR and those who did not.Conclusion. The frequency of anti-m2MAChR was higher in patients with Chagas disease for two of the receptor domains. Furthermore, patients with pacemaker therapy are more likely to have anti-m2MAChR and infection by Trypanosoma cruzi. The anti-m2MAChR response is not associated with any discernable clinical manifestation in this group of patients.
Introducción. En diferentes tipos de afecciones cardiacas, incluida la enfermedad de Chagas, se ha descrito la presencia de anticuerpos que reconocen neurorreceptores cardiacos. La respuesta más frecuente es contra receptores de acetilcolina del tipo muscarínico subtipo II (anti-m2MAChR), que reconocen este receptor.Objetivo. El objetivo del presente estudio fue establecer la frecuencia de anticuerpos anti-m2MAChR en un grupo de pacientes cardiópatas con implantación de marcapasos y enfermedad de Chagas.Materiales y métodos. Cincuenta y dos pacientes con enfermedad de Chagas e implantación de marcapasos cardiaco fueron pareados por diagnóstico de implantación con 52 individuos con marcapaso y sin enfermedad de Chagas. La presencia de anticuerpos anti-m2MAChR fue estimada mediante ELISA e inmunoblot.Resultados. El 32,7% de los casos presentaban anticuerpos contra el segundo dominio extracelular del receptor versus 3,8% de los controles (p<0,001). El 51,9% de los casos presentaron anticuerpos contra el tercer dominio intracelular del receptor versus 19,2% de los controles (p<0,001). No se encontraron diferencias clínicas entre los pacientes que presentan y los que no presentan anticuerpos anti-m2MAChR.Conclusión. El odds ratio (OR) del presente estudio muestra una mayor probabilidad de presentar anticuerpos anti-m2MAChR en pacientes con implantación de marcapaso e infección por Trypanosoma cruzi, que en aquéllos con implantación que no presentan infección por el parásito. La presencia de anticuerpos anti-m2MAChR no está relacionada con ningún tipo de manifestación clínica de las evaluadas en este estudio.
Instituto Nacional de Salud
2009-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/17
10.7705/biomedica.v29i3.17
Biomedica; Vol. 29 No. 3 (2009); 476-484
Biomédica; Vol. 29 Núm. 3 (2009); 476-484
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/17/18
https://revistabiomedica.org/index.php/biomedica/article/view/17/295
/*ref*/Abrams P, Andersson KE, Buccafusco JJ, Chapple C, de Groat WC, Fryer AD, et al. Muscarinic receptors: their distribution and function in body systems, and the implications for treating overactive bladder. J Pharmacol. 2006;148:565-78.<br />2. Myslivecek J, Nováková M, Palkovits M, Krizanová O, Kvetnanský R. Distribution of mRNA and binding sites of adrenoceptors and muscarinic receptors in the rat heart. Life Sci. 2006;79:112-20.<br />3. Wang H, Han H, Zhang L, Shi H, Schram G, Nattel S, et al. Expression of multiple subtypes of muscarinic receptors and cellular distribution in the human heart. Mol Pharmacol. 2001;59:1029-36.<br />4. Pierce KL, Lefkowitz RJ. Classical and new roles of beta-arrestins in the regulation of G-protein-coupled receptors. Nat Rev Neurosci. 2001;2:727-33.<br />5. Goin JC, Borda ES, Auger S, Storino R, Sterin L. Cardiac M2 muscarinic cholinoceptor activation by human autoantibodies: association with bradycardia. Heart. 1999;82:273-8.<br />6. Joensen L, Borda E, Kohout T, Perry S, García G, Sterin L. Trypanosoma cruzi antigen that interacts with the β1-adrenergic receptor and modifies myocardial contractile activity. Mol Biochem Parasitol. 2003;127:169-77.<br />7. Peter JC, Wallukat G, Tugler J, Maurice D, Roegel JC, Briand JP, et al. Modulation of the M2 muscarinic acetylcholine receptor activity with monoclonal anti-M2 receptor antibody fragments. J Biol Chem. 2004;279:55697-706.<br />8. Borda LE, Gorelik G, Genaro A, Goin JC, Borda ES. Human chagasic IgG interacting with lymphocyte neurotransmitter receptor triggers intracellular signal transduction. FASED J. 1990;4:1661-7.<br />9. Goin JC, Perez C, Borda E, Sterin BL. Interaction of human chagasic IgG with the second extracellular loop of the human heart muscarinic acetylholine receptor: functional and pathological implications. FASED J. 1997;10:77-83.<br />10. Goin JC, Borda E, Leiros CP, Storino R, Sterin-Borda L. Identification of antibodies with muscarinic cholinergic activity in human Chagas’ disease: Pathological implications. J Auton Nerv Syst. 1994;47:45-52.<br />11. Leiros C, Sterin-Borda L, Borda E, Goin JC, Hosey M. Desensitization and sequestration of human M2 mAChRs by autoantibodies from patients with Chagas´disease. J Biol Chem. 1997;272:12989-93.<br />12. Retondaro FC, dos Santos Costa PC, Pedrosa RC, Kurtenbach E. Presence of antibodies against the third intracellular loop of the m2 muscarinic receptor in the sera of chronic chagasic patients. FASEB J. 1999:13;2015-20.<br />13. Ribeiro AL, Giménez LE, Hernández CC, de Carvalho AC, Teixeira MM, Guedes VC, et al. Early occurrence of anti-muscarinic autoantibodies and abnormal vagal modulation in Chagas disease. Inter J Cardiol. 2007; 117:59-63.<br />14. Baba A, Yoshikawa T, Fukuda Y, Sugiyama T, Shimada M, Akaishi M, et al. Autoantibodies against M2-muscarinic acetylcholine receptors: new upstream targets in atrial fibrillation in patients with dilated cardiomyopathy. Eur Heart J. 2004;25:1108-15.<br />15. Del Corsso C, Carvalho AC, Martino HF, Varanda WA. Sera from patients with idiopathic dilated cardiomyopathy decrease ICa in cardiomyocytes isolated from rabbits. Am J Physiol Heart Circ Physiol. 2004;287:H1928-36.<br />16. Hernández CC, Barcellos LC, Giménez LE, Cabarcas RA, García S, Pedrosa RC, et al. Human chagasic IgGs bind to cardiac muscarinic receptors and impair L-type Ca2+ currents. Cardiovasc Res. 2003;58:55-65.<br />17. Ribeiro AL, Giménez LE, Hernández CC, de Carvalho AC, Teixeira MM, Guedes VC, et al. Early occurrence of anti-muscarinic autoantibodies and abnormal vagal modulation in Chagas disease. Int J Cardiol. 2007; 117:59-63.<br />18. Corrêa MB, Pedrosa RC, Pereira BB, Corrêa WB, Medeiros A, Costa PC. Chronic Chagas disease patients with sinus node dysfunction: is the presence of IgG antibodies with muscarinic agonist action independent of left ventricular dysfunction. Rev Soc Bras Med Trop. 2007;40:665-71.<br />19. Medei E, Pedrosa RC, Benchimol PR, Costa PC, Hernández CC, Chaves EA, et al. Human antibodies with muscarinic activity modulate ventricular repolarization: basis for electrical disturbance. Int J Cardiol. 2007;115:373-80.<br />20. Talvani A, Rocha MO, Ribeiro AL, Borda E, Sterin-Borda L, Teixeira MM. Levels of anti-M2 and anti-beta1 autoantibodies do not correlate with the degree of heart dysfunction in Chagas’ heart disease. Microbes Infect. 2006;8:2459-64.<br />21. Mora G, Echeverry M, Rey G, López M, Posada L, Rivas F. Frecuencia de anticuerpos anti-Trypanosoma cruzi en pacientes portadores de marcapasos de la Clínica San Pedro Claver de Bogotá. Biomédica. 2007;27:483-9.<br />22. Luetje C, Brumwel C, Gainer M, Peterson G, Schimerlik M, Nathanson N. Isolation and characterization of monoclonal antibodies specific for the cardiac muscarinic acetylcholine receptor. Biochemestry. 1987;26:6892-6.<br />23. Cremaschi G, Fernández MM, Gorelik G, Goin JC, Fossati CA, Zwirner NW, et al. Modulatory effects on myocardial physiology induced by an anti-Trypanosoma cruzi monoclonal antibody involve recognition of major antigenic epitopes from beta1-adrenergic and M2-muscarinic cholinergic receptors without requiring receptor cross-linking. J Neuroimmunol. 2004;153:99-107.<br />24. Masuda MO, Levin M, De Oliveira SF, Dos Santos PC, Bergami PL, Dos Santos NA, et al. Functionally active cardiac antibodies in chronic Chagas’ disease are specifically blocked by Trypanosoma cruzi antigens. FASEB J. 1998;12:1551-8.<br />25. Sterin-Borda L, Giordanengo L, Joensen L, Gea S. Cruzipain induces autoantibodies against cardiac muscarinic acetylcholine receptors. Functional and pathological implications. Eur J Immunol. 2003;33: 2459-68.<br />26. Fu ML. Characterization of anti-heart M2 muscarinic receptor antibodies -a combined clinical and experimental study. Mol Cell Biochem. 1996;163:343-7.<br />27. Retondaro FC, Dos Santos PC, Pedrosa RC, Kurtenbach E. Presence of antibodies against the third intracellular loop of the m2 muscarinic receptor in the sera of chronic chagasic patients. FASEB J. 1999;13:2015-20.<br />28. Marin-Neto JA, Cunha-Neto E, Maciel BC, Simões MV. Pathogenesis of chronic Chagas heart disease. Circulation. 2007;115:1109-23.
oai:oai.revistabiomedica.org:article/18
2009-12-18T16:31:11Z
biomedica:EDIT
Therapy of rabies encephalitis
Terapia de la encefalitis rábica
Jackson, Alan C.
Instituto Nacional de Salud
2009-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/18
10.7705/biomedica.v29i2.18
Biomedica; Vol. 29 No. 2 (2009); 169-176
Biomédica; Vol. 29 Núm. 2 (2009); 169-176
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/18/299
https://revistabiomedica.org/index.php/biomedica/article/view/18/1544
/*ref*/World Health Organization. WHO expert consultation on rabies: first report. Geneva: WHO; 2005.<br />2. Jackson AC, Warrell MJ, Rupprecht CE, Ertl HC, Dietzschold B, O’Reilly M, et al. Management of rabies in humans. Clin Infect Dis. 2003;36:60-3.<br />3. Jackson AC. Human disease. In: Jackson AC, Wunner WH, editors. Rabies. London: Elsevier Academic Press; 2007. p. 309-40.<br />4. Willoughby RE Jr, Tieves KS, Hoffman GM, Ghanayem NS, Amlie-Lefond CM, Schwabe MJ, et al. Survival after treatment of rabies with induction of coma. N Engl J Med. 2005;352:2508-14.<br />5. Merigan TC, Baer GM, Winkler WG, Bernard KW, Gibert CG, Chany C, et al. Human leukocyte interferon administration to patients with symptomatic and suspected rabies. Ann Neurol. 1984;16:82-7.<br />6. Kureishi A, Xu LZ, Wu H, Stiver HG. Rabies in China: recommendations for control. Bull World Health Organ. 1992; 70:443-50.<br />7. Warrell MJ, White NJ, Looareesuwan S, Phillips RE, Suntharasamai P, Chanthavanich P, et al. Failure of interferon alfa and tribavirin in rabies encephalitis. Br Med J. 1989;299:830-3.<br />8. Hemachudha T, Sunsaneewitayakul B, Mitrabhakdi E, Suankratay C, Laothamathas J, Wacharapluesadee S, et al. Paralytic complications following intravenous rabies immune globulin treatment in a patient with furious rabies. Int J Infect Dis. 2003;7:76-7.<br />9. Emmons RW, Leonard LL, DeGenaro F Jr, Protas ES, Bazeley PL, Giammona ST, et al. A case of human rabies with prolonged survival. Intervirology. 1973;1:60-72.<br />10. Hattwick MA, Corey L, Creech WB. Clinical use of human globulin immune to rabies virus. J Infect Dis. 1976;133 (Suppl):A266-72.<br />11. Basgoz N. Case 21-1998: rabies. N Engl J Med. 1999;340:64-5.<br />12. Superti F, Seganti L, Pana A, Orsi N. Effect of amantadine on rhabdovirus infection. Drugs Exp Clin Res. 1985;11:69-74.<br />13. Hu WT, Willoughby RE Jr, Dhonau H, Mack KJ. Long-term follow-up after treatment of rabies by induction of coma. N Engl J Med. 2007;357:945-6.<br />14. Lafon M. Bat rabies--the Achilles heel of a viral killer? Lancet. 2005;366:876-7.<br />15. Hattwick MA, Weis TT, Stechschulte CJ, Baer GM, Gregg MB. Recovery from rabies: a case report. Ann Intern Med. 1972;76:931-42.<br />16. Ministerio da Saude in Brazil. Rabies, human survival, bat-Brazil: (Pernambuco). ProMED-mail. 2008; 20081114.3599. [Accessed: May 19, 2009] Available at: http://www.promedmail.org/pls/otn/f?p=2400:1001:57555::::F2400_P1001_BACK_PAGE,F2400_P1001_ARCHIVE_NUMBER,F2400_P1001_USE_ARCHIVE:1001,20081114.3599,Y<br />17. Lafon M. Immunology. In: Jackson AC, Wunner WH, editors. Rabies. London: Elsevier Academic Press; 2007. p. 489-504.<br />18. Jackson AC. Recovery from rabies. N Engl J Med. 2005;352:2549-50.<br />19. Krishnamurthy KB, Drislane FW. Depth of EEG suppression and outcome in barbiturate anesthetic treatment for refractory status epilepticus. Epilepsia. 1999;40:759-62.<br />20. Bassin S, Smith TL, Bleck TP. Clinical review: status epilepticus. Crit Care. 2002;6:137-42.<br />21. Nevander G, Ingvar M, Auer R, Siesjo BK. Status epilepticus in well-oxygenated rats causes neuronal necrosis. Ann Neurol. 1985;18:281-90.<br />22. Meldrum BS, Brierley JB. Prolonged epileptic seizures in primates. Ischemic cell change and its relation to ictal physiological events. Arch Neurol. 1973;28:10-7.<br />23. Lockhart BP, Tordo N, Tsiang H. Inhibition of rabies virus transcription in rat cortical neurons with the dissociative anesthetic ketamine. Antimicrob Agents Chemother. 1992;36:1750-5.<br />24. Lockhart BP, Tsiang H, Ceccaldi PE, Guillemer S. Ketamine-mediated inhibition of rabies virus infection in vitro and in rat brain. Antivir Chem Chemother. 1991;2:9-15.<br />25. Weli SC, Scott CA, Ward CA, Jackson AC. Rabies virus infection of primary neuronal cultures and adult mice: failure to demonstrate evidence of excitotoxicity. J Virol. 2006;80:10270-3.<br />26. Cheng YD, Al-Khoury L, Zivin JA. Neuroprotection for ischemic stroke: two decades of success and failure. NeuroRx. 2004;1:36-45.<br />27. Ginsberg MD. Current status of neuroprotection for cerebral ischemia: synoptic overview. Stroke. 2009;40(Suppl 3):S111-4.<br />28. Willoughby RE, Roy-Burman A, Martin KW, Christensen JC, Westenkirschner DF, Fleck JD, et al. Generalised cranial artery spasm in human rabies. Dev Biol (Basel). 2008;131:367-75.<br />29. McDermid RC, Saxinger L, Lee B, Johnstone J, Noel Gibney RT, Johnson M, et al. Human rabies encephalitis following bat exposure: failure of therapeutic coma. Can Med Assoc J. 2008;178:557-61.<br />30. Wilde H, Hemachudha T, Jackson AC. Viewpoint: management of human rabies. Trans R Soc Trop Med Hyg. 2008;102:979-82.<br />31. Rubin J, David D, Willoughby RE Jr, Rupprecht CE, Garcia C, Guarda DC, et al. Applying the Milwaukee protocol to treat canine rabies in Equatorial Guinea. Scand J Infect Dis. 2009;41:372-5.<br />32. Daily Telegraph Online. Rabies, human - United Kingdom (04): (Northern Ireland) ex South Africa. ProMED-mail. 2009; 20090107.0065. [Accessed: May 19, 2009]. Available at: http://www.promedmail.org/pls/otn/f?p=2400:1202:19224::NO::F2400_P1202_CHECK_DISPLAY,F2400_P1202_PUB_MAIL_ID:X,75493
oai:oai.revistabiomedica.org:article/19
2009-12-18T16:31:11Z
biomedica:CASO
Endocarditis due to infection by Paecilomyces variotii
Endocarditis infecciosa por Paecilomyces variotii
Senior, Juan Manuel
Saldarriaga, Clara
Endocarditis
mycoses
Paecilomyces
mitral valve
cardiac surgical procedures
amphotericin B
Fungal endocarditis is a cardiac complication that has been increasing throughout the world. We present a case of infective endocarditis by Paecilomyces variotii in a male patient with a prosthetic mitral valve. Successful treatment consisted of administration of amphotericin B (total dose 3,670 mg) and mitral valve replacement. Only six cases have been reported previously, with a 100% mortality rate.
La endocarditis infecciosa por hongos es una complicación cada vez más frecuente en el mundo. Presentamos un caso de endocarditis infecciosa por Paecilomyces variotii en un paciente de sexo masculino con bioprótesis mitral, que respondió satisfactoriamente al tratamiento con cirugía de reemplazo valvular mitral y anfotericina B (dosis total de 3.670 mg). Hasta la fecha, sólo se han reportado seis casos similares en el mundo, con una mortalidad del 100%.
Instituto Nacional de Salud
2009-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/19
10.7705/biomedica.v29i2.19
Biomedica; Vol. 29 No. 2 (2009); 177-180
Biomédica; Vol. 29 Núm. 2 (2009); 177-180
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/19/20
https://revistabiomedica.org/index.php/biomedica/article/view/19/300
/*ref*/Ostermiller WE, Dye W, Seinberg M. Fungal endocarditis following cardiovascular surgery. J Thorac Cardiovasc Surg. 1971;61:670-5.<br />2. Joachim H, Polayes SH. Subacute endocarditis and systemic mycosis. JAMA. 1940;115:205-8.<br />3. Koelle WA, Pastor B. Candida albicans endocarditis after aortic valvulotomy. N Engl J Med. 1956;255:997-9.<br />4. Pierrotti LC, Baddour LM. Fungal endocarditis, 1995-2000. Chest. 2002;122:302-10.<br />5. Allevato PA, Ohorodnik JM, Mezger E, Eisses JF. Paecilomyces javanicus endocarditis of native and pros-thetic aortic valve. Am J Clin Pathol. 1984;82:247-52.<br />6. Kalish SB, Goldschmidt R, Li C, Knop R, Cook FV, Wilner G, et al. Infective endocarditis caused by Paecilomyces varioti. Am J Clin Pathol. 1982;78:249-52.<br />7. Rubinstein E, Noriega ER, Simberkoff MS, Holzman R, Rahal JJ. Fungal endocarditis: Analysis of 24 cases and review of the literature. Medicine. 1975;54: 331-44.<br />8. Uys CJ, Don PA, Schrire V, Barnard CN. Endocarditis following cardiac surgery due to the fungus Paecilomyces. S Afr Med J. 1963;37:1276-80.<br />9. Silver MD, Tuffnell PG, Bigelow WG. Endocarditis caused by Paecilomyces varioti affecting an aortic valve allograft. J Thorac Cardiovasc Surg. 1971;61:278-81.<br />10. Haldane EV, MacDonald JL, Gittens WO, Yuce K, van Rooyen CE. Prosthetic valvular endocarditis due to the fungus Paecilomyces. Can Med Assoc J. 1974;111:963-8.<br />11. McClellan JR, Hamilton JD, Alexander JA, Wolfe WG, Reed JB. Paecilomyces varioti endocarditis on a prosthetic aortic valve. J Thorac Cardiovasc Surg. 1976;71:472-5.<br />12. Wang SM, Shieh CC, Liu CC. Successful treatment of Paecilomyces variotii splenic abscesses: a rare complication in a previously unrecognized chronic granulomatous disease child. Diagn Microbiol Infect Dis. 2005;53:149-52.<br />13. Chamilos G, Kontoyiannis DP. Voriconazole-resistant disseminated Paecilomyces variotii infection in a neutropenic patient with leukaemia on voriconazole prophylaxis. J Infect. 2005;51:e225-8.
oai:oai.revistabiomedica.org:article/20
2009-12-18T16:31:11Z
biomedica:CASO
Allergy and intolerance to nonsteroidal antinflammatory drugs: successful desensitization in three cases
Alergia e intolerancia a antiinflamatorios no esteroides: desensibilización exitosa en tres casos y revisión de la literatura
Cardona, Ricardo
Ramírez, Ruth Helena
Reina, Zulma
Escobar, Mauricio Fernando
Morales, Edison
hipersensibilidad a los medicamentos
aspirina
agentes antiinflamatorios no esteroides
desensibilización inmunológica
asma
anafilaxis
pólipos nasales
sinusitis
Drug hypersensitivity
aspirin
anti-inflammatory agents
non-steroidal
desensitization
immunologic
asthma
anaphylaxis
nasal polyps
sinusitis
Adverse reactions to nonsteroidal antinflammatory drugs are the second cause of reactions to drugs after beta-lactams. Prevalence of these reactions among general population is between 0.1-0.3%, and prevalence of nonsteroidal antinflammatory drug-induced anaphylaxis is 0.01%.Acetylsalicylic acid or nonsteroidal antinflammatory drug sensitivity can be manifested as acute urticaria, angioedema, acute asthma, acetylsalicylic acid exacerbated respiratory disease and anaphylaxis.An updated review based on three cases of patientes with acetylsalicylic acid or nonsteroidal antinflammatory drug intolerance is presented in which, because of their concomitant diseases, permanent treatment with acetylsalicylic acid was required. After undergoing a fast acetylsalicylic acid desentization protocol in an intensive care unit, these patients were able to receive daily acetylsalicylic acid doses without any adverse effects.
Los antiinflamatorios no esteroides son la segunda causa de reacciones a medicamentos después de los beta-lactámicos. La prevalencia de las reacciones a antiinflamatorios no esteroideos en la población general es de 0,1% a 0,3% y la prevalencia de anafilaxia inducida por ellos es de 0,01%.La intolerancia al ácido acetilsalicílico o a los antiinflamatorios no esteroides se presenta con síntomas como urticaria aguda, angioedema, crisis asmática, enfermedad respiratoria exacerbada por ácido acetilsalicílico y anafilaxia.Presentamos una revisión actualizada basada en tres casos de pacientes con intolerancia al ácido acetilsalicílico o a los antiinflamatorios no esteroideos que, por sus enfermedades concomitantes, requerían tratamiento permanente conácido acetilsalicílico. Después de someterlos a un protocolo de desensibilización rápida ácido acetilsalicílico en una unidad de cuidados intensivos, estos pacientes pudieron continuar recibiendo ácido acetilsalicílico diariamente sin efectos adversos.
Instituto Nacional de Salud
2009-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/20
10.7705/biomedica.v29i2.20
Biomedica; Vol. 29 No. 2 (2009); 181-190
Biomédica; Vol. 29 Núm. 2 (2009); 181-190
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/20/21
https://revistabiomedica.org/index.php/biomedica/article/view/20/301
/*ref*/Demoly P, Hillaire-Buys D. Classification and epidemiology of hypersensitivity drug reactions. Immunol Allergy Clin North Am. 2004;24:345-56.<br />2. Sánchez-Borges M. Clinical management of nonsteroidal anti-inflammatory drug hypersensitivity. WAO Journal. 2008;1:29-33.<br />3. Jenneck C, Juergens U, Buecheler M, Novak N. Pathogenesis, diagnosis, and treatment of aspirin intolerance. Ann Allergy Asthma Immunol. 2007;99:13-21.<br />4. Cianferoni A, Novembre E, Mugnaini L, Lombardi E, Bernardini R, Pucci N, et al. Clinical features of acute anaphylaxis in patients admitted to a university hospital: an 11-year retrospective review (1985-1996). Ann Allergy Asthma Immunol. 2001;87:27-32.<br />5. Szczeklik A, Stevenson DD. Aspirin-induced asthma: advances in pathogenesis, diagnosis, and management. J Allergy Clin Immunol. 2003;111:913-21.<br />6. Faich GA. Adverse-drug-reaction monitoring. N Engl J Med. 1986;314:1589-92.<br />7. Settipane GA. Aspirin and allergic diseases: a review. Am J Med. 1983;74:102-9.<br />8. Sánchez-Borges M, Capriles-Hulett A, Caballero-Fonseca F. NSAID-induced urticaria and angioedema: a reappraisal of its clinical management. Am J Clin Dermatol. 2002;3:599-607.<br />9. Castells M. Desensitization for drug allergy. Curr Opin Allergy Clin Immunol. 2006;6:476-81.<br />10. Berges-Gimeno MP, Simon RA, Stevenson DD. Long-term treatment with aspirin desensitization in asthmatic patients with aspirin-exacerbated respiratory disease. J Allergy Clin Immunol. 2003;111:180-6.<br />11. Gollapudi RR, Teirstein PS, Stevenson DD, Simon RA. Aspirin sensitivity: implications for patients with coronary artery disease. JAMA. 2004;292:3017-23.<br />12. Widal F, Abrami P, Lermoyez J. Anaphylaxie et idiosyncrasie. Presse Med. 1922;30:189-92.<br />13. Sweet JM, Stevenson DD, Simon RA, Mathison DA. Long-term effects of aspirin desensitization-treatment for aspirin-sensitive rhinosinusitis-asthma. J Allergy Clin Immunol. 1990;85:59-65.<br />14. Stevenson DD, Hankammer MA, Mathison DA, Christiansen SC, Simon RA. Aspirin desensitization treatment of aspirin-sensitive patients with rhinosinusitis-asthma: long-term outcomes. J Allergy Clin Immunol. 1996;98:751-8.<br />15. Pfaar O, Klimek L. Aspirin desensitization in aspirin intolerance: update on current standards and recent impro-vements. Curr Opin Allergy Clin Immunol. 2006;6:161-6.<br />16. White AA, Stevenson DD, Simon RA. The blocking effect of essential controller medications during aspirin challenges in patients with aspirin-exacerbated respiratory disease. Ann Allergy Asthma Immunol. 2005;95:330-5.<br />17. Stevenson DD, Simon RA. Selection of patients for aspirin desensitization treatment. J Allergy Clin Immunol. 2006;118:801-4.<br />18. Silberman S, Neukirch-Stoop C, Steg PG. Rapid desensitization procedure for patients with aspirin hypersensitivity undergoing coronary stenting. Am J Cardiol. 2005;95:509-10.<br />19. Sánchez-Borges M, Capriles-Hulett A, Caballero-Fonseca F. The multiple faces of nonsteroidal antiinflammatory drug hypersensitivity. J Investig Allergol Clin Immunol. 2004;14:329-34.<br />20. Stevenson DD. Aspirin and NSAID sensitivity. Immunol Allergy Clin North Am. 2004;24:491-505.<br />21. Johansson SG, Hourihane JO, Bousquet J, Bruijnzeel-Koomen C, Reborg S, Haahtela T, et al. A revised nomenclature for allergy. An EAACI position statement from the EAACI nomenclature task force. Allergy. 2001;56:813-24.<br />22. Andri L, Senna G, Betteli C, Givanni S, Scaricabarozzi I, Mezzelani P, et al. Tolerability of nimesulide in aspirin-sensitive patients. Ann Allergy. 1994;72:29-32.<br />23. Kosnik M, Music E, Matjaz F, Suskovic S. Relative safety of meloxicam in NSAID-intolerant patients. Allergy. 1998;53:1231-3.<br />24. Nettis E, Di Paola R, Ferrannini A, Tursi A. Meloxicam in hypersensitivity to NSAIDs. Allergy. 2001;56:803-4.<br />25. Quiralte J, Blanco C, Castillo R, Delgado J, Carrillo T. Intolerance to nonsteroidal antiinflammatory drugs: results of controlled drug challenges in 98 patients. J Allergy Clin Immunol. 1996;98:678-85.<br />26. Ruxrungtham K, Chantaphakul H, Tiyasatapon S, Phanupak P. Acetaminophen cross-sensitivity is common in Thai patients with aspirin/NSAIDs Sensitivity and may be life-threatening. J Allergy Clin Immunol. 2002;109:s141.<br />27. Zedlitz S, Linzbach L, Kaufmann R, Boehncke WH. Reproducible identification of the causative drug of a fixed drug eruption by oral provocation and lesional patch testing. Contact Derm. 2002;46:352-3.<br />28. Talhari C, Lauceviciute I, Enderlein E, Ruzicka T, Homey B. COX-2-selective inhibitor valdecoxib induces severe allergic skin reactions. J Allergy Clin Immunol. 2005;115:1089-90.<br />29. Pichler WJ, Tilch J. The lymphocyte transformation test in the diagnosis of drug hypersensitivity. Allergy. 2004;59:809-20.<br />30. Milewski M, Mastalerz L, Nizankowska E, Szczeklik A. Nasal provocation test with lysine-aspirin for diagnosis of aspirin-sensitive asthma. J Allergy Clin Immunol. 1998;101:581-6.<br />31. Nizankowska-Mogilnicka E, Bochenek G, Mastalerz L, Swierczynska M, Picado C, Scadding G, et al. EAACI/GA2LEN guideline: aspirin provocation tests for diagnosis of aspirin hypersensitivity. Allergy. 2007;62:1111-8.
oai:oai.revistabiomedica.org:article/21
2009-12-18T16:31:12Z
biomedica:CASO
Human rabies encephalitis by a vampire bat bite in an urban area of Colombia
Encefalitis rábica humana por mordedura de murciélago en un área urbana de Colombia
Pradilla, Gustavo
Mantilla, Julio César
Badillo, Reynaldo
encefalitis
rabia
quirópteros
zoonosis
autopsia
Colombia
Encephalitis
rabies
chiroptera
zoonoses
autopsy
Colombia
A case of rabies encephalitis is presented in a teenaged male, which developed four months after a bat bite in the urban area of Floridablanca, Santander Province, Colombia. The complex clinical manifestations prevented the confirmation of an antemortem diagnosis, principally because of the lengthy incubation period and the absence of other similar urban cases. Despite application of several therapies, including the Milwaukee protocol, the patient died 19 days after hospital admission. The autopsy revealed a necrotic, acute, pan-encephalitis of rabies virus etiology. The test of direct immunofluorescence in brain tissue was positive, as well as the biologic test in mice. Serological tests indicated it to be an antigenic variant type 3, whose main reservoir is the hematophagous vampire bat, Desmodus rotundus. This is probably the first case of bat-induced rabies reported in an urban community of Colombia and one of the few in Latin America. Although rabies encephalitis by a bat bite is rare, the case serves as a notice to health authorities and to the medical community to be alert to this risk.
Se presenta el caso de un adolescente con encefalitis rábica adquirida cuatro meses después de ser mordido por un murciélago en el área urbana de Floridablanca (Santander), Colombia.La complejidad de sus manifestaciones clínicas hizo muy difícil confirmar el diagnóstico antes de su muerte, principalmente por su período de incubación y la ausencia de casos similares en áreas diferentes de las selváticas.A pesar de las diversas estrategias terapéuticas, que incluyeron el denominado Protocolo de Milwaukee, el paciente falleció luego de 19 días de evolución y la necropsia confirmó que se trataba de una panencefalitis aguda necrosante de etiología viral rábica. La prueba de inmunofluorescencia directa en tejido cerebral fue positiva, lo mismo que la prueba biológica con ratones. La tipificación viral mostró la variante antigénica 3, cuyo reservorio principal es el vampiro hematófago Desmodus rotundus.Con el reporte de este caso de encefalitis rábica por mordedura de un murciélago, probablemente el primero informado en un área urbana de Colombia y de los pocos en América Latina, alertamos a las autoridades sanitarias y a la comunidad en salud, para aumentar y fortalecer las medidas preventivas en todos los niveles.
Instituto Nacional de Salud
2009-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/21
10.7705/biomedica.v29i2.21
Biomedica; Vol. 29 No. 2 (2009); 191-203
Biomédica; Vol. 29 Núm. 2 (2009); 191-203
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/21/22
https://revistabiomedica.org/index.php/biomedica/article/view/21/303
/*ref*/Leung AK, Davies HD, Hon KL. Rabies: Epidemiology, pathogenesis, and prophylaxis. Adv Ther. 2007;24:1340-7.<br />2. Rodríguez LF. Situación de rabia canina y rabia paresiante en Colombia. Universidad Antonio Nariño. Fecha de consulta: 9 de noviembre de 2008. Disponible en: www.uan.edu.co/deans/veterinaria/publicaciones/docs/articulos/situacion_rabia.pdf.<br />3. Jackson AC. Rabies. Can J Neurol Sci. 2000;27:278-83.<br />4. Srinivasan A, Burton EC, Kuehnert MJ, Rupprecht C, Sutker WL, Ksiazek TG, et al. Transmission of rabies virus from an organ donor to four transplant recipients. N Engl J Med. 2005;352:1103-11.<br />5. Jackson AC. Update on rabies. Curr Op Neurol. 2002;15:327-31.<br />6. Hemachudha T, Laothamatas J, Rupprecht C. Human rabies: a disease of complex neuropathogenetic mechanisms and diagnostic challenges. Lancet Neurol. 2002;1:101-9.<br />7. Smith JS, Fishbein DB, Rupprecht CE, Clarck K. Unexplained rabies in three immigrants in the United States. A virologic investigation. N Engl J Med. 1991;324:205-11.<br />8. Takayama N. Rabies: a preventable but incurable disease. J Infect Chemother. 2008;14:8-14.<br />9. McDermid RC, Saxinger L, Lee B, Johnstone J, Gibney RT, Jhonson M, et al. Human rabies encephalitis following bat exposure: failure of therapeutic coma. CMAJ. 2008;178:557-61.<br />10. Valderrama J, García I, Figueroa G, Rico E, Sanabria J, Rocha N, et al. Brotes de rabia humana transmitida por vampiros en los municipios de Bajo y Alto Baudó, departamento del Chocó, Colombia 2004-2005. Biomédica. 2006;26:387-96.<br />11. Alvis N. De la rabia humana de origen canino y otras vergüenzas. Rev MVZ Córdoba. 2006;11:779-80.<br />12. Escobar E. La rabia: crónica de una experiencia. Medicina. 2005;27:249-55.<br />13. Escobar E. La rabia transmitida por vampiros. Biomédica. 2004;24:231-6.<br />14. Instituto Nacional de Salud. Rabia. Guía práctica para la atención de personas agredidas por un animal potencialmente transmisor de rabia. Serie de notas e informes técnicos No. 4. Sexta Edición. Bogotá: Instituto Nacional de Salud; 2002.<br />15. Schneider MC, Santos-Burgoa C, Aron J, Muñoz B, Ruiz-Velasco S, Uieda W. Potential force of infection of human rabies transmitted by vampire bats in the Amazonian region of Brazil. Am J Trop Med Hyg. 1996;55:680-4.<br />16. Sireno MA, Cantú PC. Presencia del virus rábico en fauna silvestre en la jurisdicción sanitaria No. II del estado de San Luís Potosí (México). Revista Salud Pública y Nutrición. 2001;2. Fecha de consulta: 17 de noviembre de 2008. Disponible en: http://www.respyn.uanl.mx/ii/2/articulos/rabia-fs.html.<br />17. Schneider MV, Belotto A, Adé MP, Leanes LF, Correa E, Tamayo H, et al. Situación epidemiológica de la rabia humana en América Latina en 2004. Boletín Epidemiológico. 2005;26:2-4.<br />18. Briones S, Marín-Pech E. Estudio de caso de rabia humana transmitida por murciélago hematófago en Yucatán, México. Rev Biomed. 2006;17:118-22.<br />19. Navarro AM, Bustamante J, Sato A. Situación actual y control de la rabia en el Perú. Rev Perú Med Exp Salud Pública. 2007;24:46-50.<br />20. López A, Mirana P, Tejada E, Fishbein DB. Outbreak of human rabies in the Peruvian jungle. Lancet. 1992;339:408-11.<br />21. Castillo B, Mike E, De Bernard C. Caso clínico patológico. Rabia selvática en humanos por mordedura de vampiro: primer caso en humanos. Fecha de consulta: 17 de noviembre de 2008. Disponible en: http://www.telmeds.net/modules.php?name=News&file=article&sid=447.<br />22. da Rosa ES, Kotait I, Barbosa FS, Carrieri ML, Brandao PE, Pinheiro AS, et al. Bat-transmitted human rabies out-breaks, Brazilian Amazon. Emerg Infect Dis. 2006;12:1197-202.<br />23. Sampedro AC, Martínez CM, De la Ossa K, Otero YL, Santos LM, Osorio S, et al. Nuevos registros de especies de murciélagos para el departamento de Sucre y algunos datos sobre su ecología en esta región colombiana. Caldasia. 2007;29:355-62.<br />24. Centro Panamericano de Fiebre Aftosa. América contra la rabia. Plan de acción para la prevención y el control de la rabia en las Américas: etapa 2005-2009. Río de Janeiro: PANAFTOSA, OPS, OMS; 2007. p. 4.<br />25. Noah DL, Drenzek CL, Smith JS, Krebs JW, Orciaria L, Shaddock J, et al. Epidemiology of human rabies in the United States, 1098 to 1996. Ann Int Med. 1998;128:922-30.<br />26. Loza-Rubio E, de Mattos CC, Aguilar A, de Mattos CA. Aislamiento y caracterización molecular de un virus rábico, obtenido de un murciélago no hematófago en la ciudad de México. Vet Mex. 2000;31:147-51.<br />27. Favic M, Yung V, Pavletic C, Ramírez E, de Mattos C, de Mattos CA. Rol de los murciélagos insectívoros en la transmisión de la rabia en Chile. Arch Med Vet. 1999;31:157-65.<br />28. de Mattos CA, Favi M, Yung V, Pavletic C, de Mattos CC. Bat rabies in urban centers in Chile. J Wildl Dis. 2000;36:231-40.<br />29. Favi M, de Mattos CA, Yung V, Chala E, López LR, de Mattos CC. First case of human rabies in Chile caused by an insectivorous bat virus variant. Emerg Infect Dis. 2002;8:79-81.<br />30. Amasino CF, Garbi CJ, Amasino MF. La rabia urbana en la provincia de Buenos Aires, Argentina: origen-evolu-ción-actualidad. Analecta Veterinaria. 2002;22:17-31.<br />31. Paéz A, Núñez G, García C, Boshell J. Epidemiología molecular de epizootias de rabia en Colombia, 1994-2002: evidencia de rabia humana y canina asociada con quirópteros. Biomédica. 2003:23:19-30.<br />32. Brito E, Palacios H, Yunda HR, Martínez J, Reyes L. Construcción de un modelo espacial para determinar áreas de riesgo en Colombia. Rabia de origen silvestre en Colombia. ICA 2005. Fecha de consulta: 17 de noviembre de 2008]. Disponible en: www.ica.gov.co/getattachment/9a95b63a-fc49-435d-8013-d6b7aeaf506b/Publicacion-8.aspx.<br />33. Ferraz C, Achkar SM, Kotait I. First report of rabies in vampire bats (Desmodus rotundus) in an urban area, Ubatuba, Sao Paulo State, Brazil. Rev Inst Med Trop Sao Paulo. 2007;49:389-90.<br />34. Hemachudha T, Phuapradit P. Rabies. Curr Opin Neurol. 1997;10:260-7.<br />35. Hemachudha T, Phanuphak P, Sriwanthana B, Manutsathit S, Siriprasomsup W, Ukachoke C, et al. Immunologic study of human encephalitic and paralytic rabies: preliminary report of 16 patients. Am J Med.1988;84:673-7.
oai:oai.revistabiomedica.org:article/22
2009-12-18T16:31:12Z
biomedica:CASO
An anatomical variation: the aberrant termination of the thoracic duct
Una variación anatómica: la desembocadura aberrante del conducto torácico
Peña, Elizabeth
Zuñiga, Janneth
variación (genética)
conducto torácico
anomalías cardiovasculares
anomalías linfáticas
anomalías múltiples
Variation (Genetics)
thoracic duct
cardiovascular abnormalities
lymphatic abnormalities
abnormalities
multiple
In a male cadaver dissected at the Department of Morphology, University del Valle, Cali (Colombia), a rarely described anatomical variation was found. It consisted of an aberrant termination or drainage of the thoracic lymph duct. Normally, this duct ascends in the thorax behind the esophagus, gradually diverges towards the left side of the neck and ends in the left jugulo-subclavian confluent--either in the internal jugular vein or in the subclavian vein. In the case of this cadaver, the thoracic duct diverged towards the right side of the neck to end in the right internal jugular vein. The present work describes the embryonic origin of the duct and offers a possible explanation for the anatomical variation encountered.
En uno de los cadáveres disecados durante el primer semestre de 2006 en el anfiteatro del Departamento de Morfología de la Universidad del Valle en Cali (Colombia), se encontró una variación anatómica poco descrita en la literatura científica mundial. Se trata de la desembocadura aberrante del conducto torácico. Normalmente, este conducto linfático asciende en el tórax y se desvía hacia el lado izquierdo del cuello para desembocar en el confluente venoso yúgulo-subclavio izquierdo. En este cadáver masculino de etnia mestiza, el conducto se desvió hacia el lado derecho del cuello y desembocaba en la vena yugular interna derecha. El trabajo describe el origen embrionario del conducto torácico y ofrece una posible explicación para la anomalía encontrada.
Instituto Nacional de Salud
2009-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/22
10.7705/biomedica.v29i2.22
Biomedica; Vol. 29 No. 2 (2009); 204-208
Biomédica; Vol. 29 Núm. 2 (2009); 204-208
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https://revistabiomedica.org/index.php/biomedica/article/view/22/23
https://revistabiomedica.org/index.php/biomedica/article/view/22/304
/*ref*/Márquez JP, García C. Caso radiológico pediátrico. Rev Chil Enf Respir. 2004;20:85-8.<br />2. Epstein DA, Debord JR. Abnormalities associated with aberrant right subclavian arteries – a case report. Vasc Endovascular Surg. 2002;36:297-303.<br />3. Solis JH, Sánchez C, Gutiérrez R. Variantes anatómicas del conducto torácico. Angiología. 1984;36:289-92.<br />4. Williams P, Warwick R. Gray anatomía. Tomo I. 36ª ed. Barcelona: Salvat Editores S.A.; 1985.<br />5. Sadler TW. Embriología médica con orientación clínica. Novena edición. Madrid: Editorial Médica Panamericana; 2004.<br />6. van der Putte SC, van Limborgh J. The embryonic development of the main lymphatics in man. Acta Morphol Neerl Scand. 1980;18:323-35.<br />7. van Pernis PA. Variations of the thoracic duct. Surgery. 1949;26:806-9.<br />8. Kausel HW, Reeve TS, Stein AA, Alley RD, Stranahan A. Anatomic and pathologic studies of the thoracic duct. J Thorac Surg. 1957;34:631-42.<br />9. Rodrigues CFS, Wafae N, Olave E, Gabrielli C, Sgrott EA, Braga MT. Variaciones de las comunicaciones linfático-venosas en la fosa supraclavicular izquierda del hombre. Rev Chil Anat. 1997;15:175-9.<br />10. Kinnaert P. Anatomical variations of the cervical portion of the thoracic duct in man. J Anat. 1973;115:45-52.
oai:oai.revistabiomedica.org:article/23
2009-12-18T16:31:12Z
biomedica:ARTI
DNA sequence analysis indicates human origin of rotavirus and hepatitis A virus strains from western Colombia
Análisis filogenético de las cepas de rotavirus y virus de la hepatitis A encontradas en agua de consumo en el municipio de Quibdó, Chocó
Gutiérrez, María Fernanda
Moreno, Sandra
Alvarado, Mónica Viviana
Bermúdez, Andrea
rotavirus
virus de la hepatitis A
contaminación del agua
filogenia
diarrea
rotavirus
hepatitis A virus
water pollution
phylogeny
diarrhea
Introduction. Quibdó, the capital of Chocó Province, is one of the poorest cities in Colombia. Enteric viruses such as rotavirus and hepatitis A virus was found to occur commonly in city drinking water and indicated poor water quality and high risk of becoming infected. The source of these viruses was unknown, but humans and cattle were suspect sources.Objective. City water was assessed to determine source and persistence of diarrhea and hepatitis among the human populations in the environs of Quibdó.Material and methods. Four thousand liters of water were collected, filtered by tangential ultrafiltration and centrifuged in Centriprep Ultracel YM-50 tubes. Sixty samples of untreated and 20 of treated water were probed by RT-PCR.Results. Six samples were positive for rotavirus and 2 for hepatitis A virus in both, treated and non treated water. DNA sequence analysis identified the presence of human G2 rotavirus and human hepatitis A virus.Conclusion. The evidence indicated a high level of contamination with pathogenic viruses in consumable water sources in Quibdó, Colombia.
Introducción. Quibdó, capital del departamento del Chocó, se ha caracterizado por ser una de las regiones más deprimidas en Colombia. La presencia de virus entéricos tipo rotavirus y virus de la hepatitis A en el agua de consumo, además de ser un indicador de su mala calidad, es una importante fuente de contaminación para los individuos que la consumen.Objetivo. Demostrar la presencia de estos dos agentes virales en el agua de consumo para contribuir con la explicación de la morbilidad por enfermedad diarreica aguda y hepatitis en la región, y aclarar que el origen de estos virus es por contaminación de desechos humanos más que por la materia fecal de bovinos o porcinos.Materiales y métodos. Se procesaron 4.000 litros de agua que se llevaron a ultrafiltración tangencial y a centrifugación con filtros Centriprep Ultracel YM-50. Se aplicó la prueba de RT-PCR a 60 muestras de agua no tratada y a 20 muestras de agua tratada por el acueducto. Las muestras positivas fueron secuenciadas y con el análisis de dichas secuencias se elaboraron árboles filogenéticos.Resultados. Seis de las muestras resultaron positivas para rotavirus y dos más para virus de la hepatitis A. Éstos aparecieron tanto en aguas tratadas como no tratadas. Los análisis filogenéticos demostraron que el rotavirus pertenece al serotipo G2 humano y que el virus de la hepatitis A fue también de origen humano.Conclusión. El agua analizada presenta un alto nivel de contaminación, demostrado por la presencia de virus patógenos para el hombre.
Instituto Nacional de Salud
2009-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/23
10.7705/biomedica.v29i2.23
Biomedica; Vol. 29 No. 2 (2009); 209-217
Biomédica; Vol. 29 Núm. 2 (2009); 209-217
2590-7379
0120-4157
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https://revistabiomedica.org/index.php/biomedica/article/view/23/24
https://revistabiomedica.org/index.php/biomedica/article/view/23/305
/*ref*/Bosch A, Guix S, Sano D, Pintó R. New tools for the study and direct surveillance of viral pathogens in water. Curr Opin Biotechnol. 2008;19:295-301.<br />2. Procuraduría General de la Nación, Ministerio del Medio Ambiente, UNICEF. Agua para la vida, Colombia y el mundo. Panorama nacional: Los niños, el agua y el ambiente sano. La infancia, el agua y el saneamiento básico en los planes de desarrollo departamentales y municipales. Primera edición. Bogotá, D.C.: CMYK Impresiones Ltda.; 2006. p. 18-29.<br />3. Eltiempo.com/archivo. La tragedia del Chocó. El Tiempo. Enero 2005; Editorial Opinión. Fecha de consulta: 15 de febrero de 2007. Disponible en: http://www.eltiempo.com/archivo/documento/MAM-1674069<br />4. Byun K, Kim J, Song K, Baek L, Song J, Park S, et al. Molecular studies: Hepatitis A virus and hepatectomy. Molecular epidemiology of hepatitis A in Korea. J Gastroenterol Hepatol. 2001;16:519-24.<br />5. Cuthbert JA. Hepatitis A: Old and new. Clin Microbiol Rev. 2001;14:38-58.<br />6. Costa-Mattioli M, Cristina J, Romero H, Pérez-Bercof R, Casane D, Colina R, et al. Molecular evolution of hepatitis A virus: A new classification based on the complete Vp1 protein. J Virol. 2002;76:9516-25.<br />7. Fiore A. Hepatitis A transmitted by food. Clin Infect Dis. 2004;38:705-15.<br />8. Hernández OA. El agua de aquí, es la que cae del cielo. Fecha de consulta: 15 de febrero de 2007. Disponible en: http://www.latarde.com/2007/2/15/nac1.htm<br />9. Martínez L, Matiz A, Trespalacios AA, Ajami N, Mora CI, Serrano P, et al. Etiología de la enfermedad diarreica aguda en niños menores de 5 años en la población de Quibdó. El calicivirus, un nuevo hallazgo. Pediatría. 2005;40:43-52.<br />10. Rubio MP, Castro J, Gutiérrez E, Tanaka J. Seroprevalencia de la hepatitis A y varicela en Bogotá, Colombia. Revista Panamericana de Infectología. 2006. Fecha de consulta: 15 de febrero de 2007. Disponible en: http://encolombia.com/medicina/ infectologia/revista panadeinfev4-1-investigaseroprevaha.htm<br />11. Rodríguez C. Actualización sobre hepatitis virales: Etiología, patogenia, diagnóstico microbiológico y prevención. Rev Cubana Med Gen Integr. 2000;16:574-85.<br />12. Costa-Mattioli M, Di Napoli A, Ferré V, Billaudel S, Pérez R, Cristina J. Genetic diversity of hepatitis A virus. J Gen Virol. 2003;84:3191-201.<br />13. Deng M, Day S, Cliver D. Detection of hepatitis a virus in environmental samples by antigen-capture PCR. Appl Environ Microbiol. 1994;60:1927-33.<br />14. Brooks H, Gersberg R, Dhar A. Detection and quantification of hepatitis A virus in seawater via real-time RT-PCR. J Virol Methods. 2005;127:109-18.<br />15. Gouvea V, Glass R, Woods P, Taniguchi K, Clark H, Forrester B, et al. Polymerase chain reaction amplification and typing of rotavirus nucleic acid from stool specimens. J Clin Microbiol. 1990;28:276-82.<br />16. Dubois E, Hennechart C, Merle G, Burger C, Hmila N, Ruelle S, et al. Detection and quantification by real time RT-PCR of hepatitis A virus from inoculated tap waters, salad vegetables and soft fruits: Characterization of the method performances. Int J Food Microbiol. 2007;117:141-9.<br />17. Espinosa A, Mazari-Hiriart M, Espinosa R, Maruri-Avidal L, Méndez E, Arias C. Infectivity and genome persistence of rotavirus and astrovirus in groundwater and surface water. Water Res. 2008;42:2618-28.<br />18. Deetz TR, Smith EM, Goyal SM, Gerba CP, Vollet JJ, Tsai L, et al. Occurrence of rota-and enteroviruses in drinking and environmental water in a developing nation. Water Res. 1984;18:567-71.<br />19. Keswick BH, Gerba CP, DuPont HL, Rose JB. Detection of enteric viruses in treated drinking water. Appl Environ Microbiol. 1984;47:1290-4.<br />20. Gutiérrez M, Alvarado M, Martínez E, Ajami N. Presence of viral proteins in drinkable water-sufficient condition to consider water a vector of viral transmission? Water Res. 2007;41:373-8.<br />21. Haramoto E, Katayama H, Utagawa E, Ohgaki S. Development of sample storage methods for detecting enteric viruses in environmental water. J Virol Methods. 2008;151:1-6.<br />22. Duan Z, Li D, Zhang Q, Liu N, Huang C, Jiang X, et al. Novel human rotavirus of genotype G5P(6) identified in a stool specimen from a Chinese girl with diarrhea. J Clin Microbiol. 2007;45:1614-7.
oai:oai.revistabiomedica.org:article/24
2009-12-18T16:31:12Z
biomedica:ARTI
Clonal expansion and genomic characterization of the human T-cell lymphotropic virus type I during the integration process in adult T-cell leukemia/lymphoma
Expansión clónica y caracterización genómica del proceso de integración del virus linfotrópico humano tipo I en la leucemia/linfoma de células T en adultos
Salcedo-Cifuentes, Mercedes
Cabrera, Jesús
Cuesta-Astroz, Yesid
Carrascal, Edwin
Eizuru, Yoshito
Domínguez, Martha C.
Sánchez, Adalberto
García-Vallejo, Felipe
integración viral
virus linfotrópico de células T humanas tipo 1
leucemia/linfoma de células T en adultos
reacción en cadena de la polimerasa
genoma humano
biología computacional
Virus integration
human T-lymphotropic virus 1
leukaemia-lymphoma
adult T-cell
polymerase chain reaction
genome
human
computational biology
Introduction. Although the integration of human T-cell lymphotropic virus type I into the T-cells is not a random process, the mechanistic details are not understood.Objectives. The characteristics of the flanking host chromatin were evaluated at the integration sites in adult T-cell leukaemia/lymphoma (ATLL) patients infected with the virus.Materials and methods. From seven leukemic Colombian patients positive for the human T-cell lymphotropic virus type I (HTLV-I), lymphocyte DNA samples were extracted and amplified by inverse polymerase chain reaction (IPCR). Clonal expansion and human genome nucleotide composition in an extension of 50 bp was determined. To establish the characteristics of the human genome flanking provirus, 61 IPCR sequences from Colombian and Japanese ATLL patients, were analyzed in silico to obtain insights about the genomic structure, functions and nature of associated chromatin.Results. The clonal expansion of cell clones was predominantly oligoclonal. From 61 IPCR sequences, 155 alignments with homology higher than 95% (e-value <0.05) were screened. Seventy-five percent of those sequences corresponded to non coding elements that include repetitive and non-repetitive DNA. Fifty percent of the proviral integrations were associated with chromosomes of A and B groups. Viral DNA integration tended to favor exons of genes that replicated early, controlled the cell cycle, or were involved in signal transduction.Conclusions. The results indicated that HTLV-I integration was preferentially directed towards genomic environments with high C:G content, and toward genes that replicate early, regulate cell cycle or involved with signal transduction.
Introducción. Aunque la integración del virus linfotrópico humano tipo I no es al azar, se desconocen muchos de los detalles de este proceso.Objetivo. Evaluar las características de la cromatina celular adyacente a secuencias provirales en pacientes con leucemia/linfoma de células T en adultos asociada al virus.Materiales y métodos. Se extrajo el ADN de biopsias de siete pacientes colombianos con leucemia/linfoma de células T en adultos y positivos para el virus linfotrópico humano tipo I. Éste se amplificó mediante reacción inversa en cadena de la polimerasa, para determinar el grado de expansión clónica y su composición de nucleótidos. A partir de 61 secuencias de ADN humano adyacentes a provirus, provenientes de pacientes leucémicos colombianos y japoneses, se efectuó un análisis in silico para obtener datos sobre su integración, las características de la cromatina y sus funciones asociadas.Resultados. La expansión de clones celulares fue predominantemente oligoclónica. De las 61 secuencias de ADN adyacente a provirus, se seleccionaron 155 alineamientos que cumplieron con los criterios de inclusión (homologías≥95%, e-value≤0,05). De éstos, 74,84% fueron secuencias no codificantes repetidas y no repetidas. El 45,95% de las integraciones provirales se localizó en los cromosomas de los grupos A y B. Se observaron tendencias de integración hacia exones de genes que se replican tempranamente, regulan el ciclo celular y participan en la transducción de señales.Conclusiones. Los resultados permiten postular que la integración del virus linfotrópico humano tipo I se dirigiría hacia un ambiente genómico caracterizado por elevado contenido de C:G, genes de replicación temprana que regularían el ciclo celular y la transducción de señales.
Instituto Nacional de Salud
2009-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/24
10.7705/biomedica.v29i2.24
Biomedica; Vol. 29 No. 2 (2009); 218-231
Biomédica; Vol. 29 Núm. 2 (2009); 218-231
2590-7379
0120-4157
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https://revistabiomedica.org/index.php/biomedica/article/view/24/25
https://revistabiomedica.org/index.php/biomedica/article/view/24/306
/*ref*/Poiesz BJ, Ruscetti FW, Gadzar AF, Bunn PA, Minna JD, Gallo RC. Detection and isolation of type C retrovirus particles from fresh and cultured lymphocytes of a patient with cutaneous T-cell lymphoma. Proc Natl Acad Sci USA. 1980;77:7415-9.<br />2. Edlich RF, Arnette JA, Williams FM. Global epidemic of human T-cell lymphotropic virus type-I (HTLV-I). J Emerg Med. 2000;18:109-19.<br />3. Quintana M, Villalobos J, Domínguez M, Tamayo O, García-Vallejo F. Estudio de la seroprevalencia de la infección por los virus linfotrópicos humanos (HTLV) I y II en poblaciones del departamento de Córdoba, Colombia. Colombia Médica. 2004;35:22-30.<br />4. García-Vallejo F. Caracterización molecular y genómica del proceso de integración del provirus del virus linfotropico humano (HTLV) tipo I. Rev Acad Colomb Cienc. 2006;30:155-70.<br />5. Yoshida M, Seiki M, Yamaguchi K, Takatsuki K. Monoclonal integration of human T-cell leukemia provirus in all primary tumors of adult T-cell leukemia suggests causative role of human T-cell leukemia virus in the disease. Proc Natl Acad Sci USA.1984;81:2534-7.<br />6. Yoshida M. Multiple viral strategies of HTLV-1 for dysregulation of cell growth control. Annu Rev Immunol. 2001;19:475-96.<br />7. Leclerq I, Mortreux F, Gabet AS, Jonson CB, Wattel E. Basis of HTLV type I site selection. AIDS Res Hum Retroviruses. 2000;16:1653-9.<br />8. Zoubak S, Richardson J, Rynditch AV, Hollsberg P, Hafler DA, Boeri E, et al. Regional specificity of HTLV-I proviral integration in the human genome. Gene. 1994;143:155-63.<br />9. Glukhova LA, Zoubak SV, Rynditch AV, Miller GG, Titova IV, Vorovyeva N, et al. Localization of HTLV-1 and HIV-1 proviral sequences in chromosomes of persistently infected cells. Chromosome Res.1999;7:177-83.<br />10. Richarsond JH, Rose NJ, Mann S, Ferguson-Smith M, Lever AM. Chromosomal positioning of human T-lymphotropic type I proviruses by fluorescent in situ hybridisation. J Virol Methods. 2001;93 65-74.<br />11. Saccone S, De Sario A, Wiegant J, Raap AK, Della-Valle G, Bernardi G. Correlations between isochores and chromosomal bands in the human genome. Proc Natl Acad Sci USA. 1993;90:11929-33.<br />12. Woodfine K, Fiegler H, Beare DM, Collins JE, McCann OT, Young BD, et al. Replication timing of the human genome. Hum Mol Genet. 2004;13:191-202.<br />13. Saccone S, Cacciò S, Kusuda J, Andreozzi L, Bernardi G. Identification of the gene-richest bands in human chromosomes. Gene. 1996;174:85-94.<br />14. Kim MA, Johannsmann R, Grzeschik KH. Giemsa staining of the sites replicating DNA early in human lymphocyte chromosomes. Cytogenet Cell Genet. 1975;15:363-71.<br />15. Federico C, Saccone S, Bernardi G. The gene-richest bands of human chromosomes replicate at the onset of the S-phase. Cytogenet Cell Genet. 1998;80:83-8.<br />16. Albrecht B, Lairmore MD. Critical role of human T-lymphotropic virus type 1 accessory proteins in viral replication and pathogenesis. Microbiol Mol Biol Rev. 2002;66:396-406.<br />17. Yasunaga JI, Matsuoka M. Human T-cell leukemia virus type I induces adult T-cell leukemia: From clinical aspects to molecular mechanisms. Cancer Control. 2007;14:133-40.<br />18. Albrecht B, Collins ND, Burrinstom MT, Nisbet JW, Ratner L, Green PL, et al. Human T-lymphotropic virus type I open reading frame I p12(I) is required for efficient viral infectivity in primary lymphocytes. J Virol. 2000;74:9828-35.<br />19. Bindhu M, Nair A, Lairmore MD. Role of accessory proteins of HTLV-1 in viral replication, T cell activation, and cellular gene expression. Front Biosci. 2004;9: 2556-76.<br />20. Carrascal E, Cortés A, Akiba S, Tamayo O, Quiñónez F, Floréz L, et al. Epidemiología y patología de la leucemia/linfoma de células T del adulto en Cali y el suroccidente colombiano. Colombia Médica. 2004;35:12-7.<br />21. República de Colombia. Ministerio de Salud. Por la cual se establecen las normas científicas, técnicas y administrativas para la investigación en salud Resolución No 008430 de octubre 4 de 1993. Bogotá: Ministerio de Salud; 1993.<br />22. Sambrook J, Fritzch EF, Maniatis T. Molecular cloning. A laboratory manual. New York: Ed. Cold Spring Harbor Press; 1989.<br />23. Seiki M, Hattori S, Hirayama Y, Yoshida M. Human adult T-cell leukemia virus: complete nucleotide sequence of the provirus genome integrated in leukemia cell DNA. Proc Natl Acad Sci USA. 1983;80:3618-22.<br />24. Feinberg AP, Vogelstein B. Technique for radiolabeling of restriction endonuclease fragments. Anal Biochem. 1983;132:6-13.<br />25. Miyoshi I, Kubonishi I, Yoshimoto S, Akagi T, Ohtsuki Y, Shiraishi Y, et al. Type C virus particles in a cord T-cell line derived by co-cultivating normal human cord leukocytes and human leukaemic T cells. Nature.1981;294:770-1.<br />26. Takemoto S, Matsuoka M, Yamaguchi K, Takatsuki K. A novel diagnostic method of adult T-cell leukemia: Monoclonal integration of human T-cell lymphotropic virus type I provirus DNA detected by inverse polymerase chain reaction. Blood. 1994;84:3080-5.<br />27. Cavrois M, Gessain A, Wain-Hobson S, Wattel E. Proliferation of HTLV-I infected circulating cells in vivo in all asymptomatic carries and patients with TSP/HAM. Oncogen. 1996;12:2419-23.<br />28. Cabrera J, García-Vallejo F. Aumento del número de amplicones obtenidos por IPCR en el ADN de personas seropositivas para HTLV-I afectadas con PET/HAM. Colombia Médica. 2000;31:169-75.<br />29. Ozawa T, Itoyama T, Sadamori N, Yamada Y, Hata T, Tomonaga M, et al. Rapid isolation of viral integration site reveals frequent integration of HTLV-1 into expressed loci. J Hum Genet. 2004;49:154-29.<br />30. STATA CORP. Stata Statistical Software: Release 8.0. College Station TX: Stata Corporative; 2000.<br />31. Venter JC, Adams MD, Myers EW, Li PW, Mural RJ, Sutton GG, et al. The sequence of the human genome. Science. 2001;291:1304-51.<br />32. International Human Genome Sequencing Consortium. Initial sequencing and analysis of the human genome. Nature. 2001;409:860-921.<br />33. Blank A. Adult T-cell leukemia/lymphoma in southwest Colombia. En: HTLV, truths and questions. Cali: Edit Zaninovic; 1996. p. 266-71.<br />34. Wattel E, Vartanian JP, Pannetier CH, Wain-Hobson S. Clonal expansión of human T-cell leukemia and symptomatic carries without malignancy. J. Virol. 1995;69:2863-8.<br />35. Wattel E, Cavrois, Gessain MA, Wain-Hobson S. Clonal expansion of infected cells –a way of life for HTLV-I. J Acquir Immune Defic Syndr Hum Retrovirol. 1996;13(Supl.1):92-9.<br />36. Doi K, Wu X, Taniguchi Y, Yasunaga J, Satou Y, Okayama A, et al. Preferential selection of human T-cell leukemia virus type I provirus integration sites in leukemic versus carrier status. Blood. 2005;106:1048-53.<br />37. Hanai S, Nitta T, Shoda M, Tanaka M, Iso N, Mizoguchi I, et al. Integration of human T-cell leukemia virus type 1 in genes of leukemia cells of patients with adult T-cell leukemia. Cancer Sci. 2004;95:306-10.<br />38. Spence JM, Mills W, Mann K, Huxley C, Farr CJ. Increased missegregation and chromosome loss with decreasing chromosome size in vertebrate cells. Chromosoma. 2006;115:60-74.<br />39. Leclercq I, Mortreux F, Cavrois M, Leroy A, Gessain A, Wain-Hobson S, et al. Host sequences flanking the human T-cell leukemia virus type 1 provirus in vivo. J Virol. 2000;74:2305-12.<br />40. Oliver JL, Carpena P, Román-Rolatán R, Mata-Balaguer T, Mejias-Romero A, Hackenberg M, et al. Isochore chromosome maps of the human genome. Gene. 2002;300:117-27.<br />41. Lengauer C, Kinzler KW, Vogelstein B. Genetic instabilities in human cancers. Nature. 1998; 396:643-9.<br />42. Pavlícek A, Jabbari K, Paces J, Paces V, Hejnar J, Bernardi G. Similar integration but different stability of Alus and LINEs in the human genome. Gene. 2001;276:39-45.<br />43. Tsuji T, Sugahara K, Tsuruda K, Uemura A, Harasawa H, Hasegawa H, et al. Clinical and oncologic implications in epigenetic down-regulation of CD26/dipeptidyl peptidase IV in adult T-cell leukemia cells. Int J Hematol. 2004;80:254-60.<br />44. Derce D, Crise B, Li Y, Princler G, Lum N, Stewart C, et al. Human T-cell leukemia virus type 1 integration target sites in the human genome: comparison with those of other retroviruses. J Virol. 2007;81:6731-41.<br />45. Agbottah E, Deng L, Dannenberg LO, Pumfery A, Kashanchi F. Effect of SWI/SNF chromatin remodeling complex on HIV-1 Tat activated transcription. Retrovirology. 2006;3:48-67.<br />46. Mitchell RS, Beitzel BF, Schroder AR, Shinn P, Chen H, Berry CC, et al. Retroviral DNA integration: ASLV, HIV, and MLV show distinct target site preferences. PLoS Biol. 2004;2:1127-37.<br />47. Wu X, Burgess S M. Integration target site selection for retroviruses and transposable elements. Cell Mol Life Sci. 2004;61:2588-96.<br />48. Versteeg R, van Schaik BD, van Batenburg MF, Roos M, Monajemi R, Caron H, et al. The human transcriptome map reveals extremes in gene density, intron length, GC content, and repeat pattern for domains of highly and weakly wxpressed genes. Genome Res. 2003;13:1998-2004.
oai:oai.revistabiomedica.org:article/25
2009-12-18T16:31:12Z
biomedica:ARTI
Seroprevalence of hepatitis B virus and human immunodeficiency virus infection in a population of multiply-transfused patients in Colombia
Seroprevalencia de infección por virus de la hepatitis B y por virus de la inmunodeficiencia humana en una población de pacientes con múltiples transfusiones en cuatro hospitales, Colombia, Sur América
Beltrán, Mauricio
Navas, María Cristina
Arbeláez, María Patricia
Donado, Jorge
Jaramillo, Sergio
De la Hoz, Fernando
Estrada, Cecilia
Cortés, Lucía del Pilar
de Maldonado, Amalia
Rey, Gloria
transfusión sanguínea
VIH
virus de la hepatitis B
factores de riesgo
Colombia
Blood transfusion
HIV
hepatitis B virus
risk factors
Colombia
Introduction. Although the transfusion of blood products is a common therapy, it carries risk of transmission of infections, especially hepatitus B virus (HBV) and human immunodeficiency virus (HIV).Objective. As part of the blood safety initiative, the Pan American Health Organization supported studies to estimate the prevalence of human immunodeficiency virus and hepatitis B virus infection in Colombia. Materials and methods. Between February and September 2003, a cross sectional study examined 500 multiply-transfused patients at four hospital centers in the cities of Bogotá and Medellín. The serum samples were analyzed by enzyme immunoassay (EIA) using commercial kits.Results. The seroprevalence of HIV infection was 1.8% (CI 95% 0.5-3.1). The seroprevalence of HBV infection was 18.6% (CI 95% 15.1-22.1). Six risk factors were associated with HIV and HBV infection: (1) receiving more than 48 units of blood or blood components, (2) diagnosis of hemophilia, (3) receiving transfusions for more than one year, (4) receiving whole blood, (5) co-infection with hepatitis C virus and (6) receiving transfusions before 1993.Conclusions. This is the first epidemiological study with a significant sample size performed in multiply-transfused patients in Colombia. The principal finding was the high prevalence of HBV and HIV infection in patients with diagnosis of hemophilia compared with the other five groups of multiply-transfused patients.
Introducción. Aunque la transfusión de componentes sanguíneos es una terapia ampliamente utilizada, representa un riesgo de transmisión de agentes infecciosos.Objetivo. Como parte de la iniciativa sobre sangre segura promovida por la Organización Panamericana de la Salud, se realizó un estudio para estimar la seroprevalencia de infección por virus de la inmunodeficiencia humana y virus de la hepatitis B en pacientes con múltiples transfusiones en Colombia.Materiales y métodos. Entre febrero y septiembre de 2003, se llevó a cabo un estudio transversal de 500 pacientes con múltiples transfusiones, seleccionados en cuatro hospitales de las ciudades de Bogotá y Medellín. Las muestras de suero obtenidas se analizaron por inmunoensayo con estuches comerciales.Resultados. La frecuencia de seropositividad para el virus de la inmunodeficiencia humana fue de 1,8%, (IC95% 0,5-3,1). La frecuencia de seropositividad para el virus de la hepatitis B fue de 18,6% (IC95% 15,1-22,1). Los principales factores de riesgo fueron: recibir más de 48 unidades de sangre o componentes, tener diagnóstico de hemofilia, recibir transfusiones por un período mayor de un año, recibir sangre total, tener coinfección por virus de la hepatitis C y haber sido transfundido antes de 1993.Conclusiones. Este es el primer estudio epidemiológico realizado en Colombia con un número significativo de pacientes con múltiples transfusiones. El hallazgo más relevante es la elevada prevalencia de infección por virus de la hepatitis B y virus de la inmunodeficiencia humana observado en la población de hemofílicos, comparado con los otros cuatro grupos de pacientes con múltiples transfusiones.
Instituto Nacional de Salud
2009-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/25
10.7705/biomedica.v29i2.25
Biomedica; Vol. 29 No. 2 (2009); 232-243
Biomédica; Vol. 29 Núm. 2 (2009); 232-243
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/25/26
https://revistabiomedica.org/index.php/biomedica/article/view/25/307
/*ref*/Donegan E, Stuart M, Niland J. Infection with HIV-1 among recipients of antibody-positive donations. Ann Intern Med. 1990;113:733-9.<br />2. Centers for Disease Control and Prevention. Provisional public health service inter-agency recommendations for screening donated blood and plasma antibody to virus causing acquired immunodeficiency syndrome. MMWR Morb Mortal Wkly Rep. 1985;34:1-5.<br />3. Schreiber GB, Busch MP, Kleinman SH, Korelitz JJ. The risk of transfusion-transmitted viral infections. N Engl J Med. 1996;334:1685-90.<br />4. WHO/UNAIDS. Situación de la epidemia de SIDA. Programa Conjunto de las Naciones Unidas sobre el VIH/SIDA y Organización Mundial de la Salud; Génova 2006. Fecha de consulta: 14 de enero de 2007. Disponible en: <a href="http://data.unaids.org/pub/GlobalReport/2006/200605FSLatinAmerica_es.pdf">http://data.unaids.org/pub/GlobalReport/2006/200605FSLatinAmerica_es.pdf</a>.<br />5. García R, Prieto F, Arenas C, Rincón J, Caicedo S, Rey G. Reducción de la transmisión madre hijo del VIH en Colombia: dos años de experiencia nacional, 2003-2005. Biomédica. 2005;25:547-64.<br />6. Ministerio de la Protección Social, Instituto Nacional de Salud. Prevalencia de VIH en población general Colombia 2003: VI Estudio Nacional Centinela de VIH 2003-2004. Inf Quinc Epidemiol Nac. 2004;9:363-4.<br />7. Lavanchy D. Worldwide epidemiology of VHB infection, disease burden, and vaccine prevention. J Clin Virol. 2005;34:S1-S3.<br />8. Shepard CW, Simard EP, Finelli L, Fiore AE, Bell BP. Hepatitis B virus infection: epidemiology and vaccination. Epidemiol Rev. 2006;28:112-25.<br />9. Ministerio de la Protección Social, Instituto Nacional de Salud. Situación hepatitis B en Colombia. Inf Quinc Epidemiol Nac. 2004;9:113-24<br />10. Ministerio de la Protección Social, Instituto Nacional de Salud. Comportamiento epidemiológico la hepatitis B, Colombia, 2005. Inf Quinc Epidemiol Nac. 2006;11:65-7<br />11. Ministerio de la Protección Social, Instituto Nacional de Salud. Hepatitis B. Inf Quinc Epidemiol Nac. 2006;11:297-312<br />12. Schmunis GA, Zicker F, Pinheiro F, Brandling-Bennett D. Risk for transfusion-transmitted infectious diseases in Central and South America. Emerg Infect Dis. 1998; 4: 5-11.<br />13. World Health Organization. World Health Day 2000: Information for National Blood Programmers. WHO Last Update September 2000. Fecha de consulta: 14 enero de 2007. Disponible en: <a href="http://www.euro.who.int/mediacentre/PR/2000/2001090925">http://www.euro.who.int/mediacentre/PR/2000/2001090925</a><br />14. WHO/UNAIDS. Situación de la epidemia de SIDA. Programa Conjunto de las Naciones Unidas sobre el VIH/SIDA y Organización Mundial de la Salud; Génova: WHO/UNAIDS; 2006.<br />15. Busch M. HIV, HBV and HCV: New developments related to transfusion safety. Vox Sang. 2000;78(Suppl.2):253-6.<br />16. Dodd R. Germs, gels and genomes: A personal recollection of 30 years in blood safety testing. En: Stramer Sl, editor. Blood safety in the millennium. Bethesda: American Association of Blood Bank; 2001. p. 97-122.<br />17. Pillonel J, Laperche S, Saura C, Desenclos JC, Couroucé AM. Transfusion-Transmissible Agents Working Group of the French Society of Blood. Trends in residual risk of transfusion-transmitted viral infections in France between 1992 and 2000. Transfusion. 2002;42:980-8.<br />18. Dodd RY, Notari EP, Stramer SL. Current prevalence and incidence of infectious diseases markers and estimated window-period risk in the American Red Cross blood donor population. Transfusion. 2002;42:975-9.<br />19. Velati C, Fomiatti L, Baruffi L, Romanò L, Zanetti A, Gruppo Italiano per lo Studio delle Malattie Trasmissibili con la Trasfusione. Impact of nucleic acid amplification technology (NAT) in Italy in the three years following implementation (2001-2003). Euro Surveill. 2005;102:12-4.<br />20. Alvarez do Barrio M, González Díez R, Hernández Sánchez JM, Oyonarte Gómez S. Residual risk of transfusion-transmitted viral infections in Spain, 1997-2002, and impact of nucleic acid testing. Euro Surveill. 2005;10:20-2.<br />21. Cortés A, Beltrán M, Olaya B, Hernández M. Riesgo de enfermedades infecciosas transmitidas por transfusión en el Valle del Cauca, Colombia. Colombia Médica. 1999;30:13-8.<br />22. Cortés A, Beltrán M, Olaya B, Hernández M. Epidemiología de la colección, proceso y uso de la sangre y componentes sanguíneos en el Valle del Cauca, Colombia. Colombia Médica. 1999;30:29-35.<br />23. Beltrán M, Jara J. Tamizaje de enfermedades infecciosas en bancos de sangre, Colombia 1995. Biomédica. 1997;17:137-42.<br />24. Remesar M, Gamba C, Kuperman S, Marcosa MA, Miguez G, Caldarola S, et al. Antibodies to hepatitis C and other viral markers in multi-transfused patients from Argentina. J Clin Virol. 2005;34(Suppl.2):S20-6.<br />25. de Paula EV, Gonçales NS, Xueref S, Addas-Carvalho M, Gilli SC, Angerami RN, et al. Transfusion-transmitted infections among multi-transfused patients in Brazil. J Clin Virol. 2005;34 (Suppl.2):S27-32.<br />26. Ballester JM, Rivero RA, Villaescusa R, Merlín JC, Arce AA, Castillo D, et al. Hepatitis C virus antibodies and other markers of blood-transfusion-transmitted infection in multi-transfused Cuban patients. J Clin Virol. 2005;34(Suppl.2):S39-46.<br />27. Vinelli E, Lorenzana I. Transfusion-transmitted infections in multi-transfused patients in Honduras. J Clin Virol. 2005;34(Suppl.2):S53-60.<br />28. Laguna-Torres VA, Pérez-Bao J, Chauca G, Sovero M, Blichtein D, Chunga A, et al. Epidemiology of transfusion-transmitted infections among multi-transfused patients in seven hospitals in Peru. J Clin Virol. 2005;34(Suppl.2):S61-8.<br />29. López L, López P, Arango A, Rodríguez I, López J, Lima E, et al. Risk factors for hepatitis B and C in multi-transfused patients in Uruguay. J Clin Virol. 2005;34(Suppl.2):S69-74.<br />30. Neninger E, Velbes P, del Castillo C. Incidencia de infección por el virus de la hepatitis B y C. Rev Cubana Med. 2001;40:24-9.<br />31. Fontes EM, Amorim L, Carvalho SM, Farah MB. Hemophilia care in the state of Rio de Janeiro, Brazil. Rev Panam Salud Pública. 2003;13:124 -8.<br />32. Ustariz C, Rodríguez L, Delgado G, Ávila O, Gautier H, Bencomo A et al. Frecuencia de hepatitis B y C en adultos con hemopatías malignas. Rev Cubana Hematol Inmunol Hemoter. 2005;21¿Páginas?.<br />33. Covas DT, Boturão NE, Zago MA. The frequency of blood-born viral infections in a population of multitransfused Brazilian patients. Rev Inst Med Trop Sao Paulo. 2006;35:271-3.<br />34. Ministerio de Salud, Instituto Nacional de Salud. Boletín epidemiológico semana SIVIGILA. Semana epidemiológica No. 42. Bogotá D.C.: Ministerio de Salud, Instituto Nacional de Salud; 2002.<br />35. Volkow P, Marín López A, Torres I. Plasma trade and the HIV epidemic. Lancet. 1997;349:327-8.<br />36. Sepúlveda J, del Río A, Valdespino JL, García L, Velázquez-Velazquez L, Volkow P. La estrategia de prevención de la transmisión del VIH/SIDA a través de la sangre y sus derivados en México. Salud Pública Mex. 1995;37:624-35.<br />37. A transfusion HIV prevention model for Perú. Transfusion Today. 2006;67:21-3. Fecha de consulta: 14 de enero de 2007. Disponible en: <a href="http://www.isbt-web.org/files/tt/TT67.pdf">http://www.isbt-web.org/files/tt/TT67.pdf</a><br />38. Beltrán M, Ayala M. Importancia de la encuesta de selección de donantes. Experiencia en un banco de sangre, Bogotá, Colombia, 1996. Biomédica. 2000;20:123-5.<br />39. Beltrán M, Ayala M, Palomino F. Seroprevalencia del virus de la hepatitis C en el banco de sangre de un hospital de Bogotá, Colombia 1998. Medicina Transfusional al Día. 2001;1:15-7.<br />40. Gamarra G, Daza N, Díaz J, León C, Ramírez H. Prevalencia de enfermedades transfusionales en donantes del Banco de Sangre del Hospital Universitario Ramón González Valencia, 1994-1997. Med UIS. 1998;12:203-10.<br />41. Schmunis GA Cruz JR. Safety of the blood supply in Latin America. Clin Microbiol Rev. 2005;181:12-29.
oai:oai.revistabiomedica.org:article/26
2009-12-19T12:09:19Z
biomedica:ARTI
Development and validation of a multiplex polymerase chain reaction for molecular identification of Salmonella enterica serogroups B, C2, D and E
Desarrollo y validación de una reacción en cadena de la polimerasa múltiple para la identificación de los serogrupos B, C2, D y E de Salmonella enterica
Cardona-Castro, Nora
Lavalett, Lelia
Sánchez, Miryan Margot
Múñoz, Nélida
Moreno, Jaime
Salmonella enterica
serogrupos
serotipificación
tipificación molecular
PCR múltiple
Salmonella enterica
serogroups
serotyping
molecular typing
multiplex PCR
Introduction. The scheme Kauffman-White (KW) for serotyping of Salmonella recognizes 46 O antigens, and 119 H antigens, thereby permitting the characterization of 2,541 serotypes. The serotyping is a useful epidemiological tool in identifying circulating serotypes and to characterize outbreaks. However, the method presents technical limitations, difficulty in interpretation of results and high costs.Objective. A multiplex polymerase chain reaction test (M-PCR) was developed as an alternative method for the identification of serogroups B, C2, D, and E of Salmonella enterica.Materials and methods. The M-PCR detected Salmonella genes rfbJ of serogroups B and C2 and wzx of serogroups D and E. To standardize the M-PCR, reference strains of Salmonella serogroups were compared. Amplification of invA gender-specific gene of Salmonella was included as internal control of amplification. To validate the test, a blind study was conducted to identify by M-PCR 400 isolates that had been previously characterized by serology.Results. The M-PCR detected Salmonella serogroups with reproducible results (Kappa index=0.95). The sensitivity of the test was between 98% to 100% and specificity between 96% to 100%.Conclusions. The polymorphisms in the Salmonella genes rfbJ and wzx permitted the development of a method for molecular typing of Salmonella serogroups that was sensitive, specific and reproducible.
Introducción. El esquema Kaufmann-White para la serotipificación de Salmonella, reconoce 46 antígenos O y 119 antígenos H, los cuales han permitido la caracterización de 2.541 serovares. La serotipificación es una herramienta epidemiológica útil en la identificación de serovares circulantes y estudio de brotes, sin embargo, presenta limitaciones técnicas, de interpretación de resultados y alto costo.Objetivo. Desarrollar una prueba de reacción en cadena de la polimerasa múltiple (PCR-M) como alternativa para identificar los serogrupos B, C2, D y E de Salmonella enterica.Materiales y métodos. Se desarrolló una PCR-M para detectar los genes rfbJ de los serogrupos B y C2 y wzx de los serogrupos D y E. Para estandarizar la PCR-M se probaron cepas de referencia de Salmonella pertenecientes a los serogrupos de estudio. Se incluyó el gen invA específico del género Salmonella como control interno de amplificación. La técnica fue validada con un estudio ciego que incluyó 400 aislamientos de Salmonella previamente serotipificados.Resultados. La PCR-M permitió identificar los serogrupos de Salmonella con resultados reproducibles (índice kappa=0,95). La sensibilidad de la prueba estuvo entre 98% y 100% y la especificidad entre 96% y 100%.Conclusiones. El polimorfismo de los genes rfbJ y wzx permitió desarrollar un método de tipificación molecular sensible, específico y reproducible, que podría servir de apoyo a la serotipificación para identificar serogrupos de Salmonella.
Instituto Nacional de Salud
2009-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/26
10.7705/biomedica.v29i2.26
Biomedica; Vol. 29 No. 2 (2009); 244-252
Biomédica; Vol. 29 Núm. 2 (2009); 244-252
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/26/27
https://revistabiomedica.org/index.php/biomedica/article/view/26/309
/*ref*/Popoff MY, Le Minor L. Antigenic formulas of the Salmonella serovars. Paris: Institut Pasteur; 2001.<br />2. Brenner FW, Villar RG, Angulo FJ, Tauxe R, Swaminathan B. Salmonella nomenclature. J Clin Microbiol. 2000;38:2465-7.<br />3. Kauffmann F. The bacteriology of Enterobacteriaceae. Baltimore: Williams & Wilkins; 1966.<br />4. Fitzgerald C, Gheesling L, Collins M, Fields PI. Sequence analysis of the rfb loci, encoding proteins involved in the biosynthesis of the Salmonella enterica O17 and O18 antigens: serogroup-specific identification by PCR. Appl Environ Microbiol. 2006;72:7949-53.<br />5. Verma NK, Quigley NB, Reeves PR. O-antigen variation in Salmonella spp rfb gene clusters of three strains. J Bacteriol. 1998;170:103-7.<br />6. Liu D, Haase AM, Lindqvist L, Lindberg AA, Reeves PR. Glycosyl transferases of O-antigen biosynthesis in Salmonella enterica: identification and characterization of transferase genes of groups B, C2, and E1. J Bacteriol. 1993;175:3408-13.<br />7. Wyk P, Reeves PR. Identification and sequence of the gene for abequose synthase, which confers antigenic specificity on group B Salmonellae: homology with galactose epimerase. J Bacteriol. 1989;171:5687-93.<br />8. Liu D, Cole RA, Reeves PR. An O-antigen processing function for Wzx (RfbX): a promising candidate for O-unit flippase. J Bacteriol. 1996;178:2102-7.<br />9. Mortimer CK, Peters TM, Gharbia SE, Logan MJ, Arnold C. Towards the development of a DNA-sequence based approach to serotyping of Salmonella enterica. BMC Microbiol. 2004;4:31-40.<br />10. Karami A, Ranjbar R, Ahmadi Z, Safiri Z. Rapid detection of different serovares of Salmonella enterica by multiplex PCR. Iranian J Publ Health. 2007;36:38-42.<br />11. Soltani MJ, Shahhosseiny MH, Shahbazzadeh D, Karami V, Mirzahoseini H, Mahboudi F, et al. Selective amplification of prt, tyv,and invA genes by multiplex PCR for rapid detection of Salmonella typhi. Iranian J Publ Health. 2005;9:135-8.<br />12. Lim YH, Hirose K, Izumiya H, Arakawa E, Takahashi H, Terajima J, et al. Multiplex polymerase chain reaction assay for selective detection of Salmonella enterica serovar Typhimurium. Jpn J Infect Dis. 2003;56:151-5.<br />13. Luk JM, Kongmuang U, Reeves PR, Lindberg AA. Selective amplification of abequose and paratose synthase genes (rfb) by polymerase chain reaction for identification of Salmonella major serogroups (A, B, C2 and D). J Clin Microbiol. 1993;31:2118-23.<br />14. Muñoz N, Agudelo CI, Ovalle MV, Realpe MH. Vigilancia en red de la susceptibilidad antimicrobiana y de los serotipos de Salmonella spp., Shigella spp. y Vibrio cholerae O1, 1997-1999. Biomédica. 2000;20:210-7.<br />15. Haque A, Ahmed J, Qureshi JA. Early detection of typhoid by polimerase chain reaction. Ann Saudi Med. 1999;19:337-40.<br />16. Henegariu O, Heerema NA, Dlouhy SR, Vance GH, Vogt PH. Multiplex PCR: critical parameters and step-by-step protocol. Biotechniques. 1997;23:504-11.<br />17. Álvarez J, Sota M, Vivanco AB, Perales I, Cisterna R, Rementeria A, et al. Development of a multiplex PCR technique for detection and epidemiological typing of Salmonella in human clinical samples. J Clin Microbiol. 2004;42:1734-8.<br />18. Elnifro EM, Ashshi AM, Cooper RJ, Klapper PE. Multiplex PCR: optimization and application in diagnostic virology. Clin Microbiol Rev. 2000;13:559-70.<br />19. Malorny B, Hoorfar J, Bunge C, Helmuth R. Multicenter validation of the analytical accuracy of Salmonella PCR: towards an international standard. Appl Environ Microbiol. 2003;69:290-6.<br />20. Olive DM, Bean P. Principles and applications of methods for DNA-based typing of microbial organisms. J Clin Microbiol. 1999;37:1661-9.<br />21. Curd H, Liu D, Reeves PR. Relationships among the O-antigen gene clusters of Salmonella enterica groups B, D1, D2 and D3. J Bacteriol. 1998;180:1002-7.<br />22. Hellerqvist CG, Rudén U. The group C2-type modification of the B-Type lipopolysaccharide in a hybrid between Salmonella groups B and C2. Eur J Biochem. 1972;25:96-101.<br />23. Wang L, Andrianopoulos K, Liu D, Popoff MY, Reeves PR. Extensive variation in the O-Antigen gene cluster within one Salmonella enterica serogroup reveals an unexpected complex history. J Bacteriol. 2002;184:1669-77.<br />24. Herrera LS, Ramiro R, Arroyo M, Díez R, Usera MA, Echeita MA. Blind comparison of traditional serotyping with three multiplex PCR for identification of Salmonella serotypes. Res Microbiol. 2007;158:122-7.<br />25. Muñoz N, Firacative C, Realpe ME, Patiño L, Gómez ME, Murcia LM, et al. Informe anual de la vigilancia fenotípica y molecular de Salmonella spp. en Colombia, 2007. Inf Quinc Epidemiol Nac. 2008;13:207-22.<br />26. Malkawi HI, Gharaibeh R. Rapid and simultaneous identification of two Salmonella enterica serotypes, Enteritidis and Typhimurium from chicken and meat products by multiplex PCR. Biotechnology. 2004;3:44-8.<br />27. Sánchez MM, Cardona-Castro N. Desarrollo y evaluación de una prueba de reacción en cadena de la polimerasa (PCR), utilizando la secuencia del gen hilA para diagnóstico de fiebre entérica por Salmonella spp. Biomédica. 2004;24:194-9.
oai:oai.revistabiomedica.org:article/27
2009-12-18T16:31:12Z
biomedica:ARTI
Risk factors associated with the presence of pneumonia in patients with brain injury
Factores de riesgo asociados a neumonía en pacientes
Yepes, David
Molina, Francisco
Ortiz, Gloria
Aguirre, Ricardo
neumonía
respiración artificial
traumatismos craneoencefálicos
infección hospitalaria
cuidados intensivos
Pneumonia
respiration
artificial
craniocerebral trauma
cross infection
intensive care
Introduction. Pneumonia in patients with head trauma occurs commonly; however, few data are available to evaluate the effects of the infection on the prognosis.Objective. The incidence and microbiological findings were described, and the associated risk factors were established with the appearance of pneumonia in patients with severe brain trauma.Materials and methods. A prospective cohort study was conducted that included 39 patients with severe brain trauma and who required mechanical ventilation; initially, none had pneumonia. These patients were observed during a 24-month period in an attempt to discern the principal risk factors associated with the onset of pneumonia.Results. Pneumonia occurred in 31 (80%) of the 39 patients, and 28 of these presented early pneumonia. The most frequent germ in patients with pneumonia was Staphylococcus aureus with a percentage of the 42.4%. In the multivariate analysis, the single statistically significant risk factor was the presence of hypotension and vasopressor support with a RR=27.9 (95% CI=1.0-749.9, p<0.05). No significant differences in the days of mechanical ventilation or mortality in both groups. The major mortality-associated risk factor in patients with pneumonia was a low Glasgow score at admittance with an OR=2.19 (95% CI 1.03 - 4.65), p<0.05.Conclusions. The incidence of pneumonia in patients with severe brain trauma is high; however, its appearance does not affect the prognosis. The single significant risk factor was the presence of hypotension and vasopressor support.
Introducción. La neumonía en los pacientes con trauma craneoencefálico es frecuente; a pesar de esto, hay pocos datos locales y no sabemos si su aparición afecta el pronóstico.Objetivo. Describir la incidencia y los hallazgos microbiológicos, y establecer los factores de riesgo asociados con la aparición de neumonía en los pacientes con trauma craneoencefálico grave.Materiales y métodos. Se realizó un estudio de cohorte, prospectivo, en el cual se incluyeron 39 pacientes con trauma craneoencefálico grave, con asistencia respiratoria mecánica y sin neumonía al ingreso.Este estudio se desarrolló durante 24 meses, tiempo en el cual se hizo seguimiento a una población con trauma craneoencefálico grave.Resultados. Se encontró un porcentaje de 80% de casos de neumonía, de los cuales, el 90% presentó neumonía temprana. El germen más frecuentemente encontrado fue Staphylococcus aureus, con 42,4%.En el análisis multivariado, sólo se encontró como factor de riesgo significativo la presencia de hipotensión y soporte vasopresor con un odds ratio (OR) de 27,9, IC95% 1,04-749,9, y p=0,047.No hubo diferencias significativas en los días de asistencia respiratoria mecánica o en la mortalidad entre los dos grupos.El factor de riesgo asociado a mortalidad en los pacientes con neumonía fue el puntaje bajo de la escala de coma de Glasgow al ingreso, con un OR de 2,19, IC95% 1,03-4,65, y p=0,04.Conclusión. La incidencia de neumonía en pacientes con trauma craneoencefálico grave es alta; a pesar de esto, su aparición no empeora el pronóstico. El único factor de riesgo encontrado que fue significativo, fue la presencia de hipotensión y soporte vasopresor.
Instituto Nacional de Salud
2009-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/27
10.7705/biomedica.v29i2.27
Biomedica; Vol. 29 No. 2 (2009); 253-259
Biomédica; Vol. 29 Núm. 2 (2009); 253-259
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/27/28
https://revistabiomedica.org/index.php/biomedica/article/view/27/311
/*ref*/Vincent JL, Bihari DJ, Suter PM, Bruining HA, White J, Nicolas-Chanoin MH, et al. The prevalence of nosocomial infection in intensive care units in Europe. Results of the European Prevalence of Infection in Intensive Care (EPIC) Study. EPIC International Advisory Committee. JAMA. 1995;274:639-44.<br />2. Heyland DK, Cook DJ, Griffith L, Keenan SP, Brun-Buisson C. The attributable morbidity and mortality of ventilator-associated pneumonia in the critically ill patient. The Canadian Critical Trials Group. Am J Respir Crit Care Med. 1999;159:1249-56.<br />3. Chastre J, Fagon JY. Ventilator-associated pneumonia. Am J Respir Crit Care Med. 2002;165:867-903.<br />4. Papazian L, Bregeon F, Thirion X, Gregoire R, Saux P, Denis JP, et al. Effect of ventilator-associated pneumonia on mortality and morbidity. Am J Respir Crit Care Med. 1996;154:91-7.<br />5. Rello J, Ollendorf DA, Oster G, Vera-Llonch M, Bellm L, Redman R, et al. Epidemiology and outcomes of ventilator-associated pneumonia in a large US database. Chest. 2002;122:2115–21.<br />6. Cavalcanti M, Ferrer M, Ferrer R, Morforte R, Garnacho A, Torres A. Risk and prognostic factors of ventilator-associated pneumonia in trauma patients. Crit Care Med. 2006;34:1067-72.<br />7. Leone M, Delliaux S, Bourgoin A, Albanese J, Garniere F, Bojadjiev I, et al. Risk factors for late-onset ventilator-associated pneumonia in trauma patients receiving selective digestive decontamination. Intensive Care Med. 2005;31:64-70.<br />8. Ewig S, Torres A, El-Ebiari M, Fabregas M, Hernández C, González J, et al. Bacterial colonization patterns in mechanically ventilated patients with traumatic and medical head injury. Am J Respir Crit Care Med. 1999;159:188-98.<br />9. Rincón-Ferrari MD, Flores-Cordero JM, Leal-Noval SR, Murillo-Cabezas M, Cayuelas A, Muñoz-Sánchez MA, et al. Impact of ventilator-associated pneumonia in patients with severe head injury. J Trauma. 2004;57:234-40.<br />10. Leone M, Bourgoin A, Giuly E, Antonini F, Dubuc M, Vivand X, et al. Influence on outcome of ventilator-associated pneumonia in multiple trauma patients with head trauma treated with selected digestive decontamination. Crit Care Med. 2002;30:1741-6.<br />11. Ibrahim EH, Sherman G, Ward S, Fraser VJ, Kollef MH. The influence of inadequate antimicrobial treatment of bloodstream infections on patient outcomes in the ICU setting. Chest. 2000;118:146-55.<br />12. McDermott FT, Rosenfeld JV, Laidlaw JD, Cordner SM, Tremayne AB, Consultative Committee on Road Traffic Fatalities in Victoria. Evaluation of management of road trauma survivors with brain injury and neurologic disability in Victoria. J Trauma. 2004;56:137-49.<br />13. Baker AM, Meredith JW, Haponik EF. Pneumonia in intubated trauma patients. Microbiology and outcomes. Am J Respir Crit Care Med. 1996;153:343-9.<br />14. Rello J, Kollef M, Díaz E, Sandiunmengue A, del Castillo Y, Corbella X, et al. Reduced burden of bacterial airway colonization with a novel silver-coated endotracheal tube in a randomized multiple-center feasibility study. Crit Care Med. 2006;34:2766-72.<br />15. Koeman M, van del Ven AJ, Hak E, Joore HC, Kaasjager K, de Smet AC, et al. Oral decontamination with chlorhexidine reduces the incidence of ventilator-associated pneumonia. Am J Respir Crit Care Med. 2006;173:1348-55.<br />16. Kollef MH, Skubas NJ, Sundt TM. A randomized clinical trial of continuous aspiration of subglottic secretions in cardiac surgery patients. Chest. 1999;116:1339-46.<br />17. Zygun DA, Zuege DJ, Boiteau PJ, Laupland KB, Henderson EA, Kortbeek JB, et al. Ventilator-associated pneumonia in severe traumatic brain injury. Neurocrit Care. 2006;5:108-14.<br />18. Sauaia A, Moore FA, Moore EE, Haenel JB, Read RA. Pneumonia related multiple organ failure is not a primary cause of death in head trauma. Pan Am J Trauma. 1992;3:90-9
oai:oai.revistabiomedica.org:article/28
2009-12-18T16:31:12Z
biomedica:ARTI
Validity and reliability of the Center for Epidemiologic Studies-Depression scale on Colombians adolescent students
Validez y confiabilidad de la escala del Center for Epidemiologic Studies-Depression en estudiantes adolescentes de Colombia
Rueda-Jaimes, Germán Eduardo
Camacho, Paul Anthony
Latorre, José Fidel
Navarro-Mancilla, Álvaro Andrés
Escobar, Mauricio
Franco, Jorge Augusto
reproducibilidad de resultados
validez de las pruebas
trastorno depresivo mayor
psiquiatría del adolescente
escalas de valoración psiquiátrica
cribado
Reproducibility of results
validity of tests
depressive disorder
major
adolescent psychiatric
psychiatric status rating scales
Introduction. Major depressive disorder is the second major cause of adolescent psychological incapacitation in Latin-America. However, scales for detecting these disorders have not been validated for screening adolescents in Colombia.Objective. The validity and reliability of a Spanish translation of the Center for Epidemiologic Studies (CES-D)-Depression scale was assessed in adolescent students.Materials and methods. A validation study for a diagnostic scale was performed with a sample of 390 adolescent students from Bucaramanga, Santander Province, in northwestern Colombia. The students were evaluated by two methods: (a) the CPS-depression scale and (b) a semi-structured clinical interview. Three to 28 days after the interview, the scale was re-applied. Criterion validity, internal consistency and test-retest reliability was analyzed.Results. The mean age was 14.8±1.2 years old. The prevalence of major depressive disorder was 11.5%. Cronbach’s alpha was 0.85. The area under the curve produced by the receiver operating characteristic curve was 0.82, and the cut point of ≥23 showed a sensitivity of 73.3%; specificity, 73.6%; positive predictive value, 26.6%, and negative predictive value, 95.5%. Lin´s coefficient of concordance was 0.75. Conclusions. The validity and reliability of the Spanish translation of the CES-D scale were similar to those reported in the international literature although with a higher cut point.
Introducción. El trastorno depresivo mayor es la segunda causa productora de discapacidad en Latinoamérica. No hay escalas validadas en Colombia para adolescentes.Objetivo. Evaluar la validez y la confiabilidad de la escala del Centro de Estudios Epidemiológicos para la Depresión en adolescentes colombianos en edad escolar.Materiales y métodos. Se llevó a cabo un estudio de validación de la escala con una muestra de adolescentes en edad escolar de Bucaramanga. Se evaluaron con la escala para depresión y la entrevista clínica estructurada. La escala fue aplicada nuevamente 3 a 28 días después. Se determinaron la validez de criterio, la consistencia interna y la reproducibilidad prueba reprueba.Resultados. Se evaluaron 390 adolescentes con edad promedio de 14,8±1,22 años. La prevalencia de trastorno depresivo mayor fue de 11,5%. El índice de consistencia, o alfa de Cronbach, fue de 0,85. El área bajo la curva según las características receptor operador fue de 0,82 y el punto de corte mayor o igual a 23 mostró una sensibilidad de 73,3%. Se encontró: especificidad de 73,6%, valor diagnóstico positivo de 26,6% y valor diagnóstico negativo de 95,5%. El coeficiente de concordancia de Lin fue de 0,75.Conclusión. La validez y la confiabilidad de la versión en español de la escala en adolescentes en edad escolar del Centro de Estudios Epidemiológicos para la Depresión, fueron similares a las informadas anteriormente, aunque cambió el punto de corte.
Instituto Nacional de Salud
2009-12-18
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/28
10.7705/biomedica.v29i2.28
Biomedica; Vol. 29 No. 2 (2009); 260-269
Biomédica; Vol. 29 Núm. 2 (2009); 260-269
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/28/29
https://revistabiomedica.org/index.php/biomedica/article/view/28/315
/*ref*/López AD, Mathers CD, Ezzati M, Jamison DT, Murray CJ. Global burden of disease and risk factors. Washington, D.C.: Oxford University Press; 2006.<br />2. Fergusson DM, Woodward LJ. Mental health, educational, and social role outcomes of adolescents with depression. Arch Gen Psychiatry. 2002;59:225-31.<br />3. Richardson JL, Radziszewska B, Dent CW, Flay BR. Relationship between after-school care of adolescents and substance use, risk taking, depressed mood, and academic achievement. Pediatrics. 1993;92:32-8.<br />4. Shrier LA, Harris SK, Beardslee WR. Temporal associations between depressive symptoms and self-reported sexually transmitted disease among adoles-cents. Arch Pediatr Adolesc Med. 2002;156:599-606.<br />5. Evans E, Hawton K, Rodham K, Deeks J. The prevalence of suicidal phenomena in adolescents: a systematic review of population-based studies. Suicide Life Threat Behav. 2005;35:239-50.<br />6. Newman DL, Moffitt TE, Caspi A, Magdol L, Silva PA, Stanton WR. Psychiatric disorder in a birth cohort of young adults: prevalence, comorbidity, clinical significance, and new case incidence from ages 11 to 21. J Consult Clin Psychol. 1996;64:552-62.<br />7. Lewinsohn PM, Rohde P, Seeley JR. Adolescent psychopathology: III. The clinical consequences of comorbidity. J Am Acad Child Adolesc Psychiatry. 1995;34:510-9.<br />8. Stover E, Fenton W, Rosenfeld A, Insel TR. Depression and comorbid medical illness: the National Institute of Mental Health perspective. Biol Psychiatry. 2003;54:184-6.<br />9. Fergusson DM, Horwood LJ, Lynskey MT. Prevalence and comorbidity of DSM-III-R diagnoses in a birth cohort of 15-year-olds. J Am Acad Child Adolesc Psychiatry. 1993;32:1127-34.<br />10. Regier DA, Farmer ME, Rae DS, Myers JK, Kramer M, Robins LN, et al. One-month prevalence of mental disorders in the United States and sociodemographic characteristics: the Epidemiologic Catchment Area study. Acta Psychiatr Scand. 1993;88:35-47.<br />11. Blazer DG, Kessler RC, McGonagle KA, Swartz MS. The prevalence and distribution of major depression in a national community sample: The National Comorbidity Survey. Am J Psychiatry. 1994;151:979-86.<br />12. Kessler D, Lloyd K, Lewis G, Gray DP. Cross sectional study of symptom attribution and recognition of depression and anxiety in primary care. Br Med J. 1999;318:436-9.<br />13. Froom J, Schlager DS, Steneker S, Jaffe A. Detection of major depressive disorder in primary care patients. J Am Board Fam Pract. 1993;6:5-11.<br />14. Wu P, Hoven CW, Bird HR, Moore RE, Cohen P, Alegria M, et al. Depressive and disruptive disorders and mental health service utilization in children and adolescents. J Am Acad Child Adolesc Psychiatry. 1999;38:1081-90<br />15. Bauer M, Whybrow PC, Angst J, Versiani M, Moller HJ, World Federation of Societies of Biological Psychiatry (WFSBF) Task Force on Treatment Guidelines for Unipolar Depressive Disorders. World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for biological treatment of unipolar depressive disorders. Part 2: Maintenance treatment of major depressive disorder and treatment of chronic depressive disorders and subthreshold depressions. World J Biol Psychiatry. 2002;3:69-86.<br />16. Rao U, Ryan ND, Birmaher B, Dahl RE, Williamson DE, Kaufman J, et al. Unipolar depression in adolescents: Clinical outcome in adulthood. J Am Acad Child Adolesc Psychiatry. 1995;34:566-78.<br />17. Rey JM, Grayson D, Mojarrad T, Walter G. Changes in the rate of diagnosis of major depression in adolescents following routine use of a depression rating scale. Aus N Z Psychiatry. 2002;36:229-33.<br />18. McDowell I. Measuring Health. Depression. In: McDowell I, Newell C. A guide to rating scales and questionnaires. Second edition. Washington, D.C.: Oxford University Press; 1996.<br />19. Wilcox H, Field T, Prodromidis M, Scafidi F. Correlations between the BDI and CES-D in a sample of adolescent mothers. Adolescence. 1998;33:565-74.<br />20. Radloff L. A self-report depression scale for research in the general population. Applied Psychological Measure. 1977;1:385-401.<br />21. Campo-Arias A, Díaz-Martínez LA, Rueda-Jaimes GE, Cadena-Afanador LP, Hernández NL. Psychometric properties of CES-D scale among Colombian adults from the general population. Rev Col Psiquiatr. 2007;36:664-74.<br />22. Obuchowski NA. Sample size calculations in studies of test accuracy. Stat Methods Med Res. 1998;7:371-92.<br />23. Silva L. Diseño razonado de muestras y captación de datos para la investigación sanitaria. Primera edición. Madrid: Díaz de Santos; 2000.<br />24. First MB, Spitzer RL, Gibbon M, Williams JB. Entrevista clínica estructurada para los trastornos de eje I del DSM-IV (versión clínica) SCID-I. Barcelona: Masson; 1999.<br />25. Cronbach LJ. Coefficient alpha and the internal structure of test. Psychometrika. 1951;16:297-334.<br />26. DeLong ER, DeLong DM, Clarke-Pearson DL. Comparing the areas under two or more correlated receiver operating curves: a nonparametric approach. Biometrics. 1988;44:837-45.<br />27. Beck JR, Shultz EK. The use of relative operating characteristics (ROC) curves in test performance evaluation. Arch Lab Pathol Med. 1986;110:13-20.<br />28. Kraemer H. Sensitivity and specificity: The signal detection approach. Evaluating medical tests: Objective and quantitative guidelines. First edition. California: Sage Publications; 1992.<br />29. Lin LI-K. A concordance correlation coefficient to evaluate reproducibility. Biometrics. 1989;45:255-68.<br />30. Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet. 1986;1:307-10.<br />31. Bradley EL, Blackwood LG. Comparing paired data: a simultaneous test for means and variances. American Statistician. 1989;43:234-5.<br />32. StataCorp. Stata statistic software: release 9.0. College Station, TX: StataCorp LP; 2005.<br />33. Irwing L, Bossuyt P, Glasziou P, Lijmer J. Designing studies to ensure that estimates of test accuracy are transferable. BMJ. 2002;324:669-71.<br />34. Radloff LS, Locke BZ. The Community Mental Health Assessment Survey and the CES-D scale. En: Weissman M, Myers J, Ross C, editors. Community surveys. New Brunswick, NJ: Rutgers University Press; 1986.<br />35. Schoenbach VJ, Kaplan BH, Grimson RC, Wagner EH. Use of a symptom scale to study the prevalence of a depressive syndrome in young adolescents. Am J Epidemiol. 1982;116:791-800.<br />36. Radloff LS. The use of the Center for Epidemiologic Studies Depression scale in adolescents and young adults. J Youth Adolesc. 1991;20:149-66.<br />37. Roberts RE, Andrews JA, Lewinsohn PM, Hops H. Assessment of depression in adolescents using the Center for Epidemiologic Studies Depression Scale. Psychol Assessment. 1990;2:122-8.<br />38. Rushton JL, Forcier M, Schectman RM. Epidemiology of depressive symptoms in the National Longitudinal Study of Adolescent Health. J Am Acad Child Adolesc Psychiatry. 2002;41:199-205.<br />39. Schoenbach VJ, Kaplan BH, Grimson RC, Wagner EH. Use of a symptom scale to study the prevalence of a depressive syndrome in young adolescents. Am J Epidemiol. 1982; 116:791-800.<br />40. Fava GA. Assessing depressive symptoms across cultures: Italian validation of the CES-D self-rating scale. J Clin Psychol. 1983;39:249-51.<br />41. Roberts RE, Lewinsohn PM, Seeley JR. Screening for adolescent depression: A comparison of depression scales. J Am Acad Child Adolesc Psychiatry. 1991;30:58-66.<br />42. Beekman AT, Deeg DJ, van Limbeek J, Braam AW, De Vries MZ, van Tilburg W. Criterion validity of the Center for Epidemiologic Studies Depression scale (CES-D): results from a community-based sample of older subjects in The Netherlands. Psychol Med. 1997;27:231-5.<br />43. Boyd JH, Weissman MM, Thompson D, Myers JK. Screening for depression in a community sample. Arch Gen Psychiatry. 1982;39:195-9.<br />44. Breslau N. Depressive symptoms, major depression, and generalized anxiety: a comparison of self-reports on CES-D and results from diagnostic interviews. Psychiatry Res. 1985;15:219-29.<br />
oai:oai.revistabiomedica.org:article/29
2009-12-24T18:06:59Z
biomedica:ARTI
Changes in retinol, hemoglobin and ferritin concentrations in Colombian children with malaria
Cambios en las concentraciones de retinol, hemoglobina y ferritina en niños palúdicos colombianos
Uscátegui, Rosa Magdalena
Correa, Adriana M.
Carmona-Fonseca, Jaime
malaria
vitamina A
anemia
niño
Colombia
malaria
vitamin A
anemia
child
Colombia
Introduction. Malaria, anemia and intestinal parasitism can co-exist in certain populations of Colombian children. The effects of retinol supplementation and anti-intestinal parasite treatment in children with malaria is unknown. Changes after this treatment of with respect to hemoglobin, retinol, ferritin and C reactive protein levels have not been previously monitored.Objective. The effect of simultaneous intervention with antimalarial, retinol supplementation and anti-intestinal parasites treatment will be monitored by examining levels of hemoglobin, ferritin, retinol and C reactive protein in children with malaria.Materials and methods. A non-blind experimental study was conducted in 93 children with malaria, aged 4-10 years. Each was randomly allocated to one of the following groups: (1) treatment with antimalarial and retinol supplement (Group MA); (2) treatment with antimalarial-retinol supplement and anti-parasitic drug (Group MAP); (3) treatment with antimalarial and anti-parasitic drug (Group MP), and (4) treatment only with antimalarials (Group M). The groups were observed for 30 days, with haemoglobin, ferritin, retinol and C reactive protein evaluated on days 0, 8 and 30 after treatment.Results. Mean values for the children at day 0 were as follows: hemoglobin 10.3±1.6 g/dL, retinol 19.1±6.0 μg/dL, C reactive protein 75±63 mg/L and ferritin 213±203 μg/L. On day 30 after treatment, hemoglobin and plasma retinol concentrations increased in 1.4±1.4 g/dL and 11.5±8.1 μg/dL, whereas the C reactive protein and ferritin concentrations decreased to 66±60 mg/L, and 184±203 μg/L, respectively. No statistically significant differences appeared among the groups. On day 8, significant differences between the groups were observed in hemoglobin concentrations Group MAP was higher when compared to other groups.Conclusion. On day 30, hemoglobin and retinol were high, whereas C reactive protein was low. Simultaneous administration of a retinol supplement and anti-parasite treatment prevented hemoglobin reduction observed on day 8 without changes in other variables.
Introducción. La malaria, la anemia y las parasitosis coexisten en niños colombianos. Se desconoce el efecto del suplemento de retinol y de los antiparasitarios sobre estos problemas de salud y la evolución de la hemoglobina, el retinol, la ferritina y la proteína C reactiva, en niños palúdicos.Objetivo. Comparar el efecto de la intervención simultánea con antipalúdicos, antiparasitarios y un suplemento de retinol sobre la evolución de la hemoglobina, la ferritina, el retinol y la proteína C reactiva, en niños palúdicos.Materiales y métodos. Estudio experimental no ciego de 93 niños palúdicos de 4 a 10 años, con asignación aleatoria a uno de los siguientes grupos: uno recibió antipalúdico y suplemento de retinol (grupo MA); otro, antipalúdico, suplemento de retinol y antiparasitarios (grupo MAP); otro, antipalúdico y antiparasitarios (grupo MP) y otro, sólo antipalúdico (grupo M); se siguieron 30 días, se evaluaron los cambios de hemoglobina, ferritina, retinol y proteína C reactiva, 8 y 30 días después.Resultados. En el total de los niños, el día del ingreso los promedios de las determinaciones fueron: hemoglobina, 10,3±1,6 g/dl; retinol, 19,1±6,0 μg/dl; proteína C reactiva, 75±63 mg/L, y ferritina, 213±203 μg/L. Al día 30, las concentraciones de hemoglobina y retinol aumentaron en 1,4±1,4g/dl y 11,5±8,1 μg/dl, respectivamente, mientras que las concentraciones de proteína C reactiva y ferritina disminuyeron en 66±60 mg/L y 184±203 μg/L, respectivamente, sin diferencias estadísticamente significativas entre los grupos de tratamiento. Los cambios el día 8 sólo fueron diferentes por grupo para la hemoglobina, que incrementó en el grupo MAP, diferente a los otros grupos.Conclusión. El día 30, la hemoglobina y el retinol aumentaron, y la proteína C reactiva y la ferritina disminuyeron. El suplemento de retinol y antiparasitarios simultáneos previno la reducción de hemoglobina al día 8, sin afectar los cambios en otras variables.
Instituto Nacional de Salud
2009-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/29
10.7705/biomedica.v29i2.29
Biomedica; Vol. 29 No. 2 (2009); 270-281
Biomédica; Vol. 29 Núm. 2 (2009); 270-281
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/29/30
https://revistabiomedica.org/index.php/biomedica/article/view/29/317
/*ref*/Dirección Seccional de Salud de Antioquia. Eventos de interés en salud pública, Antioquia 2006. Fecha de consulta: 20 de mayo de 2008. <a href="http://www.dssa.gov.co/dowload/archivoseventos_2007/EnotificacionSPVer2006-2.xls">www.dssa.gov.co/dowload/archivoseventos_2007/EnotificacionSPVer2006-2.xls</a><br />2. Castro L, Nicholls S. Deficiencia de hierro, vitamina A y prevalencia de parasitismo intestinal en población infantil y anemias nutricionales en mujeres en edad fértil de Colombia en 1995-1996. Santafé de Bogotá: Instituto Nacional de Salud; 1998. p. 50-5.<br />3. Ordóñez LE, Angulo ES. Desnutrición y su relación con parasitismo intestinal en niños de una población de la Amazonia colombiana. Biomédica. 2002;22:486-98.<br />4. Carmona-Fonseca J. La malaria en Colombia, Antioquia y las zonas de Urabá y Bajo Cauca: panorama para interpretar la respuesta terapéutica antimalárica. Parte 1. Iatreia. 2003;16:299-318.<br />5. Carmona-Fonseca J. La malaria en Colombia, Antioquia y las zonas de Urabá y Bajo Cauca: panorama para interpretar la respuesta terapéutica antimalárica. Parte 2. Iatreia. 2004;17:354-69.<br />6. van den Berg H. Vitamin A intake and status. Eur J Clin Nutr. 1996;50(Suppl.3):7-12.<br />7. WHO/NHD. Iron deficiency anaemia, assessment, prevention, and control a guide for programme managers. Geneva: United Nations Children’s Fund, United Nations University, World Health Organization; 2001. p. 10.<br />8. Tomkins A. Assessing micronutrient status in the presence of inflammation. J Nutr. 2003;133(Suppl.2):1649-55.<br />9. Hurt N, Smith T, Teuscher T, Tanner M. Do high levels of C-reactive protein in Tanzanian children indicate malaria morbidity? Clin Diagn Lab Immunol. 1994; 1:437-44.<br />10. Blair S, Álvarez G, Villa A, Carmona-Fonseca J, Ríos L. Estado nutricional y niveles de inmunoglobulinas y citoquinas en niños con malaria. Anales de Pediatría. 2003;58:418-24.<br />11. Blair S, Álvarez G, Campuzano G. Relación entre anemia y malaria en una población rural colombiana. Boletín de la Dirección de Malariología y Saneamiento Ambiental. 1997;37:7-12.<br />12. Echeverri M, Tobón A, Álvarez G, Carmona J, Blair S. Clinical and laboratory findings of Plasmodium vivax malaria in Colombia, 2001. Rev Inst Med Trop Sao Paulo. 2003;45:29-34<br />13. Persson V, Ahmed F, Gebre-Medhin M, Dreiner T. Relationships between vitamin A, iron status and helminthiasis in Bangladeshi school children. Public Health Nutr. 2000;3:83-9.<br />14. Koski KG, Scott ME. Gastrointestinal nematodes, nutrition and immunity: breaking the negative spiral. Annu Rev Nutr. 2001;21:297-321.<br />15. World Health Organization. Severe falciparum malaria. Severe and complicated malaria. Trans R Soc Trop Med Hyg. 2000;94(Suppl.1):1-88.<br />16. Willows ND, Gray-Donal K. Serum retinol is associated with hemoglobin concentration in infants who are not vitamin A deficient. Nutr Res. 2003;23:891-900.<br />17. Stoltzfus RJ, Albonico M, Chwaya HM, Tielsch JM, Schulze KJ, Savioli L. Effects of the Zanzibar school-based deworming program on iron status of children. Am J Clin Nutr. 1998;68:179-86.<br />18. Stoltzfus RJ, Chway HM, Montresor A, Tielsch JM, Jape JK, Albonico M, et al. Low dose daily iron supplementation improves iron status and appetite but not anemia, whereas quarterly antihelminthic treatment improves growth, appetite and anemia in Zanzibari preschool children. J Nutr. 2004;134:348-56.<br />19. Mwanri L, Worsley A, Ryan P, Masika J. Supplemental vitamin A improves anemia and growth in anemic school children in Tanzania. J Nutr. 2000;130:2691-6.<br />20. López F, Schmunis G. Diagnóstico de malaria. Publicación científica 512. Washington, D.C.: OPS-OMS; 1988. p. 143.<br />21. Rice CP, Trull AK, Berry D, Gorman EG. Development and validation of a particle-enhanced turbidimetric immunoassay for C-reactive protein. J Immunol Methods. 1987;99:205-11.<br />22. Talwar D, Ha TK, Cooney J, Brownlee C, O’Reilly DS. A routine method for the simultaneous measurement of retinol, alpha-tocopherol and five carotenoids in human plasma by reverse phase HPLC. Clin Chim Acta. 1998;270:85-100.<br />23. Uscátegui RM, Correa AM. Estado nutricional de niños palúdicos residentes en El Bagre y Turbo, Antioquia, Colombia, 2004-2005. Biomédica. 2007;27:559-70.<br />24. Botero D, Restrepo M. Parasitosis humanas. Cuarta edición. Medellín: Corporación para Investigaciones Biológicas; 2003. p. 455-63.<br />25. Blair S, Carmona J, Correa AM. Malaria en niños: relaciones entre nutrición e inmunidad. Rev Panam Salud Pública. 2002;11:5-14.<br />26. Rosales FJ, Topping JD, Smith JE, Shankar AH, Ross AC. Relation of serum retinol to acute phase proteins and malarial morbidity in Papua, New Guinea, children. Am J Clin Nutr. 2000;71:1582-8.<br />27. Filteau SM, Willumsen JF, Sullivan K, Simmank K, Gamble M. Use of the retinol-binding protein: transthyretin ratio for assessment of vitamin A status during the acute-phase response. Br J Nutr. 2000;83:513-20.<br />28. Álvarez MC, Correa JM, Deossa GC, Estrada A, Forero Y, Gómez LF et al. Encuesta Nacional de la Situación Nutricional en Colombia. Bogotá: ICBF, Profamilia, Instituto Nacional de Salud, Universidad de Antioquia, OPS, Panamericana Formas e Impresos; 2005. p. 445.<br />29. Thurnham DI, McCabe GP, Northrop-Clewes CA, Nestel P. Effects of subclinical infection on plasma retinol concentrations and assessment of prevalence of vitamin A deficiency: meta-analysis. Lancet. 2003;362:2052-8.<br />30. Rahman MM, Wahed MA, Fuchs GJ, Baqui AH, Álvarez JO. Synergistic effect of zinc and vitamin A on the biochemical indexes of vitamin A nutrition in children. Am J Clin Nutr. 2002;75:92-8.<br />31. Zimmermann MB, Biebinger R, Rohner F, Dib A, Zeder C, Hurrell RF, et al. Vitamin A supplementation in children with poor vitamin A and iron status increases erythropoietin and hemoglobin concentrations without changing total body iron. Am J Clin Nutr. 2006;84:580-6.<br />32. Tanumihardjo SA, Permaesih D, Muhilal. Vitamin A status and hemoglobin concentrations are improved in Indonesian children with vitamin A and deworming interventions. Eur J Clin Nutr. 2004;58:1223-30.<br />33. Stephensen CB, Gildengorin G. Serum retinol, the acute phase response, and the apparent misclassification of vitamin A status in the third National Health and Nutrition Examination Survey. Am J Clin Nutr. 2000;72:1170-8.<br />34. Álvarez MC, Uscátegui RM, López C, Baracaldo CM, Castro L, Noy V. Plasma retinol concentration according to pubertal maturation in school children and adolescents of Medellin, Colombia. Eur J Clin Nutr. 2004;58:456-61.<br />35. Tanumihardjo SA. Assessing vitamin A status: past, present and future. J Nutr. 2004;134(Suppl.1):290-3.<br />36. Obonyo CO, Vulule J, Akhwale WS, Grobbee DE. In-hospital morbidity and mortality due to severe malarial anemia in western Kenya. Am J Trop Med Hyg. 2007;77:23-8.<br />37. Anderson GJ, Darshan D, Wilkins SJ, Frazer DM. Regulation of systemic iron homeostasis: how the body responds to changes in iron demand. Biometals. 2007;20:665-74.<br />38. Rodríguez-Morales AJ, Sánchez E, Vargas M, Piccolo C, Colina R, Arria M. Anemia and thrombocytopenia in children with Plasmodium vivax malaria. J Trop Pediatr. 2006;52:49-51.<br />39. Villamor E, Mbise R, Spiegelman D, Ndossi G, Fawzi WW. Vitamin A supplementation and other predictors of anemia among children from Dar Es Salaam, Tanzania. Am J Trop Med Hyg. 2000;62:590-7.<br />40. Roberts DJ, Casals-Pascual C, Weatherall DJ. The clinical and pathophysiological features of malarial anaemia. En: Sullivan J, Krishna S, editors. Malaria: drugs, disease and post-genomic biology. Berlin: Springer-Verlag Berlin Heidelberg; 2005. p. 137-8.
oai:oai.revistabiomedica.org:article/30
2009-12-18T16:31:12Z
biomedica:ARTI
Evaluation of community-based strategies for Aedes aegypti control inside houses
Evaluación de estrategias comunitarias para el control de Aedes aegypti en Cali, Colombia
Ocampo, Clara Beatriz
González, Camila
Morales, Carlos A.
Pérez, Mauricio
Wesson, Dawn
Apperson, Charles S.
Aedes aegypti
control vectorial
Bacillus thuringiensis
dengue
participación comunitaria
Aedes aegypti
vector control
Bacillus thuringiensis
dengue
consumer participation
Introduction: Dengue viruses transmitted principally by the urban mosquito Aedes aegypti, cause one of the major public health problems confronting tropical cities. Insecticide spraying has been the mainstay of mosquito control; however, its continuous use has selected for resistance. Other important methods of control involve community participation.Objective: This study evaluated two control methods for Ae. aegypti that can be used by the community: Lethal ovitraps (LOs) and Bacillus thuringiensis var israeliensis (Bti) briquettes.Materials and methods: The project study was carried out in four similar neighborhoods within a representative district in the city of Cali, Colombia. Three interventions (LO, Bti, LO+Bti plus education and one control (education only) area were evaluated for efficacy in post-intervention entomological surveys. Additionally, entomological indices were also compared to results from a pre-intervention survey carried out on a sample of city blocks in the same neighborhoods. Relative vector abundance in relation to weather conditions using the same entomological sampling methods was compared.Results: The interventions did not achieve significant differences in vector abundance among the treatments. However, the interventions achieved a significant reduction in entomological indices compared with those observed during the pre-intervention survey: House index 15.1% vs. 8.5%, mean pupae per house 1.15 vs. 0.073, and Adult index 56.3% vs. 34.8% (p<0.05).Conclusions: The lack of significant differences among the interventions, and between treated and control blocks suggested that educational activities together with periodic visits to the houses produced similar reductions of immature and adult Aedes aegypti.
Introducción. Los virus del dengue transmitidos principalmente por el mosquito urbano Aedes aegypti, causan uno de los mayores problemas de salud pública que confrontan las ciudades tropicales. La aplicación de insecticidas ha sido la base para el control de mosquitos; sin embargo, su continuo uso ha servido para seleccionar individuos resistentes en las poblaciones de mosquitos. Otro método importante para el control involucra la participación comunitaria.Objetivo. Este estudio evaluó dos métodos de control para Ae. aegypti que podrían ser usados por la comunidad: las ovitrampas letales (OL) y las briquetas de Bacillus thuringiensis var israeliensis (Bti).Materiales y métodos. El estudio se llevó a cabo en cuatro barrios similares de la Comuna 16 de Cali, Colombia. Se evaluaron tres intervenciones (OL, Bti, OL y Bti) más educación y un área control (sólo educación) para medir la eficacia de la vigilancia entomológica posterior a la intervención. Además, los índices entomológicos se compararon con los resultados de una vigilancia antes de la intervención llevada a cabo en bloques de casas seleccionadas aleatoriamente en los mismos barrios. La abundancia relativa del vector en relación con las condiciones climáticas se comparó usando los mismos métodos del muestreo entomológico.Resultados. Las intervenciones no produjeron diferencias significativas entre los tratamientos en la abundancia del vector. Sin embargo, las intervenciones lograron una reducción significativa de los índices entomológicos comparados con los observados en la vigilancia antes de la intervención: índice de casa, de 15,1% a 8,5%; promedio de pupas por casa, de 1,15 a 0,073, e índice de adultos, de 56,3% a 34,8% (p<0,05).Conclusiones. La ausencia de diferencias significativas entre las intervenciones y el bloque control sugiere que las actividades educacionales junto con las visitas periódicas a las casas producen reducciones similares de los estadios inmaduros y adultos de Ae. aegypti.
Instituto Nacional de Salud
2009-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/30
10.7705/biomedica.v29i2.30
Biomedica; Vol. 29 No. 2 (2009); 282-297
Biomédica; Vol. 29 Núm. 2 (2009); 282-297
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/30/31
https://revistabiomedica.org/index.php/biomedica/article/view/30/321
/*ref*/Spiegel J, Bennett S, Hattersley L, et al. Barriers and bridges to prevention and control of dengue: the need for a social-ecological approach. EcoHealth. 2005;2:273-90.<br />2. Guha-Sapir D, Schimmer B. Dengue fever: new paradigms for a changing epidemiology. Emerg Themes Epidemiol. 2005;2:1.<br />3. Gubler DJ. The changing epidemiology of yellow fever and dengue, 1900 to 2003: full circle? Comp Immunol Microbiol Infect Dis. 2004;27:319-30.<br />4. Gubler DJ. Resurgent vector-borne diseases as a global health problem. Emerg Infect Dis. 1998;4:442-50.<br />5. Guzman MG, Kouri G. Dengue: an update. Lancet Infect Dis. 2002;2:33-42.<br />6. Christopher RS. Aedes aegypti (L.), the yellow fever mosquito; its life history, bionomics and structure. London: Cambridge Univ. Press; 1960.<br />7. Morrison AC, Costero A, Edman JD, Clark GG, Scott TW. Increased fecundity of Aedes aegypti fed human blood before release in a mark-recapture study in Puerto Rico. J Am Mosq Control Assoc. 1999;15:98-104.<br />8. Perich MJ, Davila G, Turner A, Garcia A, Nelson M. Behavior of resting Aedes aegypti (Culicidae: Diptera) and its relation to ultra-low volume adulticide efficacy in Panama City, Panama. J Med Entomol. 2000;37:541-6.<br />9. Focks DA, Chadee DD. Pupal survey: an epidemiologically significant surveillance method for Aedes aegypti: an example using data from Trinidad. Am. J Trop Med Hyg. 1997;56:159-67.<br />10. Gubler DJ, Clark GG. Dengue/Dengue Hemorraghic Fever. The emergence of a global health problem. Emerg Infect Dis. 1995;1:55-7<br />11. Gubler D. The emergence of epidemic dengue fever and dengue hemorrhagic fever in the Americas: a case of failed public health policy. Rev Panam Salud Pública. 2005;17:221-4.<br />12. Ministerio de Salud de Colombia. Prevención y control del dengue. Boletín epidemiológico, semana 42. Sivigila, Ministerio de Salud, Colombia. Nov 2001; 2001.<br />13. Ministerio de Salud de Colombia. Comportamiento por regiones del dengue en el 2000. Boletín epidemiológico nacional, semana 2. Sivigila, Ministerio de Salud, Colombia; 2002:2.<br />14. Suárez-Rubio M, Suárez M. The use of copepod Mesocyclops longisetus as a biological control agent for Aedes aegypti in Cali, Colombia. Am J Trop Med Hyg. 2004;20:401-4.<br />15. Suarez MF, Gonzales R, Morales CA. Themephos resistance to Aedes aegypti in Cali, Colombia. Am J Trop Med Hyg. 1998;55(Suppl.):257.<br />16. Hernandez VC, Segura I, Wesson DM, Ocampo CB. Insecticide resistance dynamics in Aedes aegypti from Cali, Colombia. Am J Trop Med Hyg. 1999;61(Suppl.):436.<br />17. Ocampo CB, Wesson DM. Population dynamics of Aedes aegypti from dengue hyper-endemic urban setting in Colombia. Am J Trop Med Hyg. 2004;71:506-13.<br />18. Zeichner BC, Perich MJ. Laboratory testing of a lethal ovitrap for Aedes aegypti. Med Vet Entomol. 1999;13:234-8.<br />19. Perich MJ, Kardec A, Braga IA, Portal IF, Burge R, Zeichner BC. Field evaluation of the lethal ovitrap against dengue vectors in Brazil. Med Vet Entomol. 2003;17:205-10.<br />20. Sulaiman S, Jeffery J, Sohadi AR, Yunus H, Busparani V, Majid R. Evaluation of Bactimos wettable powder, granules and briquets against mosquito larvae in Malaysia. Acta Tropica. 1990;47:189 -95.<br />21. WHO. Environmental Health Criteria, No 217: Bacillus thuringiensis; 1999.<br />22. Reiter P, Amador MA, Colon N. Enhancement of the CDC ovitrap with hay infusions for daily monitoring of Aedes aegypti populations. Am J Mosq Control Assoc. 1991;7:52-5.<br />23. Sithiprasasna R, Mahapibul P, Noigamol C, et al. Field evaluation of a lethal ovitrap for the control of Aedes aegypti (Culicidae) in Thailand. J Med Entomol. 2003;40:455-62.<br />24. Giraldo-Calderon G, Pérez M, Morales CA, Ocampo CB. Evaluación del triflumurón y la mezcla de Bacillus thuringiensis más Bacillus sphaericus para el control de las formas inmaduras de Aedes aegypti y Culex quinquefasciatus en sumideros de Cali, Colombia. Biomédica 2008;28:224-33.<br />25. Reiter P, Amador MA, Anderson RA, Clark GG. Short report: dispersal of Aedes aegypti in an urban area after blood feeding as demonstrated by rubidium-marked eggs. Am J Trop Med Hyg. 1995;52:177-9.<br />26. Russell R, Webb C, Williams C, SA R. Mark-release-recapture study to measure dispersal of the mosquito Aedes aegypti in Cairns, Queensland, Australia. Med Vet Entomol. 2005;19:451-7.<br />27. Honorio NA, Silva WdC, Goncalves JM, Lounibos LP, Lourenco-de-Oliveira R. Dispersal of Aedes aegypti and Aedes albopictus (Diptera: Culicidae) in an urban endemic dengue area in the State of Rio de Janeiro, Brazil. Mem Inst Oswaldo Cruz 2003;98:191-8.<br />28. Focks DA, Brenner RJ, Hayes J, Daniels E. Transmission thresholds for dengue in terms of Aedes aegypti pupae per person with discussion of their utility in source reduction efforts. Am J Trop Med Hyg. 2000;62:11-8.
oai:oai.revistabiomedica.org:article/31
2009-12-18T16:31:13Z
biomedica:ARTI
Distribution of Porphyromonas gingivalis fimA genotypes in isolates from subgingival plaque and blood sample during bacteremia
Distribución de los genotipos de fimA en cepas de Porphyromonas gingivalis aisladas de placas subgingivales y de sangre durante bacteriemias
Bonnaure-Mallet, Martine
Pérez-Chaparro, Paula Juliana
Gracieux, Patrice
Meuric, Vincent
Tamanai-Shacoori, Zohreh
Castellanos, Jaime Eduardo
Porphyromonas gingivalis
bacteriemia
periodontitis
reacción en cadena de la polimerasa
Porphyromonas gingivalis
bacteremia
periodontitis
polymerase chain reaction
Introduction. Porphyromonas gingivalis is considered as a major etiological agent in the onset and progression of chronic destructive periodontitis. Porphyromonus gingivalis fimA type has been correlated to the virulence potential of the strain; therefore this gene could be involved in the ability of P. gingivalis to reach blood stream.Objective. The classifications of P. gingivalis fimA types will be compared in subgingival plaque and blood samples collected after scaling and root root planing of periodontitis patients.Materials and methods. Fifteen periodontitis patients requiring scaling and root planing were enrolled. P. gingivalis isolates were classed to genotype with fimA type-specific PCR assay. fimA gene was sequenced if the isolate was listed as unclassifiable after PCR technique.Results. Six patients showed positive P. gingivalis bacteremia. The most frequent fimA was fimA type II, followed by Ib, III and IV. In blood strains, type II was followed by IV, Ib and III.Conclusion. Type II was the most frequent genotype in blood samples and in subgingival plaque samples. However, no correlation was found between the frequency of any fimA type with SRP induced bacteremia. P. gingivalis fimA type appears to be conserved within individual patients throughout the times of sample collection. fimA gene sequence results were not in agreement with results of fimA genotyping by PCR.
Introducción. Porphyromonas gingivalis es el principal agente etiológico de la periodontitis. El gen fimA ha sido relacionado con la virulencia del microorganismo, lo cual sugiere la participación de dicho gen en la capacidad del microorganismo para alcanzar el torrente sanguíneo.Objetivo. Estudiar la distribución de los tipos de fimA de P. gingivalis en muestras de placa subgingival y de sangre obtenidas durante bacteriemias después de raspaje y alisado radicular.Materiales y métodos. Se practicó un alisado radicular a 15 pacientes con periodontitis. Se obtuvieron aislamientos clínicos de P. gingivalis de la placa subgingival y durante la bacteriemia inducida por el procedimiento. Para la genotipificación se utilizó la técnica de reacción en cadena de la polimerasa (PCR) específica para fimA. En los aislamientos no clasificables por PCR se realizó secuenciación del gen fimA.Resultados. Seis pacientes fueron positivos para bacteriemia por P. gingivalis. La distribución de fimA evaluada en 30 aislamientos de placa subgingival y de sangre mostró una mayor frecuencia del fimA tipo II de P. gingivalis. En los aislamientos de placa subgingival, la detección de fimA tipo II fue seguida por Ib, III y IV; sin embargo, en los aislamientos de sangre el tipo II fue seguido por los tipos IV, Ib y III.Conclusión. En los aislamientos de sangre y de placa subgingival de pacientes con periodontitis el fimA más frecuente fue el tipo II; no fue posible correlacionar el tipo de fimA con la bacteriemia inducida por el alisado radicular. Los resultados de la secuenciación del gen fimA no concuerdan con los obtenidos por PCR.
Instituto Nacional de Salud
2009-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/31
10.7705/biomedica.v29i2.31
Biomedica; Vol. 29 No. 2 (2009); 298-306
Biomédica; Vol. 29 Núm. 2 (2009); 298-306
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/31/32
https://revistabiomedica.org/index.php/biomedica/article/view/31/323
/*ref*/Burt B. Position paper: epidemiology of periodontal diseases. J Periodontol. 2005;76:1406-19.<br />2. Hamada S, Amano A, Kimura S, Nakagawa I, Kawabata S, Morisaki I. The importance of fimbriae in the virulence and ecology of some oral bacteria. Oral Microbiol Immunol. 1998;13:129-38.<br />3. Eskan MA, Hajishengallis G, Kinane DF. Differential activation of human gingival epithelial cells and monocytes by Porphyromonas gingivalis fimbriae. Infect Immun. 2007;75:892-8.<br />4. Hajishengallis G, Sharma A, Russell MW, Genco RJ. Interactions of oral pathogens with toll-like receptors: possible role in atherosclerosis. Ann Periodontol. 2002;7:72-8.<br />5. Khlgatian M, Nassar H, Chou HH, Gibson FC 3rd, Genco CA. Fimbria-dependent activation of cell adhesion molecule expression in Porphyromonas gingivalis-infected endothelial cells. Infect Immun. 2002;70:257-67.<br />6. Lee JY, Sojar HT, Bedi GS, Genco RJ. Porphyromonas (Bacteroides) gingivalis fimbrillin: size, amino-terminal sequence, and antigenic heterogeneity. Infect Immun. 1991;59:383-9.<br />7. Koehler A, Karch H, Beikler T, Flemmig TF, Suerbaum S, Schmidt H. Multilocus sequence analysis of Porphyromonas gingivalis indicates frequent recombination. Microbiology. 2003;149:2407-15.<br />8. Nakagawa I, Amano A, Ohara-Nemoto Y, Endoh N, Morisaki I, Kimura S, et al. Identification of a new variant of fimA gene of Porphyromonas gingivalis and its distribution in adults and disabled populations with periodontitis. J Periodontal Res. 2002;37:425-32.<br />9. Lourbakos A, Potempa J, Travis J, D’Andrea MR, Andrade-Gordon P, Santulli R, et al. Arginine-specific protease from Porphyromonas gingivalis activates protease-activated receptors on human oral epithelial cells and induces interleukin-6 secretion. Infect Immun. 2001;69:5121-30.<br />10. Cueto A, Mesa F, Bravo M, Ocana-Riola R. Periodontitis as risk factor for acute myocardial infarction. A case control study of Spanish adults. J Periodontal Res. 2005;40:36-42.<br />11. Offenbacher S, Boggess KA, Murtha AP, Jared HL, Lieff S, McKaig RG, et al. Progressive periodontal disease and risk of very preterm delivery. Obstet Gynecol. 2006;107:29-36.<br />12. Renvert S, Pettersson T, Ohlsson O, Persson GR. Bacterial profile and burden of periodontal infection in subjects with a diagnosis of acute coronary syndrome. J Periodontol. 2006;77:1110-9.<br />13. Scannapieco FA, Stewart EM, Mylotte JM. Colonization of dental plaque by respiratory pathogens in medical intensive care patients. Crit Care Med. 1992;20:740-5.<br />14. Forner L, Larsen T, Kilian M, Holmstrup P. Incidence of bacteremia after chewing, tooth brushing and scaling in individuals with periodontal inflammation. J Clin Periodontol. 2006;33:401-7.<br />15. Heimdahl A, Hall G, Hedberg M, Sandberg H, Soder PO, Tuner K, et al. Detection and quantitation by lysis-filtration of bacteremia after different oral surgical procedures. J Clin Microbiol. 1990;28:2205-9.<br />16. Kinane DF, Riggio MP, Walker KF, MacKenzie D, Shearer B. Bacteraemia following periodontal procedures. J Clin Periodontol. 2005;32:708-13.<br />17. Lafaurie GI, Mayorga-Fayad I, Torres MF, Castillo D, Aya MR, Baron A, et al. Periodontopathic microorganisms in peripheric blood after scaling and root planing. J Clin Periodontol. 2007;34:873-9.<br />18. Bodet C, Chandad F, Grenier D. Modulation of cytokine production by Porphyromonas gingivalis in a macrophage and epithelial cell co-culture model. Microbes Infect. 2005;7:448-56.<br />19. Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol. 1999;4:1-6.<br />20. Perez-Chaparro PJ, Gracieux P, Lafaurie GI, Donnio PY, Bonnaure-Mallet M. Genotypic characterization of Porphyromonas gingivalis isolated from subgingival plaque and blood sample in positive bacteremia subjects with periodontitis. J Clin Periodontol. 2008;35:748-53.<br />21. Ashimoto A, Chen C, Bakker I, Slots J. Polymerase chain reaction detection of 8 putative periodontal pathogens in subgingival plaque of gingivitis and advanced periodontitis lesions. Oral Microbiol Immunol. 1996;11:266-73.<br />22. Amano A, Kuboniwa M, Nakagawa I, Akiyama S, Morisaki I, Hamada S. Prevalence of specific genotypes of Porphyromonas gingivalis fimA and periodontal health status. J Dent Res. 2000;79:1664-8.<br />23. Amano A, Nakagawa I, Kataoka K, Morisaki I, Hamada S. Distribution of Porphyromonas gingivalis strains with fimA genotypes in periodontitis patients. J Clin Microbiol. 1999;37:1426-30.<br />24. Nakagawa I, Amano A, Kimura RK, Nakamura T, Kawabata S, Hamada S. Distribution and molecular characterization of Porphyromonas gingivalis carrying a new type of fimA gene. J Clin Microbiol. 2000;38:1909-14.<br />25. Missailidis CG, Umeda JE, Ota-Tsuzuki C, Anzai D, Mayer MP. Distribution of fimA genotypes of Porphyromonas gingivalis in subjects with various periodontal conditions. Oral Microbiol Immunol. 2004;19:224-9.<br />26. Fujiwara T, Morishima S, Takahashi I, Hamada S. Molecular cloning and sequencing of the fimbrilin gene of Porphyromonas gingivalis strains and characterization of recombinant proteins. Biochem Biophys Res Commun. 1993;197:241-7.<br />27. Xie H, Lamont RJ. Promoter architecture of the Porphyromonas gingivalis fimbrillin gene. Infect Immun. 1999;67:3227-35.<br />28. Eick S, Rodel J, Einax JW, Pfister W. Interaction of Porphyromonas gingivalis with KB cells: comparison of different clinical isolates. Oral Microbiol Immunol. 2002;17:201-8.<br />29. Davila-Perez C, Amano A, Alpuche-Solis AG, Patino-Marin N, Pontigo-Loyola AP, Hamada S, et al. Distribution of genotypes of Porphyromonas gingivalis in type 2 diabetic patients with periodontitis in Mexico. J Clin Periodontol. 2007;34:25-30.<br />30. Enersen M, Olsen I, Kvalheim O, Caugant DA. fimA genotypes and multilocus sequence types of Porphyromonas gingivalis from patients with periodontitis. J Clin Microbiol. 2008;46:31-42.<br />31. Beikler T, Peters U, Prajaneh S, Prior K, Ehmke B, Flemmig TF. Prevalence of Porphyromonas gingivalis fimA genotypes in Caucasians. Eur J Oral Sci. 2003;111:390-4.<br />32. Nelson KE, Fleischmann RD, DeBoy RT, Paulsen IT, Fouts DE, Eisen JA, et al. Complete genome sequence of the oral pathogenic Bacterium Porphyromonas gingivalis strain W83. J Bacteriol. 2003;185:5591-601.<br />33. Naito M, Hirakawa H, Yamashita A, Ohara N, Shoji M, Yukitake H, et al. Determination of the genome sequence of Porphyromonas gingivalis strain ATCC 33277 and genomic comparison with strain W83 revealed extensive genome rearrangements in P. gingivalis. DNA Res. 2008;15:215-25.
oai:oai.revistabiomedica.org:article/32
2009-12-18T16:31:13Z
biomedica:ARTI
Therapeutic efficacy of a regimen of artesunate-mefloquine-primaquine treatment for Plasmodium falciparum malaria and treatment effects on gametocytic development
Estudio piloto de la eficacia y de los efectos sobre los gametocitos del esquema artesunato-mefloquina-primaquina para la malaria por Plasmodium falciparum
Vásquez, Ana María
Sanín, Felipe
Álvarez, Luis Gonzalo
Tobón, Alberto
Ríos, Alexandra
Blair, Silvia
Plasmodium falciparum
malaria
artesunato
mefloquina
primaquina
resultado del tratamiento
falciparum
malaria
artesunate
mefloquine
primaquine
treatment outcome
Introduction. The treatment of Plasmodium falciparum malaria requires a safe and effective therapeutic treatment regimen, which in turn has high impact on the transmission. In 2006, an artesunate (AS)-mefloquine (MQ) treatment program was implemented in Antioquia. In addition, primaquine (PQ) was added to eliminate malaria gametocytes in the bloodstream.Objective. The efficacy and gametocytocidal activity was evaluated for two treatment regimens, AS-MQ-PQ and AS-MQ, in patients with uncomplicated P. falciparum malaria.Materials and methods. Between April 2007 and February 2008, 50 patients were recruited for the trial in Turbo, Antioquia. A randomized clinical trial was conducted. Treatment compliance was supervised, with a clinical and parasitological assessment on days 1, 2, 3, 7, 14, 21, 28, 35, and 42 to evaluate response rate according to the WHO 2003 protocol.Results. Clinical response and parasite elimination efficacy of AS-MQ (with or without PQ) was 100% (95% CI 86.3%-100%), and parasitemia and fever were absent on day 3 of treatment in all patients. Gametocyte elimination was superior when PQ was used--92% (95% CI: 74%-99%) of patients who received PQ had no gametocytes on day 3, compared to 78.3% (95% CI: 59%-93%) of patients who only received AS-MQ. Furthermore, circulating gametocytes were eliminated on average one week faster when the AS-MQ-PQ treatment scheme was used compared to the scheme without PQ. Conclusion. These studies recommend the use of AS-MQ to treat P. falciparum malaria given its good therapeutic efficacy. However, further assessment is suggested concerning the benefit of adding PQ to this treatment scheme.
Introducción. El tratamiento de la malaria por P. falciparum requiere de un esquema seguro, eficaz y de impacto en la transmisión. En 2006, se implementó en Antioquia el esquema artesunato-mefloquina y se adicionó primaquina para eliminar los gametocitos.Objetivo. Evaluar la eficacia y acción gametocida de los esquemas artesunato-mefloquina-primaquina y artesunato-mefloquina en pacientes con malaria no complicada por P. falciparum de Turbo, Antioquia.Materiales y métodos. Ensayo clínico aleatorio; los tratamientos se suministraron de forma supervisada y se realizó seguimiento clínico-parasitológico en los días 1, 2, 3, 7, 14, 21, 28, 35, y 42, para evaluar la respuesta según el protocolo OMS-2003 modificado.Resultados. Entre abril de 2007 y febrero de 2008, 50 pacientes fueron reclutados; los resultados mostraron una eficacia de 100% (IC95% 86,3%-100%) para el esquema artesunato-mefloquina (con/sin primaquina); la parasitemia y la fiebre fueron eliminadas completamente al tercer día de tratamiento en todos los pacientes. La eliminación de gametocitos fue mayor con el uso de primaquina; al tercer día de seguimiento, el 92% (IC95% 74%-99%) de los pacientes que recibieron primaquina no tuvieron gametocitos, en comparación con 78,3% (IC95% 59%-93%) de pacientes del grupo artesunato-mefloquina. Además, el esquema artesunato-mefloquina-primaquina eliminó la gametocitemia una semana antes que el esquema sin primaquina.Conclusión. Se recomienda el uso del esquema artesunato-mefloquina para la malaria por P. falciparum por su alta eficacia y se sugieren futuras evaluaciones del beneficio de la PQ en la reducción de la densidad y prevalencia de gametocitos.
Instituto Nacional de Salud
2009-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/32
10.7705/biomedica.v29i2.32
Biomedica; Vol. 29 No. 2 (2009); 307-319
Biomédica; Vol. 29 Núm. 2 (2009); 307-319
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/32/33
https://revistabiomedica.org/index.php/biomedica/article/view/32/324
/*ref*/WHO-UNICEF. Roll-back malaria. World Malaria Report 2005. Geneva: World Health Organization; 2005. Fecha de consulta: diciembre de 2007. Disponible en: <a href="http://www.rbm.who.int/wmr2005">http://www.rbm.who.int/wmr2005</a>.<br />2. Phillips RS. Current status of malaria and potential for control. Clin Microbiol Rev. 2000;14:208-26.<br />3. Bloland PB. Drug resistance in malaria. WHO/CDS/CSR/ DRS/2001.4. Geneva: World Health Organization; 2001.<br />4. Wongsrichanalai C, Pickard AL, Wernsdorfer WH, Meshnick SR. Epidemiology of drug-resistant malaria. Lancet Infect Dis. 2002;2:209-18.<br />5. WHO. Assessment and monitoring of antimalarial drug efficacy for the treatment of uncomplicated falciparum malaria. WHO/HTM/RBM/2003.50. Geneva: World Health Organization; 2003.<br />6. WHO. Monitoring antimalarial drug resistance. WHO/CDS/CSR/EPH/2002.17. Geneva: World Health Organization; 2001.<br />7. Blair S, López M, Piñeros J, Álvarez T, Tobón A, Carmona J. Eficacia terapéutica de tres esquemas de tratamiento de malaria no complicada por Plasmodium falciparum, Antioquia, Colombia, 2002. Biomédica. 2003;23:318-27.<br />8. Osorio LE, Giraldo LE, Grajales LF, Arriaga AL, Andrade AL, RuebushII T, et al. Assessment of therapeutic response of Plasmodium falciparum to chloroquine and sulfadoxine/pyrimethamine in a low malaria transmission area in Colombia. Am J Trop Med Hyg. 1999;61:968-72.<br />9. Blair S, Lacharme L, Carmona-Fonseca J, Piñeros J, Ríos A, Álvarez T, et al. Therapeutic efficacy test in malaria falciparum in Antioquia, Colombia. Malar J. 2006;5:14.<br />10. Orjuela P, González I, Osorio L. Terapia combinada como estrategia en la prevención de la resistencia a los antimaláricos. Biomédica. 2004;24:423-37.<br />11. WHO. Guidelines for the treatment of malaria. WHO/HTM/MAL/2006.1108. Geneva: World Health Organization; 2006.<br />12. WHO. Susceptibility of Plasmodium falciparum to anti-malarial drugs monitoring antimalarial drug resistance. Report on global monitoring 1996-2004. WHO/HTM/MAL/ 2005.1103. Geneva: World Health Organization; 2005.<br />13. Nosten F, van Vugt M, Price R, Luxemburger C, Thway KL, Brockman A, et al. Effects of artesunate-mefloquine combination on incidence of Plasmodium falciparum malaria and mefloquine resistance in western Thailand: a prospective study. Lancet. 2000;356:297-302.<br />14. Davis TM, Karunajeewa HA, Ilett KF. Artemisinin-based combination therapies for uncomplicated malaria. Med J Aust. 2005;182:181-5.<br />15. Suputtamongkol Y, Chindarat S, Silpasakorn S, Chaikachonpatd S, Lim K, Chanthapakajee K, et al. The efficacy of combined mefloquine-artesunate versus mefloquine-primaquine on subsequent development of Plasmodium falciparum gametocitemia. Am J Trop Med Hyg. 2003;68:620-3.<br />16. Dirección Seccional de Salud de Antioquia. Protocolo de vigilancia epidemiológica para malaria, Antioquia 2007. Fecha de consulta: diciembre de 2007. Disponible en: <a href="http://www.dssa.gov.co/dowload/P0841.pdf">http://www.dssa.gov.co/dowload/P0841.pdf</a><br />17. Talisuna A, Staedke S, D´Alessandro U. Pharmaco-vigilance of antimalarial treatment in Africa: is it possible? Malar J. 2006;5:50.<br />18. Davis T. Addition of artesunate to standard antimalarial drugs reduces treatment failure. Evidence Based Healthcare. 2004;8:156-8.<br />19. Nosten F, Luxemburger C, ter Kuile FO, Woodrow C, Eh JP, Chongsuphajaisiddhi T, et al. Treatment of multidrug-resistant Plasmodium falciparum malaria with 3-day artesunate-mefloquine combination. J Infect Dis. 1994;170:971-7.<br />20. Price RN, Nosten F, Luxemburger C, Kham A, Brockman A, Chongsuphajaisiddhi T, et al. Artesunate versus artemether in combination with mefloquine for the treatment of multidrug-resistant falciparum malaria. Trans R Soc Trop Med Hyg. 1995;89:523-7.<br />21. Bunnag D, Kanda T, Karbwang J, Thimasarn K, Pungpak S, Harinasuta T. Artemether or artesunate followed by mefloquine as a possible treatment for multidrug resistant falciparum malaria. Trans R Soc Trop Med Hyg. 1996;90:415-7.<br />22. Bunnag D, Kanda T, Karbwang J, Thimasarn K, Pungpak S, Harinasuta T. Two doses of artemether/mefloquine or artesunate/mefloquine combination for multidrug resistant falciparum malaria. Southeast Asian J Trop Med Public Health. 1997;28:727-30.<br />23. Thimasarn K, Sirichaisinthop J, Chanyakhun P, Palananth C, Rooney W. A comparative study of artesunate and artemether in combination with mefloquine on multidrug resistant falciparum malaria in eastern Thailand. Southeast Asian J Trop Med Public Health. 1997;28:465-71.<br />24. Price RN, Nosten F, Luxemburger C, van Vugt M, Phaipun L, Chongsuphajaisiddhi T, et al. Artesunate/mefloquine treatment of multi-drug resistant falciparum malaria. Trans R Soc Trop Med Hyg. 1997;91:574-7.<br />25. Price R, Luxemburger C, van Vugt M, Nosten F, Kham A, Simpson J, et al. Artesunate and mefloquine in the treatment of uncomplicated multidrug-resistant hyperparasitaemic falciparum malaria. Trans R Soc Trop Med Hyg. 1998;92:207-11.<br />26. van Vugt M, Brockman A, Gemperli B, Luxemburger C, Gathmann I, Royce C, et al. Randomized comparison of artemether-benflumetol and artesunate-mefloquine in treatment of multidrug-resistant falciparum malaria. Antimicrob Agents Chemother. 1998;42:135-9.<br />27. Massougbodji A, Kone M, Kinde-Gazard D, Same-Ekobo A, Cambon N, Mueller EA. A randomized, double-blind study on the efficacy and safety of a practical three-day regimen with artesunate and mefloquine for the treatment of uncomplicated Plasmodium falciparum malaria in Africa. Trans R Soc Trop Med Hyg. 2002;96:655-9.<br />28. Marquiño W, Huilca M, Calampa C, Falconí E, Cabezas C, Naupay R, et al. Efficacy of mefloquine and a mefloquine-artesunate combination therapy for the treatment of uncomplicated Plasmodium falciparum malaria in the Amazon Basin of Peru. Am J Trop Med Hyg. 2003;68:608-12.<br />29. Smithuis F, Shahmanesh M, Kyaw MK, Savran O, Lwin S, White NJ. Comparison of chloroquine, sulfadoxine/pyrimethamine, mefloquine and mefloquine-artesunate for the treatment of falciparum malaria in Kachin State, North Myanmar. Trop Med Int Health. 2004;9:1184-90.<br />30. Stohrer JM, Dittrich S, Thongpaseuth V, Vanisaveth V, Phetsouvanh R, Phompida S, et al. Therapeutic efficacy of artemether-lumefantrine and artesunate-mefloquine for treatment of uncomplicated Plasmodium falciparum malaria in Luang Namtha Province, Lao People’s Democratic Republic. Trop Med Int Health. 2004;9:1175-83.<br />31. Smithuis F, van der Broek I, Katterman N, Kyaw MK, Brockman A, Lwin S, et al. Optimising operational use of artesunate-mefloquine: a randomized comparison of four treatment regimens. Trans R Soc Trop Med Hyg. 2004;98:182-92.<br />32. Avila JC, Villaroel R, Marquiño W, Zegarra J, Mollinedo R, Ruebush TK. Efficacy of mefloquine and mefloquine-artesunate for the treatment of uncomplicated Plasmodium falciparum malaria in the Amazon region of Bolivia. Trop Med Int Health. 2004;9:217-21.<br />33. van den Broek IV, Maung UA, Peters A, Liem L, Kamal M, Rahman M, et al. Efficacy of chloroquine+sulfadoxine-pyrimethamine, mefloquine+artesunate and artemether +lumefantrine combination therapies to treat Plasmodium falciparum malaria in the Chittagong Hill Tracts, Bangladesh. Trans R Soc Trop Med Hyg. 2005;99:727-35<br />34. Hutagalung R, Paiphun L, Ashley EA, McGready R, Brockman A, Thwai KL, et al. A randomized trial of artemether-lumefantrine versus mefloquine-artesunate for the treatment of uncomplicated multi-drug resistant Plasmodium falciparum on the western border of Thailand. Malar J. 2005;4:46.<br />35. Tangpukdee N, Krudsood S, Thanachartwet W, Chalermrut K, Pengruksa C, Srivilairit S, et al. An open randomized clinical trial of Artekin vs. artesunate-mefloquine in the treatment of acute uncomplicated falciparum malaria. Southeast Asian J Trop Med Public Health. 2005;36:1085-91.<br />36. Campbell P, Baruah S, Narain K, Rogers C. A randomized trial comparing the efficacy of four treatment regimens for uncomplicated falciparum malaria in Assam state, India. Trans R Soc Trop Med Hyg. 2006; 100: 108-18.<br />37. Vijaykadga S, Rojanawatsirivej C, Cholpol S, Phoungmanee D, Nakavej A, Wongsrichanalai C. In vivo sensitivity monitoring of mefloquine monotherapy and artesunate-mefloquine combinations for the treatment of uncomplicated falciparum malaria in Thailand in 2003. Trop Med Int Health. 2006;11:211-9.<br />38. Smithuis F, Kyaw MK, Phe O, Aye KZ, Htet L, Barends M, et al. Efficacy and effectiveness of dihydroartemisinin-piperaquine versus artesunate-mefloquine in falciparum malaria: an open-label randomized comparison. Lancet. 2006;367:2075-85.<br />39. Denis MB, Tsuyuoka R, Poravuth Y, Narann TS, Seila S, Lim C, et al. Surveillance of the efficacy of artesunate and mefloquine combination for the treatment of uncomplicated falciparum malaria in Cambodia. Trop Med Int Health. 2006;11:1360-6.<br />40. Faye B, Ndiaye JL, Ndiaye D, Dieng Y, Faye O, Gaye O. Efficacy and tolerability of four antimalarial combinations in the treatment of uncomplicated Plasmodium falciparum malaria in Senegal. Malar J. 2007;6:80.<br />41. Bhatt KM, Samia BM, Bhatt SM, Wasunna KM. Efficacy and safety of an artesunate/mefloquine combination (artequin) in the treatment of uncomplicated P. falciparum malaria in Kenya. East Afr Med J. 2006;83:236-42.<br />42. RAVREDA-AMI. Antimalarial drug efficacy studies 2002-2005. Fecha de consulta: septiembre de 2008. Disponible en: <a href="http://www.paho.org/spanish/AD/DPC/CD/ravreda-ami-areas.htm">http://www.paho.org/spanish/AD/DPC/CD/ravreda-ami-areas.htm</a><br />43. Giraldo C, Blair S. Mefloquina: revisión de tema. IATREIA. 2003;16:19-31.<br />44. Berninger E, Karlsson K, Alvan G. Quinine reduces the dynamic range of the human auditory system. Acta Otolaryngol. 1998;118:46-51.<br />45. Tange RA, Dreschler WA, Claessen FA, Perenboom RM. Ototoxic reactions of quinine in healthy persons and patients with Plasmodium falciparum infection. Auris Nasus Larynx. 1997;24:131-6.<br />46. Simoes Da Silva MV. Estudio de los efectos ototóxicos en 725 pacientes tratados con antimaláricos en el Hospital Central de Maputo (Mozambique) (tesis). Barcelona: Universidad Autónoma de Barcelona; 2004.<br />47. Chotivanich K, Sattabongkot J, Udomsangpetch R, Looareesuwan S, Day NP, Coleman RE, et al. Transmission-blocking activities of quinine, primaquine, and artesunate. Antimicrob Agents Chemother. 2006;50:1927-30.<br />48. Davis ME, Karunajeewa HA, llet KF. Artemisinin-based combination therapies for uncomplicated malaria. Med J Aust. 2005;182:181-5.<br />49. Shekalaghe S, Drakeley C, Gosling R, Ndaro A, van Meegeren M, Enevold A, et al. Primaquine clears submicroscopic Plasmodium falciparum gametocytes that persist after treatment with sulphadoxine-pyrimethamine and artesunate. PloS ONE. 2007;2:e1023. Doi:10.1371/journal.-pone.0001023<br />50.Pukrittayakamee S, Chotivanich K, Chantra A, Clemens R, Looareesuwan S, White NJ. Activities of artesunate and primaquine against asexual- and sexual-stage parasites in falciparum malaria. Antimicrob Agents Chemother. 2004;48:1329-34.
oai:oai.revistabiomedica.org:article/33
2009-12-18T16:31:13Z
biomedica:ACTU
Danger signs in the malaria patient
Signos de peligro en el paciente con malaria
Tobón, Alberto
malaria
paludismo
signos y síntomas
medicina clínica
examen físico
diagnóstico
malaria
signs and symptoms
clinical medicine
physical examination
diagnosis
Danger signs are clinical indicators of severity and are useful to predict complications or death. In the malaria patient, clinical or parasitological signs can be easily be recognized during the acute phase of the illness that indicate serious complications. Danger signs include neurological change, abnormal breathing pattern, persistent vomiting and diarrhea, jaundice, bleeding, dark urine, delayed capillary refill, intense pallor, hyperpyrexia, hyperparasitemia and schizontemia. Timely recognition of these signs can lead to a decrease in cases with complications and deaths.
Los signos de peligro son hallazgos clínicos que indican gravedad o que tienen utilidad para el pronóstico de complicación o muerte. En el paciente con malaria, o paludismo, se presentan signos clínicos o parasitológicos que pueden reconocerse fácilmente durante la fase aguda de la enfermedad y son indicadores del inicio de una complicación. Entre los signos de peligro que puede presentar el paciente con malaria se incluyen cambios neurológicos, alteraciones del patrón respiratorio, vómito y diarrea persistentes, ictericia, sangrados, orina oscura, llenado capilar lento, palidez intensa, hiperpirexia, hiperparasitemia y esquizontemia. Su reconocimiento oportuno contribuirá a la disminución de complicaciones y muertes.
Instituto Nacional de Salud
2009-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/33
10.7705/biomedica.v29i2.33
Biomedica; Vol. 29 No. 2 (2009); 320-329
Biomédica; Vol. 29 Núm. 2 (2009); 320-329
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/33/34
https://revistabiomedica.org/index.php/biomedica/article/view/33/325
/*ref*/Tobón A, Piñeros J, Blair S, Carmona J. Clínica de la malaria complicada debida a P. falciparum. Estudio de casos y controles en Tumaco y Turbo (Colombia). Iatreia. 2006;19:339-55.<br />2. Idro R, Bitarakwate E, Tumwesigire S, John CC. Clinical manifestations of severe malaria in the highlands of southwestern Uganda. Am J Trop Med Hyg. 2005;72:561-7.<br />3. Organización Mundial de la Salud, Organización Panamericana de la Salud. Evaluación de la eficacia terapéutica de los medicamentos para el tratamiento del paludismo por Plasmodium falciparum sin complicaciones en las Américas. Documento OPS/HCP/HCT/113/98. Washington, D.C.: OPS; 1998.<br />4. World Health Organization. A manual for community health workers. Geneva; World Health Organization; 1996. p. 46.<br />5. World Health Organization. Integrated management of childhood illness: conclusions. WHO Division of Child Health and Development. Bull World Health Org. 1997;75(Suppl.1):119-28.<br />6. World Health Organization. Severe falciparum malaria. World Health Organization, Communicable Diseases Cluster. Trans R Soc Trop Med Hyg. 2000;94(Suppl.1):S1-90.<br />7. Baird JK. Neglect of Plasmodium vivax malaria. Trends Parasitol. 2007;23:533-9.<br />8. Price L, Planche T, Rayner C, Krishna S. Acute respiratory distress syndrome in Plasmodium vivax malaria: case report and review of the literature. Trans R Soc Trop Med Hyg. 2007;101:655-9.<br />9. Padilla JC, Piñeros JG. Situación de la malaria en el Pacífico nariñense durante el año 2001. Inf Quinc Epidemiol Nac. 2001;6:269-73.<br />10. González L, Guzmán M, Carmona J, Lopera T, Blair S. Características clínico-epidemiológicas de 291 pacientes hospitalizados por malaria en Medellín (Colombia). Acta Med Colomb. 2000;25:163-7.<br />11. Tobón A, Giraldo C, Piñeros J, Arboleda M, Blair S, Carmona J. Epidemiología de la malaria falciparum complicada: estudio de casos y controles en Tumaco y Turbo, Colombia, 2003. Rev Bras Epidemiol. 2006;9:283-96.<br />12. Ministerio de Salud de Colombia, Grupo de Malaria Universidad de Antioquia, CIDEIM, Instituto Nacional de Salud, OPS. Manual de operaciones de la red de farmacovigilancia en malaria en Colombia. Evaluación in vivo. Buenaventura (Colombia). Bogotá: Ministerio de Salud de Colombia; Grupo de Malaria, Universidad de Antioquia; CIDEIM; Instituto Nacional de Salud; OPS; 2002. p. 32.<br />13. Bouchaud O. Diagnosis and management of imported malaria. Rev Prat. 2005;55:863-74.<br />14. Makani J, Matuja W, Liyombo E, Snow RW, Marsh K, Warrell DA. Admission diagnosis of cerebral malaria in adults in an endemic area of Tanzania: implications and clinical description. QJM. 2003;96:355-62.<br />15. Newton CR, Hien TT, White N. Cerebral malaria. J Neurol Neurosurg Psychiatry. 2000;69:433-41.<br />16. Anstey NM, Jacups SP, Cain T, Pearson T, Ziesing PJ, Fisher DA, et al. Pulmonary manifestations of uncomplicated falciparum and vivax malaria: cough, small airways obstruction, impaired gas transfer, and increased pulmonary phagocytic activity. J Infect Dis. 2002;185:1326-34.<br />17. Giraldo C, Blair S, Tobón A. Complicaciones pulmonares en malaria. Infectio. 2004;8:279-91<br />18. English M, Waruiru C, Amukoye E, Murphy S, Crawley J, Mwangi I, et al. Deep breathing in children with severe malaria: indicator of metabolic acidosis and poor outcome. Am J Trop Med Hyg. 1996;55:521-4.<br />19. Brandts C, Ndjavé M, Graninger W, Kremsner P. Effect of paracetamol on parasite clearance time in malaria. Lancet. 1997;350:704-9.<br />20. Seoh JY, Khan M, Park SH, Park HK, Shin MH, Ha EH, et al. Serum cytokine profiles in patients with Plasmodium vivax malaria: a comparison between those who presented with and without hyperpyrexia. Am J Trop Med Hyg. 2003;68:102-6.<br />21. Eiam-Ong S, Sitprija V. Falciparum malaria and the kidney: a model of inflammation. Am J Kidney Dis. 1998;32:361-75.<br />22. Peres Bota D, Lopes Ferreira F, Melot C, Vincent JL. Body temperature alterations in the critically ill. Intensive Care Med. 2004;30:811-6.<br />23. Idro R, Karamagi C, Tumwine J. Immediate outcome and prognostic factors for cerebral malaria among children admitted to Mulago Hospital, Uganda. Ann Trop Paediatr. 2004;24:17-24.<br />24. Popov AF. Algid malaria. Med Parazitol (Mosk). 2005;1:10-2.<br />25. Ustianowski A, Schwab U, Pasvol G. Case report: severe acute symptomatic hyponatraemia in falciparum malaria. Trans R Soc Trop Med Hyg. 2002;96:647-8.<br />26. Sasi P, English M, Berkley J, Lowe B, Shebe M, Mwakesi R, et al. Characterization of metabolic acidosis in Kenyan children admitted to hospital for acute non-surgical conditions. Trans R Soc Trop Med Hyg. 2006;100:401-9.<br />27. Molyneux ME, Looareesuwan S, Menzies IS, Grainger SL, Phillips RE, Wattanagoon Y, et al. Reduced hepatic blood flow and intestinal malabsorption in severe falciparum malaria. Am J Trop Med Hyg. 1989;40:470-6.<br />28. Reisinger EC, Fritzsche C, Krause R, Krejs GJ. Diarrhea caused by primarily non-gastrointestinal infections. Nat Clin Pract Gastroenterol Hepatol. 2005;2:216-22.<br />29. Planche T, Onanga M, Schwenk A, Dzeing A, Borrmann S, Faucher JF, et al. Assessment of volume depletion in children with malaria. PLoS Med. 2004;1:56-63.<br />30. Maitland K, Levin M, English M, Mithwani S, Peshu N, Marsh K, et al. Severe P. falciparum malaria in Kenyan children: evidence for hypovolaemia. QJM. 2003;96:427-34.<br />31. Gorelick MH, Shaw KN, Baker MD. Effect of ambient temperature on capillary refill in healthy children. Pediatrics. 1993;92:699-702.<br />32. Schriger DL, Baraff L. Defining normal capillary refill: variation with age, sex, and temperature. Ann Emerg Med. 1988;17:932-5.<br />33. Pamba A, Maitland K. Capillary refill: prognostic value in Kenyan children. Arch Dis Child. 2004;89:950-5.<br />34. Kochar DK, Singh P, Agarwal P, Kochar SK, Pokharna R, Sareen PK. Malarial hepatitis. J Assoc Physicians India. 2003;51:1069-72.<br />35. Nacher M, Treeprasertsuk S, Singhasivanon P, Silachamroon U, Vannaphan S, Gay F, et al. Association of hepatomegaly and jaundice with acute renal failure but not with cerebral malaria in severe falciparum malaria in Thailand. Am J Trop Med Hyg. 2001;65:828-33.<br />36. Mishra SK, Mohanty S, Satpathy SK, Mohapatra DN. Cerebral malaria in adults –a description of 526 cases admitted to Ispat General Hospital in Rourkela, India. Ann Trop Med Parasitol. 2007;101:187-93.<br />37. Campuzano G, Arbeláez M. Uroanálisis: más que un exa-men de rutina. Medicina y Laboratorio. 2006;12:511-56.<br />38. Giraldo C, Blair S. Complicaciones renales en malaria. Acta Med Colomb. 2004 29:328-36.<br />39. O’Donnell A, Weatherall DJ, Taylor AM, Reeder JC, Allen SJ. Muscle cell injury, haemolysis and dark urine in children with falciparum malaria in Papua New Guinea. Trans R Soc Trop Med Hyg. 2006;100:817-25.<br />40 Muhe L, Oljira B, Degefu H, Jaffar S, Weber MW. Evaluation of clinical pallor in the identification and treatment of children with moderate and severe anaemia. Trop Med Int Health. 2000;5:805-10.<br />41 Luby SP, Kazembe PN, Redd SC, Ziba C, Nwanyanwu OC, Hightower AW, et al. Using clinical signs to diagnose anaemia in African children. Bull World Health Org. 1995;73:477-82.<br />42 Arboleda M, Campuzano M, Restrepo BN, Cartagena G. El comportamiento clínico del dengue en pacientes hospitalizados en el Hospital Antonio Roldán Betancur, Apartado, Antioquia, 2000. Biomédica. 2006;26:286-94.<br />43 Gear JH. The hemorrhagic fevers of Southern Africa with special reference to studies in the South African Institute for Medical Research. Yale J Biol Med. 1982;55:207-12.<br />44 Brogan PA, Raffles A. The management of fever and petechiae: making sense of rash decisions. Arch Dis Child. 2000;83:506-7.<br />45 Ministerio de Salud. Guía de atención de la malaria. Norma técnica 31/03/2000. Diario oficial 43.956. Bogotá D.C.: Ministerio de Salud; 2000.<br />46 World Health Organization. Guidelines for the treatment of malaria. Documento WHO/HTM/MAL/2006.1108. Geneva: WHO; 2006. p. 266.<br />47 World Health Organization. Management of severe mala-ria. A practical handbook. Geneva: WHO; 2000. p.78.
oai:oai.revistabiomedica.org:article/34
2009-12-19T12:04:33Z
biomedica:EDIT
Malformaciones y anomalías congénitas: impacto y futuro
Bernal, Jaime
Zarante, Ignacio
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/34
10.7705/biomedica.v29i1.34
Biomedica; Vol. 29 No. 1 (2009); 7-8
Biomédica; Vol. 29 Núm. 1 (2009); 7-8
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/34/35
https://revistabiomedica.org/index.php/biomedica/article/view/34/326
/*ref*/Bernal JE, Umaña A, Ortega G. The contribution of genetic disease to paediatric mortality in a university hospital in Bogota. J Biosoc Sci. 1983;15:465-71.<br />2. DANE. Estadísticas vitales. Fecha de consulta: 21 de enero de 2009. Disponible en: <a href="http://www.dane.gov.co/index.php?option=com_content&task=category&sectionid=16&id=36&Itemid=148">http://www.dane.gov.co/index.php?option=com_content&task=category&sectionid=16&id=36&Itemid=148</a>.<br />3. Christianson A, Howson CP, Modell B. The March of Dimes global report on birth defects, The hidden toll of dying and disabled children. White Plains, New York: March of Dimes Birth Defects Foundation; 2006. [Fecha de consulta: 3 de febrero de 2009. Disponible en: <a href="http://www.marchofdimes.com/871_18587.asp">http://www.marchofdimes.com/871_18587.asp</a><br />4. Castilla EE, Orioli IM. ECLAMC: the Latin-American collaborative study of congenital malformations. Community Genet. 2004;7:76-94.<br />5. Orioli IM, Mastroiacovo P, López-Camelo JS, Saldarriaga W, Isaza C, Aiello H, et al. Clusters of sirenomelia in South America. Birth Defects Res A Clin Mol Teratol. 2009:85;112-8.<br />6. Castilla EE, Mastroiacovo P, López-Camelo JS, Saldarriaga W, Isaza C, Orioli IM. Sirenomelia and cyclopia cluster in Cali, Colombia. Am J Med Genet A. 2008;146A:2626-36.<br />7. Baltaxe E, Zarante I. Prevalence of congenital heart disease in 44,985 newborns in Colombia. Arch Cardiol Mex. 2006;76:263-8.<br />8. Calderón S, Zarante I. Congenital urological anomalies: epidemiological description and associated risk factors in Colombia 2001-2004. Arch Esp Urol. 2006;59:7-14.<br />9. Fernández N, Zarante I. Prevalencia y escala pronóstico para malformaciones congénitas en Colombia: la responsabilidad de pediatras y neonatólogos. Registro de 54.397 nacimientos. Revista de la Sociedad Colombiana de Neonatología UCIN. 2007;7:28-32.<br />10. Gómez, JC, Fernández N, Zarante I. Detección de anomalías congénitas en 12.760 nacimientos de tres hospitales en la ciudad de Bogotá, Colombia 2004-2005 mediante ecografía prenatal. Rev Colomb Obstet Ginecol. 2007;58:194-201.<br />11. Bernal JE, Suárez F. La carga de la enfermedad genética en Colombia, 1996-2025. Univérsitas Médica. 2008;49:12-28.
oai:oai.revistabiomedica.org:article/35
2009-12-19T12:04:33Z
biomedica:IMAG
Mucosal complication of cutaneous leishmaniasis
Complicación mucosa de la leishmaniasis cutánea
Zea, Diego Fernando
Prager, Martín
Figueroa, Roger Adrian
Miranda, María Consuelo
leishmaniasis cutánea
leishmaniasis mucocutánea
leishmaniasis/diagnóstico
leishmaniasis/terapia
reacción en cadena de la polimerasa
leishmaniasis
cutaneous
mucocutaneous
leishmaniasis/diagnosis
leishmaniasis/therapy
polymerase chain reaction
A 74-year-old man from the rural area of Caicedonia, Valle del Cauca Province, was diagnosed with uncontrolled hypertension, stage IV chronic renal failure and severe anemia.Fifteen years earlier, while living in Guaviare Province, he was diagnosed with leishmaniasis—with lesions located on the right upper and lower eyelids, left auricle and limbs. At that time, he received an incomplete treatment with antimonials. The patient had experienced 8 years of progressive mucosal lesions located in the upper lip, nasal mucosa and right upper and lower eyelids (figure 1). A histopathological diagnosis of leishmaniasis was made and confirmed by polymerase chain reaction (figure 2).Treatment with antimonials (Glucantime®) was contraindicated due to the patient’s comorbidities. Inpatient supervised treatment with miltefosine (Impávido ® 50 mg capsules) was initiated according to the national guidelines of 1.8 mg/kg/day for 28 days. Clinical follow up and routine laboratory tests (creatinine, BUN, liver function tests and complete blood counts) were done during and after treatment; no complications were reported. Medical follow up was continued until the eighth week post treatment; at this time, he presented clinical improvement of the lesions (figure 3).Internal medicine, ophthalmology, and plastic surgery consultations were provided for subsequent management of the pathology.Mucocutaneous leishmaniasis is a serious preventable complication of cutaneous leishmaniasis. This case illustrated a failure in opportune diagnosis and treatment of this disease as a consequence of an inadequate leishmaniasis control program. The case indicated the effectiveness of miltefosine as a therapeutic option in patients for whom antimonial treatment is contraindicated.
Se presenta el caso de un hombre de 74 años procedente del área rural de Caicedonia, Valle del Cauca, con diagnósticos de hipertensión arterial no controlada, insuficiencia renal crónica estadio IV y anemia grave.Tenía antecedentes de leishmaniasis cutánea en los párpados del ojo derecho, el pabellón auricular izquierdo y las extremidades, diagnosticada 15 años atrás en el departamento del Guaviare. Recibió tratamiento incompleto con antimoniales en esa época. Consultó al Centro Internacional de Entrenamiento e Investigaciones Médicas (CIDEIM) por un cuadro progresivo de ocho años de evolución de lesiones mucosas ulceradas en el labio superior, la mucosa nasal y los párpados del ojo derecho (figura 1). Se hizo un diagnóstico histopatológico de leishmaniasis, confirmado mediante reacción en cadena de la polimerasa (figura 2).Debido a las enfermedades concomitantes del paciente, el tratamiento con antimoniales (Glucantime®) estaba contraindicado. Se administró tratamiento supervisado intrahospitalario con miltefosine (Impávido®, cápsulas de 50 mg) a una dosis diaria de 1,8 mg/kg por 28 días, de acuerdo con las guías nacionales. Se realizó control clínico y de laboratorio durante el tratamiento y después de finalizado, sin evidencia de ningún tipo de complicación. El paciente asistió a controles médicos hasta la octava semana después del tratamiento, en los cuales presentó mejoría clínica de las lesiones (figura 3). Se remitió para continuar el manejo complementario por medicina interna, oftalmología y cirugía plástica.La leishmaniasis mucocutánea es una grave complicación evitable de la leishmaniasis cutánea. Este caso muestra fallas en el diagnóstico y tratamiento oportunos y, en general, en el programa de control de esta enfermedad. Por otra parte, el miltefosine surge como una opción terapéutica a los antimoniales para el tratamiento de pacientes en quienes estén contraindicados o presenten alto riesgo de toxicidad.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/35
10.7705/biomedica.v29i1.35
Biomedica; Vol. 29 No. 1 (2009); 9-11
Biomédica; Vol. 29 Núm. 1 (2009); 9-11
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/35/36
https://revistabiomedica.org/index.php/biomedica/article/view/35/327
oai:oai.revistabiomedica.org:article/36
2009-12-19T12:04:33Z
biomedica:CASO
Cutaneous myiasis by Cochliomyia hominivorax (Coquerel) (Díptera Calliphoridae) in Hospital Universidad del Norte, Soledad, Atlántico
Miasis cutánea por Cochliomyia hominivorax (Coquerel) (Díptera: Calliphoridae) en el Hospital Universidad del Norte, Soledad, Atlántico
Romero-Vivas, Claudia M.E.
Castro, Luis Eduardo
Visbal, Lila
Santos, Ana María
Díaz, Esther
miasis
infección por Cochliomyia hominivorax
ivermectina
Colombia
myiasis
screw worm infection
ivermectin
Colombia
Human myiasis is the parasitism of human tissues by fly larvae. Diagnoses are based on clinicalpattern of tissue damage and presence of insect stages. Herein, a case myiasis is described in a seven-year-old female child. She presented with fever associated with abscessed scalp lesions containing exposed larvae. Severe pediculosis was also observed. The patient was hospitalized and treated with clindamycin, gentamicin (for bacterial secondary infections) and ivermectin (treatment for lice) after which the patient showed clinical improvement and was discharged four days later. Since human myiasis can be caused by a number of different species, larvae were collected from the patient and identified as those of Cochliomyia hominivorax (Diptera: Calliphoridae). Because other cases of coinfestation of flies and lice are on record, health workers are to be alerted about the possible pediculosis-myasis risk.
La miasis humana es el parasitismo de órganos y tejidos producido por especies de larvas del orden Díptera.El diagnóstico se realiza con base en hallazgos clínicos y se confirma con estudios entomológicos. Se presenta el caso de una niña de siete años de edad que fue llevada por su padre al servicio de urgencias por presentar fiebre asociada a una lesión abscedada en el cuero cabelludo, con salida espontánea de larvas. Como hallazgo en el examen físico se reportó pediculosis grave. La paciente fue hospitalizada y tratada con clindamicina, gentamicina e ivermectina, y mostró mejoría de sus condiciones clínicas. Se dio alta médica al cuarto día de estancia hospitalaria. Se recolectaron larvas en estadio dos de Cochliomyia hominivorax (Diptera: Calliphoridae) directamente del área lesionada, observándose la asociación miasis-pediculosis; por lo tanto, se alerta a los trabajadores del área de la salud del riesgo potencial que representa la pediculosis para el desarrollo de la miasis.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/36
10.7705/biomedica.v29i1.36
Biomedica; Vol. 29 No. 1 (2009); 12-17
Biomédica; Vol. 29 Núm. 1 (2009); 12-17
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/36/37
/*ref*/Bermúdez SE, Espinosa JD, Cielo AB, Clavel F, Subia J, Medianero E. Incidence of myiasis in Panamá during the eradication of Cochliomyia hominivorax (Coquerel 1858, Diptera: Calliphoridae) (2002-2005). Mem Inst Oswaldo Cruz. 2007;102:675-9.<br />2. Villamizar JR, Sandoval GP. Miasis ótica. Acta de Otorrinolaringología y Cirugía de Cabeza y Cuello. 2000;28:203-6.<br />3. Mariwalla K, Langhan M, Welch KA, Kaplan DH. Cutaneous myiasis associated with scalp psoriasis. J Am Acad Dermatol. 2007;57:s51-2.<br />4. Levi F, Valderrama R, Gonzalo JA. Tratamiento de miasis oral con ivermectina: notificación de tres casos causados por Cochliomyia homninivorax (Coquerel). Rev Fac Odontol Univ Antioquia. 1998;10:41-7.<br />5. Alarcón MA. Miasis uterina. Rev Colomb Obstet Ginecol. 1988;39:130-1.<br />6. Duque CS, Marrugo G, Valderrama R. Otolaryngic manifestations of myiasis. Ear Nose Throat J. 1990;69:619-22.<br />7. Vega-Lopez F, Chopra S. Manson’s tropical diseases. 21st ed. London: Saunders; 2003. p. 374-5.<br />8. Phillips PL, Welch JB, Kramer M. Seasonal and spatial distributions of adults screwworms (Diptera: Calliphoridae) in the Panama Canal Area, Republic of Panama. J Med Entomol. 2004;41:121-9.<br />9. Vargas M, Hall MJ. Manual para la mosca del gusano barrenador del ganado, Cochliomyia hominivorax (Coquerel). Volumen 1. Roma: Organización de las Naciones Unidas para la Agricultura y la Alimentación; 1993. p. 5-6.<br />10. Hendrix CM, King-Jackson DA, Wilson PM, Blagburn BL, Kindsay DS. Furunculoid myiasis in a dog caused by Cordylobia anthropophaga. J Am Vet Med Assoc. 1995;207:1187-9.<br />11. Loredo A, Trejo J, Castilla L. Children injured: abuse or accident? Diagnosis through indicators. Bol Med Hosp Infant Mex. 2003;60:368-79.<br />12. Hope FW. On insects and their larvae occasionally found in the human body. Trans R Soc Entomol. 1840;2:256-71.<br />13. Organización de las Naciones Unidas para la Agricultura y la Alimentación. Miasis cutáneas, 2006. [Fecha de consulta: 29 de febrero de 2008]. Disponible en: <a href="http://www.rlc.fao.org/es/prioridades/transfron/miasis/cutaneas/default.htm">http://www.rlc.fao.org/es/prioridades/transfron/miasis/cutaneas/default.htm</a><br />14. Moissant de Román E, García ME, Quijada J, Simoes D, Marcial T. Miasis cutánea humana. Un caso clínico. Kasmera. 2004;32:12-5.<br />15. Duro EA, Marilvis JC, Mulieri PR. Umbilical myiasis in a human newborn. J Perinatol. 2007;27:250-1.<br />16. Powers NR, Yorgensen ML, Rumm PD, Souffront W. Myasis in humans: an overview and report of two cases in the Republic of Panama. Mil Med. 1996;161:495-7.<br />17. Osorio J, Moncada L, Molano A, Valderrama S, Gualtero S, Franco-Paredes C. Role of the ivermectin in the treatment of severe orbital myiasis due to Cochliomyia hominivorax. Clin Infec Dis. 2006;3:57-9.<br />18. Visciarelli EC, García SH, Salomón C, Cofre C, Costamanga S. Un caso de miasis humana por Cochliomyia hominivorax (Díptera: Calliphoridae) asociado a pediculosis en Mendoza, Argentina. Parasitol Latinoam. 2003;58:166-8.<br />19. Marquez AT, Mattos Mda S, Nascimento SB. Miases associadas com alguns factores sócio-econômicos em cinco áreas urbanas do Estado do Rio de Janeiro. Rev Soc Bras Med Trop. 2007;40:175-80.<br />20. Linardi PM, De Maria M, Botelho JR, Cunha HC, Ferreira J . Pediculose capitis: prevalência em escolares da rede municipal pública de Belo Horizonte, Minas Gerais, Brasil. Mem Inst Oswaldo Cruz. 1989;84:327-31.<br />21. Dourmishev AL, Dourmishev LA, Schwartz R. Ivermectin: Pharmacology and application in dermatology. Int J Dermatol. 2005;44:981-8.
oai:oai.revistabiomedica.org:article/37
2009-12-19T12:04:33Z
biomedica:CASO
Persistent type 2 lepra reaction and clofazimine-induced lethal enteropaty
Eritema nudoso leproso persistente y enteropatía letal por clofazimina
Rodríguez, Gerzaín
Pinto, Rafael
López, Fernando
Gómez, Yenny
lepra lepromatosa/complicaciones
quimioterapia
eritema nudoso
clofazimina
agentes antibacterianos/efectos adversos
abdomen agudo
lepromatous leprosy/complications
drug therapy
erythema nodosum
clofazimine
anti-bacterial agents/adverse effects
abdomen
acute
Introduction. Clofazimine enterophathy is a serious complication of clofazimine when used at high doses for treatment of type 2 lepra or or erythema nodosum leprosum.Objective. A woman is presented who had a delayed diagnosis of leprosy, persistent type 2 lepra reaction and lethal clofazimine enteropathy.Materials and methods. A 31-year-old woman presented leprosy symptoms over a 16-year period without medical diagnosis of her disease. During this period, type 2 lepra episodes occurred, but were not accurately diagnosed. These episodes became more severe during her second pregnancy. The patient and her family were interviewed, and her clinical history reviewed.Results. After twelve years of medical consults, lepromatous leprosy was diagnosed, based on perforation of her nasal septum, with a bacterial index of 5. Her husband and a 12-year-old daughter have leprosy symptoms. During multidrug therapy, she presented with repeated type 2 lepra reaction episodes for which she received daily clofazimine 400 mg doses. Two months after this treatment, severe and frequent episodes of intense abdominal pain began to occur. These persisted for more than a year and were managed with in-hospital administration of several classes of painkillers and antispasmodic medication, including morphine. She also presented with sporadic diarrhea, constipation, nausea, weight loss and mesenteric adenopathies. She died finally due to this intestinal condition. No autopsy was performed.Conclusions The patient’s clinical presentation suggested a clofazimine-induced lethal enteropathy, a complication not previously seen in Colombia. This connection was not recognized by the medical officers that treated the patient.
Introducción. La enteropatía por clofazimina es una complicación grave de este fármaco, cuando se usa a dosis altas para la reacción leprosa tipo 2 y otras enfermedades.Objetivo. Presentar una mujer de 31 años con síntomas de lepra, incluidos episodios de eritema nudoso leproso, agravados durante el embarazo, sin diagnóstico médico preciso. Relatar la evolución de su enteropatía letal por clofazimina.Materiales y métodos. Entrevista con la paciente y sus familiares, revisión de la historia clínica y de la literatura pertinente.Resultados. La paciente presentó lesiones cutáneas anestésicas y varios episodios de eritema nudoso, agravados durante sus embarazos. Luego de epistaxis repetidas y perforación del tabique nasal, se diagnóstico lepra lepromatosa, 12 años después de numerosas consultas médicas. Su esposo y su hija de 12 años presentaron signos de lepra para la cual se trataron.La paciente tuvo episodios de reacción tipo 2 durante la poliquimioterapia, para los cuales recibió 400 mg diarios de clofazimina. A los dos meses de este tratamiento comenzó a presentar dolor abdominal persistente durante más de un año, muy serio y episódicamente exacerbado, manejado con analgésicos y antiespasmódicos, incluida la morfina. Tuvo, además, diarrea, estreñimiento, náuseas, pérdida de peso y adenopatías mesentéricas. Falleció sin diagnóstico de su afección intestinal. No se hizo autopsia.Conclusiones. La clínica final de la paciente sugiere que se trata de un caso de enteropatía letal por clofazimina, una complicación que no se había reconocido previamente en nuestros pacientes. Es necesario aumentar el conocimiento de la lepra entre los médicos.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/37
10.7705/biomedica.v29i1.37
Biomedica; Vol. 29 No. 1 (2009); 18-24
Biomédica; Vol. 29 Núm. 1 (2009); 18-24
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/37/38
https://revistabiomedica.org/index.php/biomedica/article/view/37/332
/*ref*/<br />1. Arrieta R, Garcés MT, Ordóñez N, Fadul S, Pinto R, Rodríguez G. Lepra familiar. Biomédica. 2001;21:248-55.<br />2. Oskam l, Bakker MI. Report of the workshop on the use of chemoprophylaxis in the control of leprosy held in Amsterdam, the Netherlands on 14 December 2006. Lepr Rev. 2007;78:173-85.<br />3. Smith WC, Smith CM, Cree IA, Jadhav RS, Macdonald M, Edward VK, et al. An approach to understanding the transmission of Mycobacterium leprosy using molecular and immunological methods: results of the MILEP2 study. Int J Lepr Other Mycobact Dis. 2004;72:269-77.<br />4. Rodríguez G, Pinto R. Mujer joven con episodios de epistaxis, fiebre y nódulos cutáneos, agravados durante su segundo embarazo. Cuadernos de Medicina en Investigación y Salud. 2007;1:60-75.<br />5. Mansfield RE. Tissue concentrations of clofazimine (B663) in man. Am J Trop Med Hyg. 1974;23:1116-9.<br />6. Desikan KV, Balakrishnan S. Tissue levels of clofazimina in a case of leprosy. Lepr Rev. 1976;47:107-13.<br />7. Desikan KV, Ramanujam K, Ramu G, Balakrishnan S. Autopsy findings in a case of lepromatous leprosy treated with clofazimina. Lepr Rev. 1975;46:181-9.<br />8. World Health Organization. The final push towards elimination of leprosy: strategic plan 2000-2005. Geneva: WHO; 2000.<br />9. Arbiser Jl, Moschella SL. Clofazimine: A review of its medical uses and mechanisms of action. J Am Acad Dermatol. 1995;32:247-7.<br />10. Hastings RC. Leprosy. New York: Churchill Livinstone; 1985.<br />11. Meyers WM. Leprosy. Dermatol Clin. 1992;10:73-96.<br />12. Atkinson AJ Jr, Sheagren JN, Rubio JB, Knight V. Evaluation of B.663 in human leprosy. Int J Lepr. 1967;35:119-27.<br />13. Plock H, Lieker DL. A long term trial with cofazimine in reactive lepromatous leprosy. Lep Rev. 1976;47:25-34.<br />14. Jopling WJ. Complications of treatment with clofazimine (lamprene: B663). Lep Rev. 1976;47:1-3.<br />15. Parizhskaya M, Youssef NN, Di Lorenzo C, Goyal RK. Clofazimine enteropathy in a pediatric bone marrow transplant recipient. J Pediatr. 2001;138: 574-6.<br />16. Kumar B, Kaur S, Kaur I, Gangowar DN. More about clofazimine- 3 years experience and review of literature. Indian J Lepr. 1987;59:63-74.<br />17. Deps PD, Nasser G, Guerra P, Simm M, Birshner RC, Rodrigues L. Adverse effects from multidrug therapy in Leprosy. A Brazilian study. Lepr Rev. 2007;78:216-22.<br />18. Venencie YP, Cortez A, Orieux G, Jost JL, Chomette G, Puissant A. Clofazimine enteropathy. J Am Acad Dermatol. 1986;15:290-1.<br />19. Sukpanichnant S, Hargrove NS, Kachintorn U, Manatsathit S, Chanchairujira T, Siritanararatkul N, et al. Clofazimine-induce crystal-storing histiocytosis producing chronic abdominal pain in a leprosy patient. Am J Surg Pathol. 2000;24:19-35.<br />20. Pais AV, Pereira S, Garg I, Stephen J, Antony M, Inchara YK. Intra-abdominal, crystal-storing histiocytosis due to clofazimine in a patient with lepromatous leprosy and concurrent carcinoma of the colon. Lepr Rev. 2004;75:171-6.<br />21. Mason GH, Ellis-Pegler B, Arthur JF. Clofazimine and eosinophilic enteritis. Lepr Rev. 1977;48:175-80.<br />22. Belaube P, Devaux J, Pizzi M, Boutboul R, Privat Y. Small bowell deposition of crystals associated with the use of clofazimine (Lamprene®) in the treatment of prurigo nodularis. Int J Lepr Other Mycobact Dis. 1983;51:328-30.<br />23. McDougall AC, Horsfall WR, Hede JE, Chaplin AJ. Splenic infarction and tissue accumulation of crystals associated with the use of clofazimine (Lamprene; B663) in the treatment of pyoderma gangrenosum. Br J Dermatol. 1980;102:227-30.<br />24. Bryceson A. Unnecesary laparotomy for abdominal pain and fever due to clofazimine. Lepr Rev. 1979;50:258-9.<br />25. de Bergeyck E, Janssens PG, de Muynck A. Radio-logical abnormalities of the ileum associated with the use of clofazimine (Lamprene; B663) in the treatment of skin ulceration due to Mycobacterium ulcerans. Lepr Rev. 1980;51:221-8.<br />26. Ramu G, Iyer GG. Side effects of clofazimine therapy. Lepr India. 1976;48 (4 Suppl):722-31.<br />27. Harvey RF, Harman RR, Black C, Read AD, Baddeley H, Davies J, et al. Abdominal pain and malabsorption due to tissue deposition of clofazamine (Lamprene) crystals (Abstract). Br J Dermatol. 1977;97:19.<br />28. Hameed A, Beach FX, Kennedy RH, Barry RE. A case of clofazimine enteropathy. Int J Clin Pract. 1998;52:439-40.<br />29. Rodríguez G, Pinto R. La lepra. Imágenes y conceptos. Medellín: Universidad de Antioquia; 2007.
oai:oai.revistabiomedica.org:article/38
2009-12-19T12:04:34Z
biomedica:CASO
Four cases of Jarcho-Levin’s syndrome in the province of Antioquia, Colombia
Reporte de cuatro casos de pacientes con síndrome de Jarcho-Levin en el departamento de Antioquia, Colombia
Montoya, Jorge Hernán
Morales, Olga Lucía
patrón de herencia
frecuencia de los genes
anomalías congénitas
columna vertebral
costillas
hipertensión portal
inheritance patterns
gene frequency
congenital abnormalities
spine
ribs
hypertension
portal
Jarcho-Levin’s syndrome is a skeletal dysplasia with changes in the morphogenesis and costal vertebrae segmentation. It is manifested by hemivertebrae, fused vertebral bodies, absent vertebrae or fused ribs. This entity has also been called spondylo-costal or spondylo-thoracic dysplasia-dysostosis.This paper presents four cases evaluated at the Hospital University San Vicente de Paúl, Medellín, Colombia. Three had family origins in southwestern Antioquia and one in Medellin, indicating the possibility of a predisposing genetic allele with elevated frequency in this population.The clinical and radiological manifestations were described, a well as the most notable complications, such as restrictive lung disease with permanent oxygen requirement (all 4 patients) and portal hypertension etiology (1 patient). The latter has not been reported previously as a manifestation of this syndrome.
El síndrome de Jarcho-Levin es una displasia esquelética con alteraciones en la morfogénesis vertebral y en la segmentación costal, que se manifiesta con hemivertebras, fusión vertebral o agenesia vertebral, y fusión costal. Esta entidad también se ha denominado displasia-disostosis espóndilo-costal o espóndilo-torácica.En este artículo se presentan cuatro casos evaluados en el Hospital Universitario San Vicente de Paúl, Medellín, Colombia. Tres tienen origen familiar en el suroeste del departamento de Antioquia y uno en Medellín, lo que podría estar relacionado con un alelo con acentuada frecuencia en esta población.En este artículo se describen las características clínicas y radiológicas, y las complicaciones más importantes, entre las cuales podemos citar la presencia de enfermedad pulmonar restrictiva, con necesidad permanente de oxígeno en todos los pacientes y, en uno, hipertensión portal de etiología por esclarecer, lo cual no se ha reportado como manifestación de este síndrome.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/38
10.7705/biomedica.v29i1.38
Biomedica; Vol. 29 No. 1 (2009); 25-32
Biomédica; Vol. 29 Núm. 1 (2009); 25-32
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/38/39
https://revistabiomedica.org/index.php/biomedica/article/view/38/334
/*ref*/<br />1. Jarcho S, Levin PM. Hereditary malformation of the vertebral bodies. Bull Johns Hopkins Hosp. 1938;68:216-26.<br />2. Kulkarni ML, Navaz SR, Vani HN, Manjunath KS, Matani D. Jarcho-Levin syndrome. Indian J Pediatr. 2006;73:245-7.<br />3. Herrera MR, Beltran M. P44.14: Jarcho-Levin syndrome: second and first trimester ultrasound features. Ultrasound Obstet Gynecol. 2007;30:621-2.<br />4. Wong G, Levine D. Jarcho-Levin syndrome: two consecutive pregnancies in a Puerto Rican couple. Ultrasound Obstet Gynecol. 1998;12:70-3.<br />5. Shimizu K, Arai H, Sakamoto T, Sunamori M, Suzuki A. Jarcho-Levin syndrome associated with atrial septal defect and partial anomalous pulmonary venous return: a case report. J Card Surg. 1997;12:198-200.<br />6. Hatakeyama K, Fuse S, Tomita H, Chiba S. Jarcho-levin syndrome associated with a complex congenital heart anomaly. Pediatr Cardiol. 2003;24:86-8.<br />7. Hull AD, James G, Pretorius DH. Detection of Jarcho-Levin syndrome at 12 weeks’ gestation by nuchal translucency screening and three-dimensional ultrasound. Prenat Diagn. 2001;21:390-4.<br />8. Bulman MP, Kusumi K, Frayling TM, McKeown C, Garrett C, Lander ES, et al. Mutations in the human delta homologue, DLL3, cause axial skeletal defects in spondylocostal dysostosis. Nat Genet. 2000;24:438-41.<br />9. Whittock NV, Sparrow DB, Wouters MA, Sillence D, Ellard S, Dunwoodie SL, et al. Mutated MESP2 causes spondylocostal dysostosis in humans. Am J Hum Genet. 2004;74:1249-54.<br />10. Cornier AS, Staehling-Hampton K, Delventhal KM, Saga Y, Caubet JF, Sasaki N, et al. Mutations in the MESP2 gene cause spondylothoracic dysostosis/Jarcho-Levin syndrome. Am J Hum Genet. 2008;82:1334-41.<br />11. Sparrow DB, Chapman G, Wouters MA, Whittock NV, Ellard S, Fatkin D, et al. Mutation of the Lunatic Fringe gene in humans causes spondylocostal dysostosis with a severe vertebral phenotype. Am J Hum Genet. 2006;78:28-37.<br />12. Eliyahu S, Weiner E, Lahav D, Shalev E. Early sonographic diagnosis of Jarcho-Levin syndrome: a prospective screening program in one family. Ultrasound Obstet Gynecol. 1997;9:314-8.<br />13. Kauffmann E, Roman H, Barau G, Dumas H, Laffitte A, Fourmaintraux A, et al. Case report: a prenatal case of Jarcho-Levin syndrome diagnosed during the first trimester of pregnancy. Prenat Diagn. 2003.23:163-5.<br />14. Onay OS, Kinik ST, Otgün Y, Arda IS, Varan B. Jarcho-Levin syndrome presenting with diaphragmatic hernia. Eur J Pediatr Surg. 2008;18:272-4.<br />15. Hurst JA, Firth HV, Smithson S. Skeletal dysplasias. Semin Fetal Neonatal Med. 2005;10:233-41.<br />16. Bannykh SI, Emery SC, Gerber JK, Jones KL, Benirschke K, Masliah E. Aberrant Pax1 and Pax9 expression in Jarcho-Levin syndrome: Report of two Caucasian siblings and literature review. Am J Med Genet. 2003;120:241-6.<br />17. DANE. Resultados censo general 2005. Población censada después de compensada por omisiones de cobertura geográfica y contingencia de transferencia, Andes (Antioquia). (Fecha de consulta: 1 de junio de 2008). Disponible en: <a href="http://www.dane.gov.co/files/censo2005/regiones/antioquia/andes.pdf">http://www.dane.gov.co/files/censo2005/regiones/antioquia/andes.pdf</a>.<br />18. Bravo ML, Valenzuela CY, Arcos-Burgos OM. Polymorphisms and phyletic relationships of the Paisa community from Antioquia (Colombia). Gene Geogr. 1996;10:11-7.
oai:oai.revistabiomedica.org:article/39
2009-12-19T12:04:34Z
biomedica:ENSA
Evidence-based medicine: an epistemological approach
Medicina basada en la evidencia: una aproximación epistemológica
Henao, Daniel Eduardo
Jaimes, Fabián Alberto
medicina basada en evidencia
epidemiología
conocimiento
ciencia
evidence-based medicine
epidemiology
knowledge
science
Evidence-based medicine gathers physician’s experience and the best scientific evidence to make medical decisions. This proposal has been widely promulgated by medical opinion leaders. Despite a large literature supporting this practice, a formal discussion has not been established regarding its epistemological consequences in daily medical work. The main proposal of evidence-based medicine consists of choosing the best medical decision according to the best available results from scientific studies. Herein, the goal was to highlight inappropriate application of the scientific method used by physics to clinical science. The inaccuracy resides in describing health and disease in strictly numeric equivalents that can be homogenized on a continuous scale. Finally, the authors consider each diseased human being as a complex system, unique and particular, and that this being is defined by an historical background as well as current actual context. Therefore, evidence-based medicine possesses certain limitations that must be recognized in order to to provide better health care to patients.
La propuesta de la medicina basada en la evidencia conjuga la experiencia del clínico con el análisis juicioso de los resultados de investigaciones clínicas de excelente calidad metodológica para la toma de decisiones médicas. Esta propuesta ha sido ampliamente divulgada por los líderes de opinión médica. Sin embargo, contrario al gran número de publicaciones que promueven esta práctica, no se evidencia en la literatura médica un espacio de discusión acerca de las implicaciones epistemológicas que ha tenido la implementación de esta práctica en el acontecer cotidiano del acto médico. La propuesta novedosa de la medicina basada en la evidencia consiste en priorizar las decisiones médicas de acuerdo con la disponibilidad del conocimiento como resultado de los estudios científicos.Presentamos en este ensayo algunas reflexiones sobre la inconveniencia de la importación "ciega" del método científico de las ciencias exactas a la ciencia clínica, que es la principal fuente de evidencia para el médico, además de lo inadecuado de definir los estados de salud y enfermedad como continuos numéricos homogenizados por una escala de medición. Finalmente, proponemos que el reconocimiento del ser humano enfermo como sistema complejo, único e irrepetible, definido a su vez por su devenir y su contexto, nos obliga a reconocer que la propuesta de la medicina basada en la evidencia no es universal ni absoluta. Sólo en la medida en que dichas particularidades se tengan en cuenta, estaremos en capacidad de brindar una atención más idónea a nuestros pacientes.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/39
10.7705/biomedica.v29i1.39
Biomedica; Vol. 29 No. 1 (2009); 33-42
Biomédica; Vol. 29 Núm. 1 (2009); 33-42
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/39/40
https://revistabiomedica.org/index.php/biomedica/article/view/39/335
/*ref*/Evidence-Based Medicine Working Group. Evidence-based medicine. A new approach to teaching the practice of medicine. JAMA. 1992;268:2420-5.<br />2. Sackett DL, Rosenberg WM, Gray JA, Haynes RB, Richardson WS. Evidence based medicine: what it is and what it isn’t. BMJ. 1996;312:71-2.<br />3. Marshall T. Evidence-based medicine. Lancet. 1995; 346:1171-2.<br />4. Rosenberg W, Donald A. Evidence based medicine: an approach to clinical problem-solving. BMJ. 1995;310: 1122-6.<br />5. Sackett D. Evidence-based medicine. Lancet. 1995;346:1171.<br />6. Feinstein AR, Horwitz RI. Problems in the “evidence” of “evidence-based medicine”. Am J Med. 1997;103:529-35.<br />7. Evidence-based medicine, in its place. Lancet. 1995; 346:785.<br />8. Grahame-Smith D. Evidence based medicine: Socratic dissent. BMJ. 1995;310:1126-7.<br />9. Sleigh JW. Evidence-based medicine and Kurt Godel. Lancet. 1995;346:1172.<br />10. Aveyard P. Evidence-based medicine. Lancet. 1995; 346: 840.<br />11. Bradley F, Field J. Evidence-based medicine. Lancet. 1995;346:838-9.<br />12. Chagla LS, McCulloch PG. Evidence-based medicine. Lancet. 1995;346:839-40.<br />13. Fowler PB. Evidence-based medicine. Lancet. 1995; 346:838.<br />14. Haynes B. Evidence-based medicine. Lancet. 1995;346: 1171.<br />15. Iggo N. Evidence-based medicine. Lancet. 1995;346:839-40.<br />16. Morgan WK. Evidence-based medicine. Lancet. 1995; 346:1172.<br />17. Shahar E. Evidence-based medicine. Lancet.1995;346: 1172.<br />18. White KL. Evidence-based medicine. Lancet. 1995;346: 837-8.<br />19. Ellis J, Mulligan I, Rowe J, Sackett DL. Inpatient general medicine is evidence based. A-Team, Nuffield Department of Clinical Medicine. Lancet. 1995;346:407-10.<br />20. Gill P, Dowell AC, Neal RD, Smith N, Heywood P, Wilson AE. Evidence based general practice: a retrospective study of interventions in one training practice. BMJ. 1996;312:819-21.<br />21. Hughes J. Evidence-based medicine. Lancet. 1995;346:839-40.<br />22. Norman G. Evidence-based medicine. Lancet. 1995;346:1300.<br />23. Canguilhem G. Augusto Comte y el “principio de Broussais”. En: Lo normal y lo patológico. Primera edición. Buenos Aires: Siglo Veintiuno; 1971. p. 25-41.<br />24. Burgos L. Introducción a la nueva biología. Primera edición. Medellín: Biogénesis; 2003.<br />25. Hubert R. Brevarios del pensamiento filosófico “Comte”. Primera edición. Buenos Aires: Editorial Sudamericana; 1943.<br />26. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL, et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289:2560-72.<br />27. Canguilhem G. Lo normal y lo patológico. Primera edición. Buenos Aires: Siglo Veintiuno; 1971. p. 83-113.<br />28. Canguilhem G. Claude Bernard y la patología experimental. En: Lo normaly lo patológico. Primera edición. Buenos Aires: Siglo Veintiuno; 1971. p. 41-62.<br />29. Canguilhem G. Las concepciones de R. Leriche. En: Lo normal y lo patológico. Primera edición. Buenos Aires: Siglo Veintiuno; 1971. p. 63-71.
oai:oai.revistabiomedica.org:article/40
2009-12-19T12:04:34Z
biomedica:ARTI
Financial cost of early rheumatoid arthritis in the first year medical attention: three clinical scenarios.
Costos directos de la artritis reumatoide temprana en el primer año de atención: simulación de tres situaciones clínicas en un hospital universitario de tercer nivel en Colombia
Quintana, Gerardo
Mora, Claudia
González, Andrés
Díaz, Jorge Díaz
artritis reumatoide
costos y análisis de costos
costo de enfermedad
Colombia
rheumatoid
arthritis
costs and cost analysis
cost of illness
Colombia
Introduction. In Colombia, the cost burden of chronic diseases is not well known, either globally or in localized areas of the health system. Rheumatoid arthritis is one of most common chronic diseases, and represents a high cost for the health system.Objective. The direct medical costs were estimated for rheumatoid arthritis patients in the in the first year of diagnosis at a level 3 university hospital in Colombia.Materials and methods. Three therapy settings for early rheumatoid arthritis patients were established in the first year of diagnosis according to national and international guidelines. Each setting included treatment with disease-modifying anti-rheumatic drugs or biologic therapy based on disease severity as measured by Disease Activity Score 28. All direct medical costs were included: specialized medical care, diagnostic tests and drugs. Cost information was obtained from the Central Military Hospital finance department in Bogotá and the national manual of drug prices based on the “Farmaprecios” 2007 guide, a reference in general use by health institutions.Results. The average of cost of medical care in patients with mild, moderate and severe disease was US$1,689, $1,805 and $23,441 respectively. The recommended retail prices of the medicines published in “Farmaprecios” was US$ 1,418, $1,821 and $31,931. When the charges levied by several major health institutions were compared, substantial increases were noted, US$ 4,936, $ 7,716 and $ 123,661, respectively. Drug costs represented 86% of total cost, laboratory costs were 10% and medical attention was only 4%.Conclusions. Drugs costs were the principal component of the total direct medical cost, and it increased 40 times when a biological therapy is used. Complete economic evaluation studies are necesary to estimate the viability and clinical relevance of biological therapy for early rheumatoid arthritis.
Introducción. En Colombia se desconoce cuál es la carga derivada de las enfermedades reumatológicas crónicas de forma global y en las diferentes esferas del sistema de salud. La artritis reumatoide es una de las enfermedades más frecuentes en su clase y, actualmente, representa un alto costo para el sistema de salud derivado de la atención de los pacientes.Objetivo. Determinar los costos médicos directos en pacientes con artritis reumatoide temprana en el primer año de diagnóstico en un hospital universitario de tercer nivel en Colombia.Materiales y métodos. De acuerdo con la gravedad de la enfermedad medida por el Disease Activity Score 28, se establecieron tres tipos de tratamiento en concordancia con las guías nacionales e internacionales vigentes, que involucran medicamentos modificadores de la enfermedad o inhibidores del factor de necrosis tumoral. Se incluyeron todos los costos directos derivados del cuidado médico, como costos por atención médica especializada, pruebas diagnósticas y medicamentos. El cálculo de los costos se basó en el sistema tarifario del hospital universitario, en el manual tarifario nacional vigente a diciembre de 2007 y en los precios de venta de los fármacos sugeridos al público por la guía Farmaprecios, usada como referencia en las instituciones de salud.Resultados. En promedio, la atención de la enfermedad leve, moderada y grave cuesta US$ 1.689, US$ 1.805 y US$ 23.441, respectivamente. Al utilizar los precios recomendados en Farmaprecios y el manual tarifario nacional, el costo total para cada categoría osciló entre US$ 1.418 y US$ 4.936, US$ 1.821 y US$ 7.716, US$ 31.931 y US$ 123.661, respectivamente. El 86% de estos costos se deriva del costo de los medicamentos, 10% de los exámenes de laboratorio y 4% de la atención médica.Conclusión. El principal elemento de los costos médicos directos en la artritis reumatoide temprana son los costos por medicamentos y se incrementa 40 veces con el uso de la terapia biológica. Deben realizarse estudios de evaluación económica completos para determinar la viabilidad y pertinencia clínica y económica del uso de la terapia biológica en estos pacientes.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/40
10.7705/biomedica.v29i1.40
Biomedica; Vol. 29 No. 1 (2009); 43-50
Biomédica; Vol. 29 Núm. 1 (2009); 43-50
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/40/41
https://revistabiomedica.org/index.php/biomedica/article/view/40/336
/*ref*/<p> </p><p>1. Guzmán R, Restrepo J. Artritis reumatoide temprana. Rev Colomb Reumatol. 2002;9:171-5.<br />2. Choy EH, Panayi GS. Cytokine pathways, and joint inflammation in rheumatoid arthritis. N Engl J Med. 2001;344:907-16.<br />3. Merkesdal S, Ruof J, Schoffski O, Bernitt K, Zeidler H, Mau W. Indirect medical cost in early rheumatoid arthritis. Arthritis Rheum. 2001;44:528-34.<br />4. Combe B. Early rheumatoid arthritis: strategies for prevention and management. Best Pract Res Clin Rheumatol. 2007:21:27-42.<br />5. Rovira J. Evaluación económica en salud: de la investigación a la toma de decisiones. Rev Esp Salud Pública. 2004;78:293-5.<br />6. Mora C, González A, Quintana G. Guía de manejo artritis reumatoide temprana en un Hospital Universitario de Colombia. Rev Colomb Reumatol. 2008;15:79-91.<br />7. Combe B, Landewe R, Lukas C, Bolosiu H D, Breedveld F, Dougados M, et al. EULAR recommendations for the management of early arthritis: report of a task force of the European Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2007;66:34-45.<br />8. Luqmani R, Hennell S, Estrach C, Birrell F, Bosworth A, Davenport G, et al. British Society for Rheumatology and British Health Professionals in Rheumatology Guideline for the Management of Rheumatoid Arthritis (the first 2 years). Rheumatology. 2006;45:1167-9.<br />9. Vinicio C, Chalem P, Londoño L, Restrepo J, Iglesias A, Vélez P, et al. Primer consenso colombiano sobre el tratamiento de la artritis reumatoide temprana. Rev Col Reumatol. 2002;9:323-31.<br />10. Loët X, Berthelot J M, Cantagrel A, Combe B, De Bandt M, Fautrel B, et al. Clinical practice decision tree for the choice of the first disease modifying antirheumatic drug for very early rheumatoid arthritis: a 2004 proposal of the French Society of Rheumatology. Ann Rheum Dis. 2006;65:45-50.<br />11. Arnett FC, Edworthy SM, Bloch DA, McShane DJ, Fries JF, Cooper NS, et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum. 1988;31:315- 24.<br />12. Byford S, Torgerson D, Raftery J. Economic note: Cost of illness studies. BMJ. 2000;320;1335.<br />13. Rat AC, Boissier MC. Rheumatoid arthritis: direct and indirect costs. Joint Bone Spine. 2004;71:518-24.<br />14. Michaud K, Messer J, Choi H, Wolfe F. Direct medical costs and their predictors in patients with rheumatoid arthritis a three-year study of 7,527 patients. Arthritis Rheum. 2003;48:2750-62.<br />15. Kavanaugh A. The pharmacoeconomics of newer therapeutics for rheumatic diseases. Rheum Dis Clin North Am. 2006;32:45-56.<br />16. Cooper NJ. Economic burden of rheumatoid arthritis: a systematic review. Rheumatology. 2000;39:28-33.<br />17. Pineda-Tamayo R, Arcila G, Restrepo P, Tobón GJ, Camargo JF, Anaya JM. Costos médicos directos de la artritis reumatoide temprana. Rev Colomb Reumatol. 2004;11:89-96.<br />18. Delgado-Vega A, Martín J, Granados J, Anaya JM. Epidemiología genética de la artritis reumatoide: ¿qué esperar de América Latina? Biomédica. 2006;26:562-84.</p>
oai:oai.revistabiomedica.org:article/41
2010-09-15T20:54:17Z
biomedica:ARTI
Anti-tubercular activity of eleven aromatic and medicinal plants occurring in Colombia
Actividad antituberculosa de plantas colombianas
Bueno-Sánchez, Juan Gabriel
Martínez-Morales, Jairo René
Stashenko, Elena E.
Ribón, Wellman
Mycobacterium tuberculosis
tuberculosis
anti-infective agents
plants
medicinal
phytotherapy
Colombia
Mycobacterium tuberculosis
tuberculosis
agentes antiinfecciosos
plantas medicinales
fitoterapia
Colombia
Introduction. Human tuberculosis is a contagious-infectious disease mainly caused by Mycobacterium tuberculosis. Although regimens exist for treating tuberculosis, they are far from ideal. Development of effective strategies for treatment of human tuberculosis has posed a challenge, considering the increase in infections associated with the human immunodeficiency virus and immunocompromised patients. Essential oils -volatile, aromatic oil extracts from plants-have been used in traditional treatment of many diseases; however careful investigation of these oils has not been undertaken with respect to treatments of tuberculosis.Objective. The in vitro antitubercular activity of essential oils from 11 medicinal plants grown in Colombia were assessed for efficacy as new medications (phytomedicines) for treatment of M. tuberculosis H37Rv.Material and methods. Essential oil extraction and analysis were performed as described Stashenko et al. (2004). Minimal inhibitory concentrations were determined by a colorimetric macrodilution method, following the protocol described by Abate et al. (1998). Isoniazide and rifampin were used as control treatments. Bactericidal and bacteriostatic activity was measured using the method developed by the Clinical and Laboratory Standards Institute consigned in the M26-A protocol.Results. Essential oils from Achyrocline alata and Swinglea glutinosa were the most active with minimal inhibitory concentrations of 62.5±0.1 and 100±36 μg ml-1, respectively. Carvacrol, thymol, p-cymene, 1,8-cineole, limonene, and β-pinene were the major components ,most often identified in the 11 plant extracts of essential oils. Time-kill curve assays demonstrated the bacteriostatic activity of these essential oils.Conclusions. The essential oils from A. alata and S. glutinosa plants, and the components identified therein, are candidates as potential phytotherapeutic agents for human tuberculosis control.
Introducción. La tuberculosis es una enfermedad infectocontagiosa causada por Mycobacterium tuberculosis. Aunque existen protocolos para su tratamiento, no son ideales. Actualmente, el desarrollo de estrategias terapéuticas efectivas ha tomado nuevos rumbos, considerando el incremento de pacientes positivos para el virus de la inmunodeficiencia humana. Los medicamentos basados en plantas medicinales se usan ampliamente en la medicina tradicional para el tratamiento de diversas afecciones. Los aceites esenciales obtenidos de plantas medicinales presentan amplia actividad antimicrobiana, sin embargo, existen pocos estudios que reporten la actividad antituberculosa de los mismos.Objetivo. Evaluar la actividad antituberculosa in vitro de 11 aceites esenciales provenientes de plantas medicinales que crecen en Colombia, los cuales podrían ser candidatos para el desarrollo de futuros fitofármacos. Materiales y métodos. La extracción y el análisis de los aceites esenciales se realizó bajo la metodología desarrollada por Stashenko et al.. La obtención de la concentración inhibitoria mínima se llevó a cabo por un método colorímetrico de macrodilución en caldo descrito por Abate y et al.; la isoniacida y la rifampicina se usaron como medicamentos control. La actividad bactericida y bacteriostática se determinaron mediante el protocolo M26-A del Clinical and Laboratory Standards Institute.Resultados. Los aceites esenciales provenientes de las plantas Achyrocline alata y Swinglea glutinosa fueron los más activos con concentraciones inhibitorias mínimas de 62,5±0,01 y 100±36 μg ml-1, respectivamente. Carvacrol, timol, p-cymene, 1,8-cineole, limoneno, y β-pineno fueron los componentes mayoritarios identificados en los 11 aceites. Los ensayos de curva de letalidad evidenciaron que ambos aceites son bacteriostáticos.Conclusiones. Los aceites esenciales obtenidos de las plantas A. alata y S. glutinosa, así como sus componentes, son candidatos potenciales como fitoterapéuticos para el control de la tuberculosis.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/41
10.7705/biomedica.v29i1.41
Biomedica; Vol. 29 No. 1 (2009); 51-60
Biomédica; Vol. 29 Núm. 1 (2009); 51-60
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/41/42
https://revistabiomedica.org/index.php/biomedica/article/view/41/337
/*ref*/Ducati RG, Ruffino-Netto A, Basso LA, Santos DS. The resumption of consumption-a review on tuberculosis. Mem Inst Oswaldo Cruz. 2006;101:697-714.<br />2. Zumla A, Grange J. Tuberculosis. BMJ. 1998; 316: 1962-4.<br />3. Chang Blanc D, Nunn P. Incentives and disincentives for new anti-tuberculosis drug development. Geneva: World Health Organization; 1999.<br />4. National Institute of Allergy and Infectious Diseases. NIAID Global Health Research Plan for HIV/AIDS, malaria, and tuberculosis. Bethesda: National Institute of Allergy and Infectious Diseases; 2001.<br />5. Heinrich M, Gibbons S. Ethnopharmacology in drug discovery: an analysis of its role and potential contribution. J Pharm Pharmacol. 2001;53:425-32.<br />6. Gautam R, Saklani A, Jachak SM. Indian medicinal plants as a source of antimycobacterial agents. J Ethnopharmacol. 2007;110:200-34.<br />7. Edris AE. Pharmaceutical and therapeutic potentials of essential oils and their individual volatile constituents: a review. Phytother Res. 2007;21:308-23.<br />8. Cantrell CL, Franzblau SG, Fischer NH. Anti-myco-bacterial plant terpenoids. Planta Med. 2001;67:685-94.<br />1. Ducati RG, Ruffino-Netto A, Basso LA, Santos DS. The resumption of consumption-a review on tuberculosis. Mem Inst Oswaldo Cruz. 2006;101:697-714.<br />2. Zumla A, Grange J. Tuberculosis. BMJ. 1998; 316: 1962-4.<br />3. Chang Blanc D, Nunn P. Incentives and disincentives for new anti-tuberculosis drug development. Geneva: World Health Organization; 1999.<br />4. National Institute of Allergy and Infectious Diseases. NIAID Global Health Research Plan for HIV/AIDS, malaria, and tuberculosis. Bethesda: National Institute of Allergy and Infectious Diseases; 2001.<br />5. Heinrich M, Gibbons S. Ethnopharmacology in drug discovery: an analysis of its role and potential contribution. J Pharm Pharmacol. 2001;53:425-32.<br />6. Gautam R, Saklani A, Jachak SM. Indian medicinal plants as a source of antimycobacterial agents. J Ethnopharmacol. 2007;110:200-34.<br />7. Edris AE. Pharmaceutical and therapeutic potentials of essential oils and their individual volatile constituents: a review. Phytother Res. 2007;21:308-23.<br />8. Cantrell CL, Franzblau SG, Fischer NH. Anti-myco-bacterial plant terpenoids. Planta Med. 2001;67:685-94.
oai:oai.revistabiomedica.org:article/42
2009-12-19T12:04:34Z
biomedica:ARTI
Mutations in the BRCA1 gene (185delAG and 5382insC) are not present in any of the 30 breast cancer patients analyzed from eastern Colombia
Análisis de las mutaciones más frecuentes del gen BRCA1 (185delAG y 5382insC) en mujeres con cáncer de mama en Bucaramanga, Colombia
Sanabria, María Carolina
Muñoz, Gerardo
Vargas, Clara Inés
Breast neoplasms/genetics
genes
neoplasm
suppressor
BRCA1
germ-line mutation
genetic predisposition to disease
Introduction. Breast cancer is considered a worldwide public health problem, and, in Santander Province, Colombia, it is the first leading cause of morbidity and mortality by cancer in women. All cancers are considered genetic diseases, and mutations in BRCA (BReast CAncer) genes raises the risk for breast cancer by 60%-80%. The current study searched for the two most frequent BRCA1 mutations reported in the Breast Cancer Core Information database.Objective. The presence of specific mutations (185delAG, exon 2 and 5382insC, exon 20) was determined for the BRCA1 gene in women with familial/hereditary breast cancer.Materials and methods. The sample included 30 female patients using the oncology services in Bucaramanga, eastern Colombia; an informed consent, a questionnaire and a blood sample were obtained from each. The molecular analysis was done with PCR-Mismatch, to detect the insertion or eliminatation of a restriction site, and enzymatic digestion methods (HinfI or DdeI).Results. Two of the most frequent BRCA1 mutations in the international database were not found in the 30 patients studied.Conclusion. Additional mutation screening techniques are necessary involving the entire BRCA1 gene, are necessary in order to better characterize the molecular epidemiology of breast cancer in Bucaramanga, Santander, Colombia.
Introducción. El cáncer de mama es un problema de salud pública a nivel mundial y en Santander es la primera causa de morbimortalidad por cáncer en mujeres. Todo cáncer se considera una enfermedad genética y las mutaciones en los genes BRCA confieren un riesgo de 60% a 80% para el cáncer de mama. Este estudio consistió en buscar las dos mutaciones BRCA1 más frecuentes según la base de datos Breast Cancer Core Information.Objetivo. Determinar la presencia de mutaciones específicas (185delAG, exón 2, y 5382insC, exón 20) en el gen BRCA1 en mujeres con cáncer de mama heredo-familiar, atendidas en los diferentes servicios de oncología de Bucaramanga, Colombia.Materiales y métodos. La muestra incluyó 30 pacientes, de las cuales se obtuvo un consentimiento informado, un cuestionario dirigido y sangre venosa para los estudios moleculares. El análisis molecular se realizó mediante PCR-mismatch, para introducir o eliminar sitios de restricción, y digestión enzimática (HinfI o DdeI).Resultados. No se detectaron dos de las mutaciones más frecuentes en el gen BRCA1 en las 30 pacientes estudiadas.Conclusión. Se requieren más estudios en la región que abarquen la tamización de la totalidad del gen BRCA1, para hacer una mayor contribución al conocimiento de la epidemiología molecular del cáncer de mama en Bucaramanga, Santander, Colombia.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/42
10.7705/biomedica.v29i1.42
Biomedica; Vol. 29 No. 1 (2009); 61-72
Biomédica; Vol. 29 Núm. 1 (2009); 61-72
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/42/43
https://revistabiomedica.org/index.php/biomedica/article/view/42/339
/*ref*/<p>1. Parkin DM. International variation Oncogene. 2004; 23:6329-40.<br />2. Stewart SL, King JB, Thompson TD, Friedman C, Wingo PA. Cancer mortality surveillance--United States, 1990-2000. MMWR Surveill Summ. 2004;53:1-108.<br />3. Hormiga C, Rodríguez L, Uribe C. Análisis de la situación de las enfermedades neoplásicas en Santander. Revista del Observatorio de Salud Pública de Santander. 2006;2:4-30.<br />4. Miki Y, Swensen J, Shattuck-Eidens D, Futreal PA, Harshman K, Tavtigian S, et al. A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1. Science. 1994;266:66-71.<br />5. Wooster R, Bignell G, Lancaster J, Swift S, Seal S, Mangion J, et al. Identification of the breast cancer susceptibility gene BRCA2. Nature. 1995;378:789-92.<br />6. Easton D, Ford D, Peto J. Inherited susceptibility to breast cancer. Cancer Surv. 1993;18:95-113.<br />7. Marcus JN, Watson P, Page DL, Narod SA, Lenoir GM, Tonin P, et al. Hereditary breast cancer: pathobiology, prognosis, and BRCA1 and BRCA2 gene linkage. Cancer. 1996;77:697-709.<br />8. Ford D, Easton DF, Stratton M, Narod S, Goldgar D, Devilee P, et al. Genetic heterogeneity and penetrance analysis of the BRCA1 and BRCA2 genes in breast cancer families. The Breast Cancer Linkage Consortium. Am J Hum Genet. 1998;62:676-89.<br />9. National Human Genome Research Institute. The Breast Cancer Information Core Database, 2007. [Fecha de consulta: agosto de 2006 y marzo de 2007]. Disponible en: <a href="http://research.nhgri.nih.gov/bic/">http://research.nhgri.nih.gov/bic/</a><br />10. Bar-Sade RB, Kruglikova A, Modan B, Gak E, Hirsh-Yechezkel G, Theodor L, et al. The 185delAG BRCA1 mutation originated before the dispersion of Jews in the diaspora and is not limited to Ashkenazim. Hum Mol Genet. 1998;7:801-5.<br />11. Diez O, Osorio A, Robledo M, Barroso A, Domenech M, Cortés J, et al. Prevalence of BRCA1 and BRCA2 Jewish mutations in Spanish breast cancer patients. Br J Cancer. 1999;79:1302-3.<br />12. Neuhausen SL, Mazoyer S, Friedman L, Stratton M, Offit K, Caligo A, et al. Haplotype and phenotype analysis of six recurrent BRCA1 mutations in 61 families: results of an international study. Am J Hum Genet. 1996;58:271-80.<br />13. Roa BB, Boyd AA, Volcik K, Richards CS. Ashkenazi Jewish population frequencies for common mutations in BRCA1 and BRCA2. Nat Genet. 1996;14:185-7.<br />14. Struewing JP, Abeliovich D, Peretz T, Avishai N, Kaback MM, Collins FS, et al. The carrier frequency of the BRCA1 185delAG mutation is approximately 1 percent in Ashkenazi Jewish individuals. Nat Genet. 1995;11:198-200.<br />15. Abeliovich D, Kaduri L, Lerer I, Weinberg N, Amir G, Sagi M, et al. The founder mutations 185delAG and 5382insC in BRCA1 and 6174delT in BRCA2 appear in 60% of ovarian cancer and 30% of early-onset breast cancer patients among Ashkenazi women. Am J Hum Genet. 1997;60:505-14.<br />16. Mullineaux LG, Castellano TM, Shaw J, Axell L, Wood ME, Diab S, et al. Identification of germline 185delAG BRCA1 mutations in non-Jewish Americans of Spanish ancestry from the San Luis Valley, Colorado. Cancer. 2003;98:597-602.<br />17. Schorge JO, Mahoney NM, Miller DS, Coleman RL, Muller CY, Euhus DM, et al. Germline BRCA1-2 mutations in non-Ashkenazi families with double primary breast and ovarian cancer. Gynecol Oncol. 2001;83:383-7.<br />18. Osorio A, Robledo M, Albertos J, Diez O, Alonso C, Baiget M, et al. Molecular analysis of the six most recurrent mutations in the BRCA1 gene in 87 Spanish breast/ovarian cancer families. Cancer Lett. 1998;123:153-8.<br />19. Jara L, Ampuero S, Santibanez E, Seccia L, Rodríguez J, Bustamante M, et al. BRCA1 and BRCA2 mutations in a South American population. Cancer Genet Cytogenet. 2006;166:36-45.<br />20. Jara L, Ampuero S, Seccia L, Bustamante M, Blanco R, Santibanez E, et al. Frequency of the 185delAG mutation in the BRCA1 gene in Chilean healthy women with family history of breast cancer. Rev Med Chil. 2002;130:1113-23.<br />21. Backe J, Hofferbert S, Skawran B, Dork T, Stuhrmann M, Karstens JH, et al. Frequency of BRCA1 mutation 5382insC in German breast cancer patients. Gynecol Oncol. 1999;72:402-6.<br />22. De Benedetti VM, Radice P, Pasini B, Stagi L, Pensotti V, Mondini P, et al. Characterization of ten novel and 13 recurring BRCA1 and BRCA2 germline mutations in Italian breast and/or ovarian carcinoma patients. Mutations in brief Nº 178. Hum Mutat. 1998;12:215.<br />23. Tommasi S, Crapolicchio A, Lacalamita R, Bruno M, Monaco A, Petroni S, et al. BRCA1 mutations and polymorphisms in a hospital-based consecutive series of breast cancer patients from Apulia, Italy. Mutat Res. 2005;578:395-405.<br />24. van Der Looij M, Wysocka B, Brozek I, Jassem J, Limon J, Olah E. Founder BRCA1 mutations and two novel germline BRCA2 mutations in breast and/or ovarian cancer families from North-Eastern Poland. Hum Mutat. 2000;15:480-1.<br />25. Dufloth RM, Carvalho S, Heinrich JK, Shinzato JY, dos Santos CC, Zeferino LC, et al. Analysis of BRCA1 and BRCA2 mutations in Brazilian breast cancer patients with positive family history. Sao Paulo Med J. 2005;123:192-7.<br />26. Torres D, Rashid MU, Gil F, Umana A, Ramelli G, Robledo JF, et al. High proportion of BRCA1/2 founder mutations in Hispanic breast/ovarian cancer families from Colombia. Breast Cancer Res Treat. 2007; 103: 225-32.<br />27. Brose MS, Rebbeck TR, Calzone KA, Stopfer JE, Nathanson KL, Weber BL. Cancer risk estimates for BRCA1 mutation carriers identified in a risk evaluation program. J Natl Cancer Inst. 2002;94:1365-72.<br />28. Ford D, Easton DF, Bishop DT, Narod SA, Goldgar DE. Risks of cancer in BRCA1-mutation carriers. Breast Cancer Linkage Consortium. Lancet. 1994;343:692-5.<br />29. Struewing JP, Hartge P, Wacholder S, Baker SM, Berlin M, McAdams M, et al. The risk of cancer associated with specific mutations of BRCA1 and BRCA2 among Ashkenazi Jews. N Engl J Med. 1997;336:1401-8.<br />30. Thompson D, Easton DF. Cancer Incidence in BRCA1 mutation carriers. J Natl Cancer Inst. 2002;94:1358-65.<br />31. Miller SA, Dykes DD, Polesky HF. A simple salting out procedure for extracting DNA from human nucleated cells. Nucleic Acids Res. 1988;16:1215.<br />32. Elstrodt F, Hollestelle A, Nagel JH, Gorin M, Wasielewski M, van den Ouweland A, et al. BRCA1 mutation analysis of 41 human breast cancer cell lines reveals three new deleterious mutants. Cancer Res. 2006;66:41-5.<br />33. Kutner SE. Breast cancer genetics and managed care. The Kaiser Permanente experience. Cancer. 1999;86:2570-4.<br />34. Ikeda N, Miyoshi Y, Yoneda K, Shiba E, Sekihara Y, Kinoshita M, et al. Frequency of BRCA1 and BRCA2 germline mutations in Japanese breast cancer families. Int J Cancer. 2001;91:83-8.<br />35. Peto J, Collins N, Barfoot R, Seal S, Warren W, Rahman N, et al. Prevalence of BRCA1 and BRCA2 gene mutations in patients with early-onset breast cancer. J Natl Cancer Inst. 1999;91:943-9.<br />36. Ruiz-Flores P, Calderón A, Barrera-Saldaña H. Breast Cancer Genetics BRCA1 and BRCA2: Main susceptibility genes. Revista de Investigación Clínica. 2001;53:46-64.<br />37. Trincado P, Fardella C, Mayerson D, Montero L, O’Brien A, Barrueto K, et al. Prevalence of the 185Ag deletion of the BRCA1 gene in Chilean women with breast neoplasm. Rev Med Chil. 1999;127:19-22.<br />38. Jara L, Ampuero S, Seccia L, Bustamante M, Blanco R, Ojeda JM. Analysis of 5382insC (BRCA1) and 6174delT (BRCA2) mutations in 382 healthy Chilean women with a family history of breast cancer. Biol Res. 2002;35:85-93.<br />39. Mantilla A, Vesga B, Insuasty J. Registro de Cáncer, Unidad de Oncología, Hospital Universitario Ramón González Valencia, Bucaramanga, Colombia. (1996-1999). MedUNAB. 2006;9:14-9.<br />40. Palacios J, Honrado E, Osorio A, Cazorla A, Sarrio D, Barroso A, et al. Immunohistochemical characteristics defined by tissue microarray of hereditary breast cancer<br />not attributable to BRCA1 or BRCA2 mutations: differences from breast carcinomas arising in BRCA1 and BRCA2 mutation carriers. Clin Cancer Res. 2003;9:3606-14.<br />41. Easton DF, Pooley KA, Dunning AM, Pharoah PD, Thompson D, Ballinger DG, et al. Genome-wide association study identifies novel breast cancer susceptibility loci. Nature. 2007;447:1087-93.<br />42. U.S. Preventive Services Task Force (USPSTF). Genetic risk assessment and BRCA mutation testing for breast and ovarian cancer susceptibility: recommendation statement. Ann Intern Med. 2005;143:355-61.<br />43. Stoppa-Lyonnet D, Laurent-Puig P, Essioux L, Pages S, Ithier G, Ligot L, et al. BRCA1 sequence variations in 160 individuals referred to a breast/ovarian family cancer clinic. Institut Curie Breast Cancer Group. Am J Hum Genet. 1997;60:1021-30.</p>
oai:oai.revistabiomedica.org:article/43
2009-12-19T12:04:34Z
biomedica:ARTI
Sand flies (Diptera: Psychodidae) of Guaviare Province, Colombia, with 4 new records for the country
Flebótomos (Diptera: Psychodidae) del departamento de Guaviare, Colombia, con nuevos registros para el país
Cabrera, Olga Lucía
Mosquera, Laureano
Santamaría, Erika
Lutzomyia
leishmaniasis cutánea
biodiversidad
ecosistema amazónico
Colombia
Lutzomyia
leishmaniasis
cutaneous
biodiversity
Amazonian ecosystem
Colombia
Introduction. Although cases of leishmaniasis have been reported in the province of Guaviare, Colombia, no entomological studies were included to identify the Lutzomyia sand fly vector species in that area.Objective. Lutzomyia species were identified from four townships of Guaviare. Probable vectors were named based on those species involved in transmission in other areas.Materials and methods. Sampling was undertaken with CDC light traps suspended at heights between 1.5 m and 9 m. Additional sand flies were collected with Shannon traps and by aspiration of adult flies from daytime resting sites.Results. Sand flies belonging to 37 different species were collected. 35 of them were recorded for the first time in Guaviare Province. Four species were new records for Colombia: Lutzomyia begonae, L. campbelli, L. sericea and L. nematoducta. The most abundant species were L. hirsuta 24.3% (148/610), L. yuilli 15.2% (93/610), L. davisi 10.3% (63/610), followed by L. fartigi, L. carrerai, L. antunesi, L. flaviscutellata and L. olmeca bicolor.Conclusion. Seven of these species of have been associated previously with endemic or epidemic transmission of leishmaniasis.
Introducción. El registro de casos de leishmaniasis en el departamento de Guaviare evidenció la ausencia de estudios entomológicos dirigidos a identificar las especies de Lutzomyia de esa región del país.Objetivo. Determinar las especies del género Lutzomyia en los cuatro municipios del departamento del Guaviare y señalar por antecedentes vectoriales las especies con posible compromiso en la transmisión de la leishmaniasis.Materiales y métodos. El muestreo se realizó con trampas CDC colgadas entre 1,5 m y 9 m de altura. Además, se recolectaron flebótomos con trampa Shannon y en sitios de reposo.Resultados. Se recolectaron flebótomos pertenecientes a 37 especies; 35 de ellas se registran por primera vez para el departamento del Guaviare y cuatro para el país: L. begonae, L. campbelli, L. sericea y L. nematoducta. Las especies más abundantes fueron L. hirsuta 24,3% (148/610), L. yuilli 15,2% (93/610) y L. davisi 10,3% (63/610), seguidas por L. fartigi, L. carrerai, L. antunesi, L. flaviscutellata y L. olmeca bicolor.Conclusión. Se identificaron siete especies de Lutzomyia como posibles vectores de leishmaniasis.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/43
10.7705/biomedica.v29i1.43
Biomedica; Vol. 29 No. 1 (2009); 73-86
Biomédica; Vol. 29 Núm. 1 (2009); 73-86
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/43/44
https://revistabiomedica.org/index.php/biomedica/article/view/43/340
/*ref*/Young DG, Duncan MA. Guide to the identification and geographic distribution of Lutzomyia sand flies in Mexico, the West Indies, Central and South America (Diptera: Psychodidae). Mem Entomol Inst. 1994;54:1-881.<br />2. Lewis DJ, Young DG, Fairchild GB, Minter DM. Proposals for a stable classification of the phlebotomine sandflies (Diptera: Psychodidae). Syst Entomol. 1977;2:319-32.<br />3. Tesh RB, Guzmán H. Sand flies and the agents they transmit. In: Beaty BJ, Marquartdt WC, editors. The biology of disease vectors. Niwot: University Press of Colorado; 1996. p. 117-27.<br />4. Beati L, Cáceres AG, Lee JA, Munstermann LE. Systematic relationships among Lutzomyia sand flies (Diptera: Psychodidae) of Perú and Colombia based on the analysis of 12S and 28S ribosomal DNA sequences. Int J Parasitol. 2004;34:225-34.<br />5. Antunes PC. Informe sobre una investigación entomológica realizada en Colombia. Revista de la Facultad de Medicina. 1937;6:3-29.<br />6. Muñoz G. The sandfly vectors and epidemiology of cutaneous leishmaniasis in the Landázuri focus, Colombia (thesis). London: University of London; 1998. p. 257.<br />7. Davies CR, Reithinger R, Campbell-Lendrum D, Feliciangeli D, Borges R, Rodriguez N. The epidemiology and control of leishmaniasis in Andean countries.Cad Saude Publica. 2000;16:925-50.<br />8. Cárdenas R, Pabón E, Anaya H, Sandoval CM. Presencia de Lutzomyia longiflocosa (Diptera: Psychodidae) en el foco de leishmaniasis tegumentaria americana del municipio de Ábrego, Norte de Santander. Primer registro para el departamento. Clon. 2005;3:7-14.<br />9. Pardo RH, Cabrera OL, Becerra J, Fuya P, Ferro C. Lutzomyia longiflocosa, posible vector en un foco de leishmaniasis cutánea en la región subandina del departamento del Tolima, Colombia, y el conocimiento que tiene la población sobre este insecto. Biomédica. 2006;26(Supl.1):95-108.<br />10. Pardo RH. The ecology and control of cutaneous leishmaniasis in the sub-Andean region of South-West Colombia (thesis). Londres: London School of Hygiene and Tropical Medicine; 2006.p. 311.<br />11. Santamaría E, Ponce N, Zipa Y, Ferro C. Presencia en el peridomicilio de vectores infectados con Leishmania (Viannia) panamensis en dos focos endémicos en el occidente de Boyacá, piedemonte del valle del Magdalena medio, Colombia. Biomédica. 2006;26(Suppl.1):82-94.<br />12. Osorno-Mesa E, Morales-Alarcón A, De Osorno F, Ferro-Vela C. Phlebotominae de Colombia (Diptera, Psychodidae) IX. Distribución geográfica de especies de Brumptomyia y Lutzomyia Franca 1924, encontradas en Colombia. Revista Académica Colombiana de Ciencias Exactas, Físicas y Naturales. 1972;14:45-68.<br />13. Morales A, Minter DM. Estudios sobre flebotominos en Araracuara, Caquetá, Colombia, incluyendo la descripción de Lutzomyia araracuarensis (Diptera: Psychodidae). Biomédica. 1981;1:94-116.<br />14. Young DG, Morales A. New species and records of phlebotomine sand flies from Colombia (Diptera: Psychodidae). J Med Entomol. 1987;24:651-65.<br />15. Cipa Group. Computer-aided identification of phlebo-tomine sandlies of America. (Fecha de consulta: 3 de abril de 2008). Disponible en: <a href="http://cipa.snv.jussieu.fr/">http://cipa.snv.jussieu.fr/</a><br />16. Montoya-Lerma J, Ferro C. Flebótomos (Diptera: Psychodidae) de Colombia. En: Amat G, Andrade MG, Fernández F, editores. Insectos de Colombia. Volumen II. Colección Jorge Álvarez Lleras No. 13. Bogotá D.C.; Academia Colombiana de Ciencias Exactas, Físicas y Naturales; 1999. p. 211-45.<br />17. Barreto M, Burbano ME, Barreto P. Lutzomyia sand flies (Diptera: Psychodidae) from middle and lower Putumayo department, Colombia, with new records to the country. Mem Inst Oswaldo Cruz. 2000;95:633-9.<br />18. Wolff M, Sierra D, Murcia LM, Vélez ID. Phlebotominae fauna (Diptera: Psychodidae) in the department of Amazonas, Colombia. Neotrop Entomol. 2003;32:523-6.<br />19. Molina J, Hildebrand P, Olano V, Muñoz P, Barreto M, Guhl F. Fauna de insectos hematófagos del sur del Parque Nacional Chiribiquete, Caquetá, Colombia. Biomédica. 2000;20:314-26.<br />20. Barreto M, Burbano ME, Young DG. Description of Lutzomyia (Trichophoromyia) pabloi n. sp. and the female of L. howardi (Diptera: Psychodidae) from Colombia. J Med Entomol. 2002;39:601-4.<br />21. Wolff M, Bianchi Galati EA. Description of Pintomyia limafalcaoae and Pintomyia antioquiensis, two new species of phlebotomine sand fly (Diptera, Psychodidae) from the Colombian Andes. Mem Inst Oswaldo Cruz. 2002;97:317-24.<br />22. Bejarano EE, Duque P, Vélez ID. Taxonomy and distribution of the series pia of the Lutzomyia verrucarum group (Diptera: Psychodidae), with a description of Lutzomyia emberai n. sp. J Med Entomol. 2004;41:833-41.<br />23. Bejarano EE. Lista actualizada de los Psicódidos (Diptera: Psychodidae) de Colombia. Folia Entomol Mex. 2006;45:47-56.<br />24. Bejarano EE, Duque P, Vélez ID. Redescripción de la hembra de Lutzomyia vattierae (Diptera: Psychodidae, Phlebotominae) de la serranía de La Macarena, Colombia. Biomédica. 2006;26:556-61.<br />25. Martínez AG. Toda Colombia es mi pasión. Departamento del Guaviare. (Fecha de consulta: 9 de abril de 2008) Disponible en: <a href="http://www.todacolombia.com/departamentos/guaviare.html">http://www.todacolombia.com/departamentos/guaviare.html</a><br />26. Gobernación de San José del Guaviare. Departamento del Guaviare, el Guaviare en buenas manos. Información general del departamento. (Fecha de consulta: 6 de mayo de 2008). Disponible en: <a href="http://www.guaviare.gov.co/nuestromunicipio.shtml?apc=m-I1—&m=f&s=m">http://www.guaviare.gov.co/nuestromunicipio.shtml?apc=m-I1—&m=f&s=m</a><br />27. Instituto Geográfico Agustín Codazzi-IGAC. Diccionario Geográfico de Colombia. Tercera edición. Santafé de Bogotá: Instituto Geográfico Agustín Codazzi; 1996. p. 2504.<br />28. Young DG. A review of the bloodsucking psychodid flies of Colombia (Diptera: Phlebotominae and Sycoracinae). Technical Bulletin 806. Gainesville: Institute of Food and Agricultural Sciences, University of Florida; 1979. p. 266.<br />29. Llanos B, Martins AV, Da Silva JE. Estudios sobre os flebotomineos do Peru (Diptera, Psychodidae, Phlebotominae) I- Departamento de Cuzco: 2- Descricao das femeas de Lutzomyia campbelli e Lutzomyia sherlocki e redescricao do macho e descricao da femea de Lutzomyia octavioi. Rev Brasil Biol. 1975;35:655-64.<br />30. Fairchild GB, Hertig M. Notes on the Phlebotomus of Panamá XVI (Diptera, Psychodidae). Descriptions of new and little-known species from Panamá and Central America. Ann Entomol Soc Amer. 1961;54:237-55.<br />31. Fairchild GB, Theodor O. On Lutzomyia flaviscutellata (Mangabeira) and L. olmeca (Vargas and Diaz-Najera) (Diptera: Psychodidae). J Med Vet. 1971;8:153-9.<br />32. Ortíz I, Torres Rojas J. Phlebotomus begonae nov. sp. Nuevo flebotomíneo del subgénero Evandromyia Mangabeira, 1941, en la región sur-occidental amazónica venezolana (Díptera: Psychodidae). Rev Inst Nac Hig. 1975;8:101-5.<br />33. De Carvalho GM, Falcão AL, Filho JD. Taxonomic revision of phlebotomine sand fly species in the series davisi and panamensis of the subgenus Psychodopygus Mangabeira, 1941 (Diptera: Psychodidae: Phlebotominae). Mem Inst Oswaldo Cruz. 2006;101:129-36.<br />34. Feliciangeli MD, Ramírez-Pérez J, Ramírez A. The phlebotomine sandflies of Venezuelan Amazonia. Med Vet Entomol. 1988;2:47-65.<br />35. Ferro C, Morales A. Lista de las especies de flebótomos (Diptera: Psychodidae, Phlebotominae) de Colombia S.A. Biomédica. 1988;8:68-70.<br />36. Barreto M, Burbano ME, Barreto P. Registros de Lutzomyia (Diptera: Psychodidae) en nuevas localidades de Colombia. Colombia Médica. 2006;37:39-45.<br />37. Bejarano EE, Duque P, Vélez ID. Estudio de los flebotomineos (Diptera: Psychodidae) antropofílicos de la Serranía de La Macarena, Colombia. Revista Colombiana de Entomología. 2006;32:176-8.<br />38. Bejarano EE, Castro M, Pérez-Doria A, Hernández-Oviedo E, Vélez A, Vélez ID. Primer Informe de Lutzomyia franca en el departamento de Guainía, Amazonia colombiana, y de Brumptomyia mesai Sherlock (Diptera: Psychodidae) en el litoral Caribe colombiano. Neotrop Entomol. 2007;36:990-3.<br />39. Bejarano EE, Duque P, Vélez ID. Confirmacion de la presencia de Lutzomyia lutziana (Diptera: Psychodidae) en Colombia. Caldasia. 2007;29:153-7.<br />40. Martins AV. Lutzomyia (Psychodopygus) fairtigi n.sp. from Colombia (Diptera: Psychodidae: Phlebotominae) Proc Entomol Soc Wash. 1970;72:279.<br />41. Arias JR, Freitas RA. On the vectors of cutaneous leishmaniasis in the Central Amazon of Brazil. 3. Phlebotomine sand fly stratification in a terra firme florest. Acta Amazonica. 1982;12:599-608.<br />42. Campbell-Lendrum D, Dujardin JP, Martinez E, Feliciangeli MD, Perez JE, Silans LN, et al. Domestic and peridomestic transmission of American cutaneous leishmaniasis: changing epidemiological patterns present new control opportunities. Mem Inst Oswaldo Cruz. 2001; 96:159-62.<br />43. Zambrano P. Informe de leishmaniasis, Colombia, semanas 1 a 52 de 2005. Inf Quinc Epidemiol Nac. 2006;11:40-3.<br />44. Vélez ID, Wolff M, Valderrama R, Escobar JP, Osorio L. Community and environmental risk factors associated with cutaneous leishmaniasis in Montebello, Antioquia, Colombia. In: IDRC, editors. Leishmaniasis control strategies: a critical evaluation of IDRC supported research. London: IDRC Publications; 1991. p. 261-74.<br />45. Young DG, Lawyer PG. New world vectors of the leishmaniases. In: Harrris KF, editor. Current topics in vector research. Vol. 4. New York; Springer Verlag; 1987. p. 29-71.<br />46. Loiola CF, Da Silva DA, Galati EA. Phlebotomine fauna (Diptera: Psychodidae) and species abundance in an endemic area of American cutaneous leishmaniasis in southeastern Minas Gerais, Brazil. Mem Inst Oswaldo Cruz. 2007;102:581-5.<br />47. Gil LH, Basano SA, Souza AA, Silva MG, Barata I, Ishikawa EA, et al. Recent observations on the sand fly (Diptera: Psychodidae) fauna of the state of Rondonia, western Amazonia, Brazil: the importance of Psychdopygus davisi as a vector of zoonotic cutaneous leishmaniasis. Mem Inst Oswaldo Cruz. 2003;98:751-5.<br />48. Ryan L, Lainson R, Shaw JJ, Wallbanks KR. The transmission of suprapylarian Leishmania by the bite of experimentally infected sand flies (Diptera: Psychodidae). Mem Inst Oswaldo Cruz. 1987;82:425-30.<br />49. Travi BL, Montoya J, Solarte Y, Lozano L, Jaramillo C. Leishmaniasis in Colombia. I. Studies on the phlebotomine fauna associated with endemic foci in the Pacific coast region. Am J Trop Med Hyg.1988;39:261-6.
oai:oai.revistabiomedica.org:article/44
2009-12-19T12:04:34Z
biomedica:ARTI
Flu vaccine effectiveness: a metaanalysis
Efectividad de la vacuna contra influenza: metanálisis de literatura
Moreno, José
De la Hoz, Fernando
Rico, Alejandro
Cotes, Karol
Porras, Alexandra
influenza vaccines
effectiveness
efficacy
meta-analysis
vacuna contra la influenza
efectividad
eficacia
metaanálisis
Introduction. Seasonal influenza is a disease of great interest in public health due to its high rates of infection and big costs, especially in high-risk population. This situation has motivated studies related to development of control measures necessary to mitigate its impact. Immunization constitutes a key role in providing the necessary interventions; however, little information is available about its effectiveness as public health measure in tropical countries.Objective. The vaccine effectiveness was evaluated by means of published results in the scientific literature.Materials and methods. Meta-analysis techniques were used to summarize the results of epidemiological analytical studies. A critical evaluation was undertaken for each study to identify the potential biases and methodological limitations.Results. Two hundred and fifty-seven relevant studies were located, of which 28 were included in the analysis. The pooled estimator of the vaccine effectiveness for hospitalization was 0.74 [95%CI 0.68-0.81] in older adults (65 years and older) in cases-control studies. For cohort studies, the obtained estimator was 0.80 [95%CI 0.68-0.91].Conclusion. Other conclusions were analyzed, and in general, a protective effect was demonstrated in the vaccine. About 1,200,000 were involved, 530,000 of them were vaccinated. Geographically, the analyzed studies came from developed countries in Europe, America and Asia.
Introducción. Las altas tasas de infección y los grandes costos, especialmente en población de alto riesgo, hacen de la influenza estacional una enfermedad de gran interés en salud pública. Esta situación ha motivado el desarrollo de investigaciones relacionadas con las medidas de control necesarias para mitigar su impacto. Desde esta perspectiva, la inmunización constituye una pieza clave en el entramado de las intervenciones requeridas. Sin embargo, el conocimiento existente frente a su efectividad como medida de salud pública en países tropicales, es relativamente poco.Objetivos. Evaluar la efectividad de la vacuna mediante los resultados reportados en la literatura publicada sobre el tema.Materiales y métodos. Mediante técnicas de metanálisis, se resumieron los resultados de estudios epidemiológicos analíticos observacionales. Se llevó a cabo una evaluación crítica de cada uno de los estudios para identificar los potenciales sesgos y limitaciones metodológicas.Resultados. Se encontraron 257 estudios, de los cuales se incluyeron 28 en el análisis final. El estimativo agregado de efectividad de la vacuna para hospitalización fue de 0,74 (IC95% 0,68-0,81) en adultos mayores en los estudios de casos y controles. Para los estudios de cohortes el estimativo obtenido fue de 0,80, (IC95% 0,68-0,91). También se analizaron otros desenlaces y, de manera general, se evidenció un efecto protector en la vacuna.Conclusiones. Los análisis sugieren la vacunación como medida masiva de control para influenza en adultos mayores de 65 años. Existe un importante vacío de conocimiento en la efectividad de la vacuna en niños menores de dos años y madres gestantes.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/44
10.7705/biomedica.v29i1.44
Biomedica; Vol. 29 No. 1 (2009); 87-97
Biomédica; Vol. 29 Núm. 1 (2009); 87-97
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/44/45
https://revistabiomedica.org/index.php/biomedica/article/view/44/342
/*ref*/Organización Mundial de la Salud. Vacunas contra la influenza. Boletín Epidemiológico Semanal. 2005;80:279-28.<br />2. Dirección General de Salud Pública, Grupo de Vigilancia en Salud Pública, Ministerio de la Protección Social. La influenza y su situación en Colombia. Bogotá D.C.: Ministerio de la Protección Social; 2005.<br />3. Abarca K. Influenza: vacunación a nuevos grupos etarios. Rev Chil Infect. 2007;24:227-30.<br />4. Bridges CB, Harper SA, Fukuda K, Uyeki T M, Cox NJ , Singleton JA. Prevention and control of influenza. Recommendations of the advisory committee on immunization practices (ACIP). MMWR Recomm Rep. 2003;52:1-34.<br />5. World Health Organization. Guidelines on the use of vaccines and antiviral during influenza pandemics. Ginebra: WHO; 2004.<br />6. Woolacott N. Systematic review protocol. Center for Reviews and Dissemination, University of York. York, UK: University Press; 2006.<br />7. The Cochrane Collaborative Review Group on HIV Infection and AIDS. Inclusion and appraisal of experimental and non-experimental (observational) studies. Washington, D.C.: John Wiley & Sons; 2007.<br />8. Altman DG, Schulz KF, Moher D, Egger M, Davidoff F, Elbourne D, et al. The revised consort statement for reporting randomized trials: explanation and elaboration. Ann Intern Med. 2001;134:663-94.<br />9. Wells GA, Shea B, O’Connell D, Peterson J, Welch V, Losos M, et al. The Newcastle-Ottawa scale for assessing the quality of non randomized studies in meta-analyses. Leicester, UK: University of Ottawa Press; 2007.<br />10. Moreno J, De la Hoz F. Protocolo de revisión sistemática de literatura (documento institucional). Bogotá D.C.: Instituto Nacional de Salud; 2007.<br />11. Salanti G, Sanderson S, Higgins P. Obstacles and opportunities in meta-analysis of genetic association studies. Genet Med. 2005;7:11-3.<br />12. Egger M, Davey G, Phillips AN. Meta-analysis: principles and procedures. BMJ. 1997;315:1533-7.<br />13. Berlin JA. Invited commentary. Am J Epidemiol. 1995;142:383-7.<br />14. Frumkin H, Berlin J. Asbestos exposure and gastrointestinal malignancy review and meta-analysis. Am J Ind Med. 1988;14:79-95.<br />15. Cook TD, Cooper H, Cordray DS, Hartmann H, Hedges LV, Light RJ, et al. Meta-analysis for explanation: a casebook. New York: Russell Sage Foundation; 1992.<br />16. The Nordic Cochrane Centre. Review Manager (RevMan) [Computer program]. Version 4.2 for Windows. Copenhagen: The Cochrane Collaboration; 2003.<br />17. StataCorp LP .Stata 9.0 [Computer program]. Version 9.0 for Windows. College Station, TX: StataCorp LP; 2006.<br />18. Dott MM. Come distruggere in maniera scientifica il sistema immunitario, con i vaccini. Danni biologici dei vaccini e cure. Med J Aust. 2001;154:638.<br />19. Colquhoun AJ, Nicholson KG, Botha JL, Raymond NT. Effectiveness of influenza vaccine in reducing hospital admissions in people with diabetes. Epidemiol Infect. 1997,119:335-41.<br />20. Ahmed AH, Nicholson KG, Nguyen-Van JS, Pearson JC. Effectiveness of influenza vaccine in reducing hospital admissions during the 1989-90 epidemic. Epidemiol Infect. 1997;118:27-33.<br />21. Ahmed AH, Nicholson KG, Nguyen-Van JS. Reduction in mortality associated with influenza vaccine during 1989-90 epidemic. Lancet. 2001;126:71-9.<br />22. Megumi H, Tatsuhiko S, Keitaro T. Effectiveness of influenza vaccination in preventing influenza-like illness among community-dwelling elderly: population-based cohort study in Japan. Vaccine. 2006;24:5546-51.<br />23. Nichol K, Baken L, Worenma J. The health and economics benefits associated with pneumococcal vacination of elderly persons with chronic lung disease. Arch Intern Med. 1999;8:2437-42.<br />24. Moher D, Fortin P, Jadad AR. Completeness of reporting of trials published in languages other than English: implications for conduct and reporting of systematic reviews. Lancet. 1996;347:363-76.<br />25. Belshe R, Kathryn E, Vlack S, Walker R, Hultquist M, Connor G, et al. Live attenuated versus inactivated vaccine in infants and young children. N Eng J Med. 2007;356:685-96.<br />26. Mesa SS, Moreno AP, Hurtado G, Arbeláez MP. Efectividad de una vacuna antigripal en una población laboral colombiana. Rev Panam Salud Pública. 2001;10:35-9.<br />27. The Cochrane Collaboration. Eficacia y efectividad de las vacunas contra la influenza en adultos mayores. Rev Panam Salud Pública. 2005;18 447.<br />28. Egger M, Davey Smith G, Schneider M, Minder C. Bias in meta-analysis detected by a simple, graphical test. BMJ. 1997;315:629-34.<br />29. Organización Mundial de la Salud. Declaración sobre la calidad de las vacunas. Declaración de política general del Programa Mundial de Vacunas y Vacunación. Ginebra: OMS; 1997.
oai:oai.revistabiomedica.org:article/45
2009-12-19T12:04:34Z
biomedica:ARTI
Mortality by avoidable causes in preschool children
Situación de la mortalidad por causas reducibles en menores de cinco años, Colombia, 1985-2004
Lurán, Albenia
López, Elizabeth
Pinilla, Consuelo
Sierra, Pedro
mortalidad infantil
tasa de mortalidad
atención primaria de salud
diagnóstico precoz
promoción de la salud
desnutrición energética
infant mortality
mortality rate
primary health care
early diagnosis
health promotion
energy malnutrition
Introduction. The infant-mortality rate in children aged less than five is an indicator of the general state of health of a population and directly reflects the quality of life and the level of socio-economic development of a country.Objective. Avoidable mortality was assessed in preschool children as a reflection of Colombia quality of life and socio-economic development.Materials and methods. Mortality trends were analyzed in preschool children aged less than five throughout Colombia during a 20-year period from 1985-2004, and focused on mortality causes that were considered avoidable.This was a descriptive, retrospective study; the sources of information were Departamento Administrativo Nacional de Estadística records of deaths and population projections 1985-2004. Mortality rate due to avoidable causes was the statistical indicator.Results. In children aged less than one, the reducible mortality due to “early diagnosis and medical treatment” occupied the first place amongst causes for every year of the study period and accounted for more than 50% of recorded deaths. In children aged 1 to 4, the category “other important reducible causes” was associated with 40% of recorded deaths—deaths due mainly to respiratory diseases. Over the 20-year period, the avoidable mortality rate decreased by 34% in children aged less than one, in children 1-4, it decreased by 23%.Conclusions. Although the infant-mortality rate in preschool children was reduced, the decrease was small, from 80% to 77%. The situation requires more analysis with respect to strategies in public health, particularly concerning preventable diseases of the infancy.
Introducción. La tasa de mortalidad de menores de cinco años es un indicador del estado de salud de la población en general, que refleja en forma directa el nivel de vida y el grado de desarrollo de un país.Objetivo. Determinar y analizar la tendencia de la mortalidad en menores de cinco años en Colombia, entre 1985 y 2004, según causas reducibles o evitables.Materiales y métodos. Es un estudio descriptivo y retrospectivo. Las fuentes de información fueron las bases de datos de las defunciones registradas y las proyecciones de población del Departamento Administrativo Nacional de Estadística de 1985 a 2004; el indicador utilizado fue la tasa de mortalidad por causas reducibles.Resultados. En niños menores de un año, la mortalidad reducible por “diagnóstico y tratamiento médico precoz” ocupó el primer lugar en todos los años con más del 50% de las defunciones; y en los niños de uno a cuatro años, el subgrupo “otras importantes reducibles” correspondió a más del 40% de las defunciones, debido principalmente a las muertes por enfermedades del aparato respiratorio.La tasa de mortalidad por causas reducibles disminuyó en 34% en menores de un año y, en los niños de uno a cuatro años, 23%.Conclusiones. La tasa de mortalidad por causas reducibles en menores de cinco años ha disminuido. Sin embargo, entre 77% y 80% se podría reducir; situación que amerita un análisis más profundo de las estrategias utilizadas en salud pública, especialmente frente a las enfermedades prevenibles de la infancia.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/45
10.7705/biomedica.v29i1.45
Biomedica; Vol. 29 No. 1 (2009); 98-107
Biomédica; Vol. 29 Núm. 1 (2009); 98-107
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/45/46
https://revistabiomedica.org/index.php/biomedica/article/view/45/343
/*ref*/Mausner JS, Kramer S. Epidemiology. An introductory text. Segunda Edición. Philadelphia: W.B. Saunders Company; 1985.<br />2. UNICEF. Estado mundial de la infancia 2008. Supervivencia infantil: la situación actual. UNICEF, diciembre de 2007 [Fecha de consulta: mayo de 2008] Disponible: <a href="http://www.unicef.org/spanish/sowc08/docs/sowc08-sp.pdf">http://www.unicef.org/spanish/sowc08/docs/sowc08-sp.pdf</a><br />3. Silva LC, Duran E. Infant mortality and social conditions in America: a correlation analysis. Rev Saúde Pública. 1990;24:473-80.<br />4. Alcaldía Mayor de Bogotá. Política por la calidad de vida de niños, niñas y adolescentes. Bogotá 2004-2008. [Fecha de consulta: junio de 2007]. Disponible: <a href="http://www.bogota.gov.co/portel/minisites/ninosyninas">http://www.bogota.gov.co/portel/minisites/ninosyninas</a> politicainfancia.pdf<br />5. Rosero L. Determinantes del descenso de la mortalidad infantil en Costa Rica. Bol Of Sanit Panam. 1985;99:510-26.<br />6. Mora DA, Portugués CF, Sáenz I. Saneamiento, educación y su relación con los indicadores básicos de salud en el contexto mundial 2002. Rev Costarric Salud Pública. 2002;14:35-45.<br />7. Ordóñez M, Castaño L, Pinilla C, López E. La mortalidad en Colombia en el período 1982-1996. Bogotá D.C.: Instituto Nacional de Salud, Ministerio de la Protección Social; 2003.<br />8. Departamento Administrativo Nacional de Estadística. Colombia. Proyecciones quinquenales de población por sexo y edad, 1950-2050. Estudios Censales No. 1. Bogotá: DANE; 1998.<br />9. Taucher E. La mortalidad infantil en Chile. Notas de Población. 1979;7:35-72.<br />10. Gómez R. La mortalidad evitable como indicador de desempeño de la política sanitaria. Colombia 1985-2001. (Tesis de doctorado). Alicante: Programa de Doctorado de Salud Pública, Universidad de Alicante; 2006.<br />11. Chackiel J. La investigación sobre causas de muerte en América Latina. Notas de Población. 1987;44:9-30.<br />12. Organización Panamericana de la Salud. La salud en las Américas. Washington, D. C.: OPS; 2002. p. 8.<br />13. Organización Panamericana de la Salud. Estadísticas de salud de las Américas. Washington, D. C.: OPS; 2006.<br />14. Jiménez M, Del Popolo F, Bay G, Jasper-Faijer D. La reducción de la mortalidad infantil en América Latina y el Caribe: avance dispar que requiere respuestas variadas. CELADE–División de Población de la CEPAL, 19 de diciembre de 2007. [Fecha de consulta: febrero de 2008]. Disponible: http ://www.unicef.org/lac/desafios_n6_Mortalidad Infantil_Ene_08.pdf<br />15. Organización Panamericana de la Salud. Mortalidad evitable: ¿Indicador o meta? Aplicación en los países en desarrollo. Bol Epidemiol. 1990;11:1-9.<br />16. Organización Panamericana de la Salud. Mortalidad según criterios de evitabilidad. Cuba. Bol Epidemiol. 1990;11:9-14.<br />17. Riverón R, Azcuy P. Mortalidad infantil en Cuba 1959-1999. Rev Cubana Pediatr. 2001;73:143-57.<br />18. Campos TP, Carvalho MS, Barcellos CC. Mortalidade infantil no Rio de Janeiro, Brasil: áreas de risco e trajetória dos pacientes até os serviςos de sáude. Rev Panam Salud Pública. 2000:8;164-71.<br />19. UNICEF. Sala de prensa. En los últimos 5 años el país ha mejorado sus indicadores en mortalidad infantil. UNICEF. Bogotá, 13 de septiembre de 2007. [Fecha de consulta: febrero de 2008] Disponible: <a href="http://www.unicef.org/colombia/sala/prensa-sep-07.htm">http://www.unicef.org/colombia/sala/prensa-sep-07.htm</a><br />20. Organización Mundial de la Salud. Centro de prensa. La vacunación de los niños africanos contra las enfermedades neumocócicas les salva la vida. 25 de marzo de 2005. [Fecha de consulta: mayo de 2008] Disponible: <a href="http://www.who.int/mediacentre/news/statements">http://www.who.int/mediacentre/news/statements</a> /2005/s03/es/index.html21.<br />21. Ministerio de la Protección Social. Semana de la vacunación en Las Américas. Documento marco. Bogotá D.C.: Ministerio de la Protección Social; 2007.<br />22. Organización Panamericana de la Salud/Organización Mundial de la Salud. Clasificación Internacional de Enfermedades. Volumen 1. Washington, D. C.; OPS: 1975.<br />23. Organización Panamericana de la Salud/Organización Mundial de la Salud. Clasificación Estadística Internacional de Enfermedades y Problemas Relacio-nados con la Salud CIE-10. Décima revisión. Volumen 3. Washington, D. C.: OPS; 1995.
oai:oai.revistabiomedica.org:article/46
2009-12-19T12:04:34Z
biomedica:ARTI
Association between polymorphism in uncoupling proteins and type 2 diabetes in a northwestern Colombian population
Asociación de variantes en genes de las proteínas desacoplantes con diabetes mellitus tipo 2 en una población del nordeste colombiano
Franco-Hincapié, Liliana
Duque, Constanza Elena
Parra, María Victoria
Gallego, Natalia
Villegas, Alberto
Ruiz-Linares, Andrés
Bedoya, Gabriel
Diabetes mellitus/genetics
insulin resistance
obesity
polymorphism
genotype
haplotypes
diabetes mellitus/genética
resistencia a insulina
obesidad
genotipo
haplotipos
Introduction. The uncoupling proteins belong to the family of anion transporting proteins which uncouple the ATP production from the mitochondrial respiration, cause proton leakage through the inner mitochondrial membrane, and release energy as heat. Although uncoupling protein function has not been well established, specific polymorphisms in these proteins have been associated with type 2 diabetes mellitus, obesity and insulin resistance.Objective. The association was assessed between the polymorphisms in uncoupling protein genes 1, 2 and 3 genes and type 2 diabetes mellitus.Materials and methods. In a northwestern Colombian population, 545 diabetes cases and 449 controls were investigated for presence of 14 polymorphisms in uncoupling protein genes (3826A/G, ID 45, 2723T/A, 1957G/A, 866G/A, and 55C/T) by PCR and PCR-RFLP. Single associations were evaluated by chi-square test, and bayesian logistic regression analysis was done including as covariates the individual admixture estimates obtained by 54 informative markers for European, African and Amerind ancestry.Results. Association between type 2 diabetes mellitus and the polymorphisms 3826A (OR=0.78; 95%CI=0.63-0.97; p=0.02) and 55C (OR=1.41; 95%CI=1.04-1.92; p=0.03) and the haplotype D45, 866G, 1957G, 2723T, and 55C (OR=1.26; 95%CI=1.02-1.56; p=0.03) were found. These associations remained after adjustment using individual genetic admixture estimates.Conclusion. Some alleles of uncoupling protein genes 1, 2 and 3, and their haplotypes confer risk to type 2 diabetes in a northwestern Colombian population.
Introducción. Las proteínas desacoplantes pertenecen a la familia de proteínas transportadoras de aniones que desacoplan la producción de ATP de la respiración mitocondrial, causando pérdida de protones a través de la membrana mitocondrial interna y disipando la energía en forma de calor. Aunque su función no ha sido bien establecida, algunos polimorfismos en estas proteínas se han asociado con diabetes mellitus tipo 2, obesidad y resistencia a la insulina.Objetivo. Evaluar la asociación entre las variantes -3826A/G, ID 45, -2723T/A, -1957G/A, -866G/A, -55C/T de los genes de las proteínas desacoplantes 1, 2 y 3 con diabetes mellitus tipo 2 en una población del nordeste colombiano.Materiales y métodos. Se tipificaron 545 casos y 449 controles para 14 variantes de los genes de las proteínas desacoplantes por medio de PCR y PCR-RFLP. Se hicieron pruebas de asociación simples con ji al cuadrado y se corrigieron en un análisis de regresión logística bayesiana, incluyendo los estimados de mezcla individual obtenidos mediante 54 marcadores informativos de ascendencia europea, africana y amerindia.Resultados. Las variantes -3826A (OR=0,78; IC95% 0,63-0,97; p=0,02), -55C (OR=1,41; IC95% 1,04-1,92; p=0,03) de las proteínas desacoplantes 1 y 3, respectivamente, y el haplotipo D45, -866G, -1957G, -2723T, -55C (OR=1,26; IC95% 1,02-1,56; p=0,03) se asociaron con diabetes tipo 2. Estas asociaciones se conservaron después de ajustar por la mezcla genética individual.Conclusión. Algunas variantes de las proteínas desacoplantes 1, 2 y 3, y sus haplotipos, confieren riesgo para diabetes mellitus tipo 2 en una población del nordeste colombiano.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/46
10.7705/biomedica.v29i1.46
Biomedica; Vol. 29 No. 1 (2009); 108-118
Biomédica; Vol. 29 Núm. 1 (2009); 108-118
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/46/47
https://revistabiomedica.org/index.php/biomedica/article/view/46/356
/*ref*/Zimmet P, Alberti KG, Shaw J. Global and societal implica-tions of the diabetes epidemic. Nature. 2001;414:782-7.<br />2. McCarthy MI. Progress in defining the molecular basis of type 2 diabetes mellitus through susceptibility-gene identification. Hum Mol Genet. 2004;13:33-41.<br />3. Tusie Luna MT. Genes and type 2 diabetes mellitus. Arch Med Res. 2005;36:210-22.<br />4. Sokolova IM, Sokolov EP. Evolution of mitochondrial uncoupling proteins: novel invertebrate UCP homologues suggest early evolutionary divergence of the UCP family. FEBS Lett. 2005;579:313-7.<br />5. Li Y, Maedler K, Shu L, Haataja L. UCP-2 and UCP-3 proteins are differentially regulated in pancreatic beta-cells. PLoS ONE. 2008;3:e1397.<br />6. Nedergaard J, Cannon B. The ‘novel’ ‘uncoupling’ proteins UCP2 and UCP3: what do they really do? Pros and cons for suggested functions. Exp Physiol. 2003;88:65-84.<br />7. Rousset S, Alves-Guerra MC, Mozo J, Miroux B, Cassard-Doulcier AM, Bouillaud F, et al. The biology of mitochondrial uncoupling proteins. Diabetes. 2004;53 (Suppl.1):S130-5.<br />8. Pawade T, Ho PW, Kwok KH, Chu AC, Ho SL, Ramsden DB. Uncoupling proteins: targets of endocrine disruptors? Mol Cell Endocrinol. 2005;244:79-86.<br />9. Sale MM, Hsu FC, Palmer ND, Gordon CJ, Keene KL, Borgerink HM, et al. The uncoupling protein 1 gene, UCP1, is expressed in mammalian islet cells and associated with acute insulin response to glucose in African American families from the IRAS Family Study. BMC Endocr Disord. 2007;7:1.<br />10. Chan CB, Saleh MC, Koshkin V, Wheeler MB. Uncoupling protein 2 and islet function. Diabetes 2004;53 (Suppl.1):S136-42.<br />11. Hsu YH, Niu T, Song Y, Tinker L, Kuller LH, Liu S. Genetic variants in the UCP2-UCP3 gene cluster and risk of diabetes in the Women’s Health Initiative Observational Study. Diabetes. 2008;57:1101-7.<br />12. Gable DR, Stephens JW, Cooper JA, Miller GJ, Humphries SE. Variation in the UCP2-UCP3 gene cluster predicts the development of type 2 diabetes in healthy middle-aged men. Diabetes. 2006;55:1504-11.<br />13. Shin HD, Kim KS, Cha MH, Yoon Y. The effects of UCP-1 polymorphisms on obesity phenotypes among Korean female subjects. Biochem Biophys Res Commun. 2005;335:624-30.<br />14. Neel JV. Diabetes mellitus: a “thrifty” genotype rendered detrimental by “progress”? Am J Hum Genet. 1962;14:353-62.<br />15. Chakraborty R, Ferrell RE, Stern MP, Haffner SM, Hazuda HP, Rosenthal M. Relationship of prevalence of non-insulin-dependent diabetes mellitus to Amerindian admixture in the Mexican Americans of San Antonio, Texas. Genet Epidemiol. 1986;3:435-54.<br />16. Harris MI, Flegal KM, Cowie CC, Eberhardt MS, Goldstein DE, Little RR, et al. Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults. The Third National Health and Nutrition Examination Survey, 1988-1994. Diabetes Care. 1998;21:518-24.<br />17. Williams RC, Long JC, Hanson RL, Sievers ML, Knowler WC. Individual estimates of European genetic admixture associated with lower body-mass index, plasma glucose, and prevalence of type 2 diabetes in Pima Indians. Am J Hum Genet. 2000;66:527-38.<br />18. Sandoval C, De la Hoz A, Yunis E. Estructura genética de la población colombiana. Revista Facultad de Medicina Universidad Nacional de Colombia. 1993;41:3-14.<br />19. Bedoya G, Montoya P, García J, Soto I, Bourgeois S, Carvajal L, et al. Admixture dynamics in Hispanics: a shift in the nuclear genetic ancestry of a South American population isolate. Proc Natl Acad Sci USA. 2006;103:7234-9.<br />20. Gower BA, Fernández JR, Beasley TM, Shriver MD, Goran MI. Using genetic admixture to explain racial differences in insulin-related phenotypes. Diabetes. 2003;52:1047-51.<br />21. Hoggart CJ, Parra EJ, Shriver MD, Bonilla C, Kittles RA, Clayton DG, et al. Control of confounding of genetic associations in stratified populations. Am J Hum Genet. 2003;72:1492-504.<br />22. Parra EJ, Hoggart CJ, Bonilla C, Dios S, Norris JM, Marshall JA, et al. Relation of type 2 diabetes to individual admixture and candidate gene polymorphisms in the Hispanic American population of San Luis Valley, Colorado. J Med Genet. 2004;41:e116.<br />23. The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus Diabetes Care. 2002;25.<br />24. Bedoya G, García J, Montoya P, Rojas W, Amézquita ME, Soto I, et al. Análisis de isonimia entre poblaciones del noroeste de Colombia. Biomédica. 2006;26:538-45.<br />25. Shriver MD, Smith MW, Jin L, Marcini A, Akey JM, Deka R, et al. Ethnic-affiliation estimation by use of population-specific DNA markers. Am J Hum Genet. 1997;60:957-64.<br />26. Raymond M, Rousset F. GENEPOP (version 1.2): population genetics software for exact tests and ecumenicism. J Hered. 1995;86.<br />27. Schneider S, Roessli D, Excoffier L. Arlequin: A software for population genetics data analysis. Versión 2000. Ginebra: Laboratorio de Genética y Biometría, Departamento de Antropología, Universidad de Ginebra; 2000.<br />28. McKeigue PM, Carpenter JR, Parra EJ, Shriver MD. Estimation of admixture and detection of linkage in admixed populations by a Bayesian approach: application to African-American populations. Ann Hum Genet. 2000;64:171-86.<br />29. Nagai N, Sakane N, Ueno LM, Hamada T, Moritani T. The -3826 A-->G variant of the uncoupling protein-1 gene diminishes postprandial thermogenesis after a high fat meal in healthy boys. J Clin Endocrinol Metab. 2003;88:5661-7.<br />30. Forga L, Corbalan M, Marti A, Fuentes C, Martínez-González MA, Martínez A. Influencia del polimorfismo -3826 A Æ G en el gen de la UCP1 sobre los componentes del síndrome metabólico. An Sist Sanit Navar. 2003;26:231-6.<br />31. Heilbronn LK, Kind KL, Pancewicz E, Morris AM, Noakes M, Clifton PM. Association of -3826 G variant in uncoupling protein-1 with increased BMI in overweight Australian women. Diabetologia. 2000;43:242-4.<br />32. Kim KS, Cho DY, Kim YJ, Choi SM, Kim JY, Shin SU, et al. The finding of new genetic polymorphism of UCP-1 A-1766G and its effects on body fat accumulation. Biochim Biophys Acta. 2005;1741:149-55.<br />33. Salopuro T, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H, Ilanne-Parikka P, et al. Common variants in beta2- and beta3-adrenergic receptor genes and uncoupling protein 1 as predictors of the risk for type 2 diabetes and body weight changes. The Finnish Diabetes Prevention Study. Clin Genet. 2004;66:365-7.<br />34. Esterbauer H, Oberkofler H, Liu YM, Breban D, Hell E, Krempler F, et al. Uncoupling protein-1 mRNA expression in obese human subjects: the role of sequence variations at the uncoupling protein-1 gene locus. J Lipid Res. 1998;39:834-44.<br />35. Nakazaki M, Kakei M, Ishihara H, Koriyama N, Hashiguchi H, Aso K, et al. Association of upregulated activity of K(ATP) channels with impaired insulin secretion in UCP1-expressing insulinoma cells. J Physiol. 2002;540:781-9.<br />36. Bernal-Mizrachi C, Weng S, Li B, Nolte LA, Feng C, Coleman T, et al. Respiratory uncoupling lowers blood pressure through a leptin-dependent mechanism in genetically obese mice. Arterioscler Thromb Vasc Biol. 2002;22:961-8.<br />37. Carroll AM, Porter RK. Starvation-sensitive UCP 3 protein expression in thymus and spleen mitochondria. Biochim Biophys Acta. 2004;1700:145-50.<br />38. Lengacher S, Magistretti PJ, Pellerin L. Quantitative rt-PCR analysis of uncoupling protein isoforms in mouse brain cortex: methodological optimization and comparison of expression with brown adipose tissue and skeletal muscle. J Cereb Blood Flow Metab. 2004;24:780-8.<br />39. Moulin K, Arnaud E, Nibbelink M, Viguerie-Bascands N, Penicaud L, Casteilla L. Cloning of BUG demonstrates the existence of a brown preadipocyte distinct from a white one. Int J Obes Relat Metab Disord. 2001;25:1431-41.<br />40. Villarroya F, Iglesias R, Giralt M. PPARs in the control of uncoupling proteins gene expression. PPAR Res. 2007;2007:74364.<br />41. Meirhaeghe A, Amouyel P, Helbecque N, Cottel D, Otabe S, Froguel P, et al. An uncoupling protein 3 gene polymorphism associated with a lower risk of developing type II diabetes and with atherogenic lipid profile in a French cohort. Diabetologia. 2000;43:1424-8.<br />42. Damcott CM, Feingold E, Moffett SP, Barmada MM, Marshall JA, Hamman RF, et al. Genetic variation in uncoupling protein 3 is associated with dietary intake and body composition in females. Metabolism. 2004;53:458-64.<br />43. Schrauwen P, Xia J, Walder K, Snitker S, Ravussin E. A novel polymorphism in the proximal UCP3 promoter region: effect on skeletal muscle UCP3 mRNA expression and obesity in male non-diabetic Pima Indians. Int J Obes Relat Metab Disord. 1999;23:1242-5.<br />44. Krook A, Digby J, O’Rahilly S, Zierath JR, Wallberg-Henriksson H. Uncoupling protein 3 is reduced in skeletal muscle of NIDDM patients. Diabetes. 1998;47:1528-31.<br />45. Clapham JC, Arch JR, Chapman H, Haynes A, Lister C, Moore GB, et al. Mice overexpressing human uncoupling protein-3 in skeletal muscle are hyperphagic and lean. Nature. 2000;406:415-8.<br />46. Choi CS, Fillmore JJ, Kim JK, Liu ZX, Kim S, Collier EF, et al. Overexpression of uncoupling protein 3 in skeletal muscle protects against fat-induced insulin resistance. J Clin Invest. 2007;117:1995-2003.<br />47. Esterbauer H, Schneitler C, Oberkofler H, Ebenbichler C, Paulweber B, Sandhofer F, et al. A common polymorphism in the promoter of UCP2 is associated with decreased risk of obesity in middle-aged humans. Nat Genet. 2001;28:178-83.<br />48. Ochoa MC, Santos JL, Azcona C, Moreno-Aliaga MJ, Martínez-González MA, Martínez JA, et al. Association between obesity and insulin resistance with UCP2-UCP3 gene variants in Spanish children and adolescents. Mol Genet Metab. 2007;92:351-8.<br />49. Aschner P, King H, Triana de Torrado M, Rodríguez BM. Glucose intolerance in Colombia. A population-based survey in an urban community. Diabetes Care. 1993;16:90-3.<br />50. Mejía S, Vélez A, Buriticá O, Arango M, Del-Río J. La política farmacéutica nacional en Colombia y la reforma de la seguridad social: acceso y uso racional de medicamentos. Cad Saude Publica. 2002;18:1025-39.<br />51. Qi L, Hu FB, Hu G. Genes, environment, and interactions in prevention of type 2 diabetes: a focus on physical activity and lifestyle changes. Curr Mol Med. 2008;8:519-32.<br />52. Colditz GA, Willett WC, Rotnitzky A, Manson JE. Weight gain as a risk factor for clinical diabetes mellitus in women. Ann Intern Med. 1995;122:481-6.<br />53. Leahy JL. Pathogenesis of type 2 diabetes mellitus. Arch Med Res. 2005;36:197-209.<br />54. Rothman KJ, Greenland S. Modern Epidemiology. Second edition. Filadelfia, EU: Lippincott-Raven; 1998.<br />55. Cheurfa N, Dubois-Laforgue D, Ferrarezi DA, Reis AF, Brenner GM, Bouche C, et al. The common -866G>A variant in the promoter of UCP2 is associated with decreased risk of coronary artery disease in type 2 diabetic men. Diabetes. 2008;57:1063-8.
oai:oai.revistabiomedica.org:article/47
2009-12-19T12:04:34Z
biomedica:ARTI
Life cycle of Triatoma dimidiata Latreille, 1811 (Hemiptera, Reduviidae) under laboratory conditions: production of nymphs for biological tests
Ciclo de vida de Triatoma dimidiata Latreille, 1811 (Hemiptera, Reduviidae) en condiciones de laboratorio: producción de ninfas para ensayos biológicos
Reyes, Marlene
Angulo, Víctor Manuel
Triatominae
triatoma
etapas del ciclo de vida
enfermedad de Chagas
Colombia
Triatominae
triatoma
life cycle stages
Chagas disease
Colombia
Introduction. Despite the importance of Triatoma dimidiata as a vector of Chagas disease, little is known of its life cycle and the efficient production of these insects for biological tests.Objective. Life cycle characteristics in the laboratory were described and optimum nutritional conditions were established for the efficient production of nymphs V stage for biological tests.Materials and methods. We determined the time of development of the nymphal stage under controlled laboratory conditions until reaching the adult stage. In a massive rearing of stage V nymphs, fed and weighted after varying periods of fasting, distributed in weight ranges to obtain the largest proportion of individuals.Results. The time mean from egg to adult was 269 days, with a wide range of duration (174 to 598 days) and the times required for 1st, 2nd, 3rd, 4th and 5th stage development was 33, 37, 41, 61 and 69 days, respectively, with a mortality of 22%. The optimum treatment was 22 days of fasting, in which 76% of the nymphs reached stage V with a weight range from 201 to 300 mg.Conclusion. Triatoma dimidiata presented development time with broad range for some individuals, possibly due to the irregularity in the food availability. A homogenous weight range was attained with a regime of 22 days of fasting with an optimum production of stage V nymphs.Production of similarly sized insects facilitate the application of standardized protocols to establish criteria for selecting compounds insecticides used in control programs.
Introducción. A pesar de la importancia de Triatoma dimidiata como vector de la enfermedad de Chagas, poco se conoce de su ciclo biológico y de la producción eficiente de insectos disponibles para ensayos biológicos.Objetivo. Determinar las características del ciclo de vida en el laboratorio y establecer las condiciones del estado nutricional para la producción eficiente de ninfas de V estadio para ensayos biológicos.Materiales y métodos. Se determinaron los tiempos de desarrollo de los estadios de ninfa en condiciones controladas de laboratorio hasta alcanzar la fase adulta. Se llevó a cabo una cría masiva de ninfas de V estadio, alimentadas y pesadas después de diferentes periodos de ayuno, distribuidas en rangos de peso para obtener la mayor proporción de individuos.Resultados. El tiempo medio de paso de huevo a adulto fue de 269 días, con un amplio rango de duración (174 a 598 días) y, para los estadios I, II, II, IV y V, fue de 33, 37, 41, 61 y 69 días, respectivamente, con una mortalidad de 22%. Se obtuvo una eficiencia de 76% en ninfas de V estadio, alimentadas después de 22 días de ayuno, en el rango de 201 a 300 mg de peso.Conclusión. T. dimidiata presentó un tiempo de desarrollo intermedio entre los triatominos con amplio rango para algunos individuos, posiblemente debido a la irregularidad en su alimentación. La identificación de un rango de peso homogéneo después de 22 días de ayuno con gran producción de ninfas de V estadio, facilita la aplicación de protocolos estandarizados para establecer criterios de selección de compuestos insecticidas utilizables en los programas de control.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/47
10.7705/biomedica.v29i1.47
Biomedica; Vol. 29 No. 1 (2009); 119-126
Biomédica; Vol. 29 Núm. 1 (2009); 119-126
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/47/48
https://revistabiomedica.org/index.php/biomedica/article/view/47/357
/*ref*/Moncayo A. Chagas disease: Current epidemiological trends after the interruption of vectorial and transfusional transmission in the Southern Cone Countries. Mem Inst Oswaldo Cruz. 2003;98:577-91.<br />2. Guhl F, Angulo V, Restrepo M, Nicholls S, Montoya R. Estado del arte de la enfermedad de Chagas en Colombia y estrategias de control. Biomédica. 2003;23:31-4.<br />3. Molina JA, Gualdrón LE, Brochero LH, Olano VA, Barrios D, Guhl F. Distribución actual e importancia epidemiológica de las especies de triatominos (Reduviidae: Triatominae) en Colombia. Biomédica. 2000;20:344-60.<br />4. Guhl F, Vallejo GA. Interruption of Chagas disease transmission in the Andean countries: Colombia. Mem Inst Oswaldo Cruz. 1999;94:413-5.<br />5. Christensen AH, Sousa EO, Vasquez AM. Host feeding profiles of Triatoma dimidiata in peridomestic habitats of Western Panama. Am J Trop Med Hyg. 1988;38:477-9.<br />6. Calderón AO, Chinchilla M, García F, Vargas M. Preferencias alimentarias de Triatoma dimidiata (Hemiptera: Reduviidae) procedente de la meseta central de Costa Rica a finales del siglo XX. Parasitología al Día. 2001;25:3-4.<br />7. Zeledón R, Solano G, Zúñiga A, Swartzwelder JC. Biology and ethology of Triatoma dimidiata (Latreille, 1811) II. Habitats and blood sources. J Med Entomol. 1973;10:363-70.<br />8. Zeledón R, Calvo N, Montenegro V, Seixas L E, Arévalo C. A survey on Triatoma dimidiata in an urban area of the province of Heredia, Costa Rica Rio de Janeiro. Mem Inst Oswaldo Cruz. 2005;100:607-12.<br />9. Angulo VM. Comportamiento de Triatoma dimidiata: Un reto para su control. Biomédica. 2005;25:80-3.<br />10. Zeledón R, Guardia VM, Zúñiga A, Swartzwelder JC. Biology and ethology of Triatoma dimidiata (Latreille, 1811). I: Life cycle, amount of blood ingested, resistance to starvation and size of adults. J Med Entomol. 1970;7:313-9.<br />11. World Health Organization. Control of Chagas disease. Second report of the WHO Expert Committee. Technical report 2002. Series 905. Geneva: WHO; 2002. p. 39-40.<br />12. Fontán A, Zerba EN. Influence of the nutritional state of Triatoma infestans over the insecticidal activity of DDT. Comp Biochem Physiol C. 1992;101:589-91.<br />13. Rojas A, Lehane MJ, Schofield CJ, Fournet A. Comparative evaluation of pyrethroid insecticide formulations against Triatoma infestans (Klug): Residual efficacy on four substrates. Mem Inst Oswaldo Cruz. 2003;98:975-80.<br />14. Reyes M, Angulo VM, Sandoval CM. Efecto tóxico de ß-cipermetrina, deltametrina y fenitrotión en cepas de Triatoma dimidiata (Latreille, 1811) y Triatoma maculata (Erichson, 1848) (Hemiptera, Reduviidae). Biomédica. 2007;27(Suppl.1):75-82.<br />15. Oliveira Filho AM. Differences of susceptibility of five triatomine species to pyrethroid insecticides: implications for Chagas’ disease vector control. Mem Inst Oswaldo Cruz.1999;94:425-8.<br />16. Wood E, Picollo MI, Zerba E. Comparación entre la variación de la capacidad detoxificante y la diferente susceptibilidad al insecticida malatión entre ninfas V de distinta edad de Triatoma infestans. Rev Asoc Med Arg.1993;81:153-62.<br />17. Fontán A, Zerba E. Mode of entry of insecticides in Triatoma infestans. Arch Insect Biochem Physiol. 1987;43:13-323.<br />18. Nelson MJ. Experiencias en el monitoreo de niveles de susceptibilidad de los triatominos a los insecticidas en las Américas. Acta Toxicol Arg. 1994;2:29-58.<br />19. World Health Organization. Protocolo de evaluación de efecto insecticida sobre triatominos. Acta Tóxico Arg. 1994;2:29-32.<br />20. Fontán A, Zerba EN. Influence of the nutritional state of Triatoma infestans over the insecticidal activity of DDT. Comp Biochem Physiol C. 1992;101:589-91.<br />21. Paz RR. Ciclo de vida y datos biométricos de Triatoma Longipennis (Usinger) (Hemiptera: Reduviidae,Triatominae) (tesis). Ciudad de México: Universidad Nacional Autónoma de México; 1996. p. 96.<br />22. Otálora B. Triatoma dimidiata (Latreille). Anal Soc Biol Bogotá. 1952;5:135-7.<br />23. Hernández MC. Infección natural Triatoma capitata Usinger, 1939 por el Trypanosoma cruzi. Rev Fac Med Unal. 1947;15:465-76.<br />24. Canale MD, Jurberg J, Carcavallo UR, Galvao C, Mena SC, Silva RD, et al. Bionomics of some species. In: Carcavallo UR, Galindez GI, Jurberg J, Lent H, editores. Atlas of Chagas disease vectors in the Américas. Volumen III. Río de Janeiro: Fiocruz-Inc; 1999. p. 839-90.<br />25. Martínez JA, Gala KD. Biology of Triatoma pallidipennis Stal 1945 (Hemiptera: Reduviidae: Triatominae) under laboratory conditions. Mem Inst Oswaldo Cruz. 1999;94:837-9.<br />26. Rabinovich JE. Vital statistics of Triatominae (Hemiptera: Reduviidae) under laboratory conditions. I. Triatoma infestans Klug. J Med Entomol. 1972;9:351-70.<br />27. Moura JF, Vargas A, Almeida E, Esperança G, Souza R, Ramos E, et al. A Triatoma maculata (Hemiptera, Reduviidae, Triatominae) population from Roraima, Amazon region, Brazil, has some bionomic characteristics of a potential Chagas’ disease vector. Rev Inst Med Trop Sao Paulo. 2005;47:131-7.<br />28. Feliciangeli MD, Rabinovich JE. Vital statistics of Triatominae (Hemiptera: Reduviidae) under laboratory condition. J Med Entomol.1985;22:43-8.<br />29. Malo EA, Ramírez RA, Cruz L, Rojas J. Lyfe cycle and influence of age and feeding on the first mating of Triatoma mazoottii (Hemiptera:Reduviidae) Mem Inst Oswaldo Cruz. 1993;88:203-6.<br />30. Arévalo A, Carranza J, Guhl F, Clavijo J, Vallejo G. Comparación del ciclo de vida de Rhodnius colombiensis Moreno, (Jurberg & Galvao,1999) y Rhodnius prolixus (Stal,1872) (Hemiptera, Reduviidae, Triatominae) en condiciones de laboratorio. Biomédica. 2007;27(Suppl.1):119-29.<br />31. Carcavallo UR, Mena SC,Canale MD. Ciclo de vida de Triatoma lenti Sherlock, Serafim,1967 (Hemiptera, Reduviidae, Triatominae). Entomología y Vectores. 1994;1:43-9.<br />32. Dorn P, Monrroy C, Curtis A. Triatoma dimidiata (Latreille, 1811): A review of its diversity across its geographic range and the relationship among populations. Infect Genet Evol. 2007;7:343-52.<br />33. Bargues M, Klisiowicz D, Gonzalez F, Ramsey J, Monroy C, Ponce C, et al. Phylogeography and genetic variation of Triatoma dimidiata, the main Chagas’ disease vector in Central America, and its position within the genus triatoma. PLoS Negl Trop Dis. 2008;2:1-19.<br />34. Arroyo CM, Esteban L, Catalá S, Angulo VM. Variación del fenotipo antenal de poblaciones del domicilio, peridomicilio y silvestres de Triatoma dimidiata (Hemiptera: Reduviidae) en Santander, Colombia. Biomédica. 2007;27(Suppl.1):92-100.<br />35. Zeledón R. El Triatoma dimidiata (Latreille,1811) y su relación con la enfermedad de Chagas. San José: Editorial EUNED; 1981. p .146.<br />36. Friend WG, Smith JJ. Fisiología de los triatominos con especial referencia a la alimentación por sangre. En: Carcavallo RU, Rabinovich JE, Tonn RJ, editores. Factores biológicos y ecológicos en la enfermedad de Chagas. Tomo I. Epidemiología-vectores. Washington: OPS/OMS; 1985. p. 55-81.<br />37. Zeledón R, Alvarado R, Jirón LF. Observations on the feeding and defecation patterns of three triatomine species (Hemiptera: Reduviidae) Acta trop. 1977;34:65-77.<br />38. Canale D,Carcavallo RU. Triatoma infestans (Klug). En: Carcavallo RU, Rabinovich JE, Tonn RJ, editores. Factores biológicos y ecológicos en la enfermedad de Chagas. Tomo I. Epidemiología -vectores. Washington, D.C.: OPS/OMS; 1985. p. 237-50.<br />39. Carcavallo RU, Tonn R. Rhodnius prolixus (Stal). En: Carcavallo RU, Rabinovich JE, Tonn RJ, editores. Factores biológicos y ecológicos en la enfermedad de Chagas. Tomo I. Epidemiología -vectores. Washington, D.C.: OPS/OMS; 1985. p. 209-17.<br />40. Angulo VM. Ensayo de estrategias de control y vigilancia de Triatoma dimidiata en Colombia. En: Guhl F, editor. Primer Taller Internacional sobre Control de la Enfermedad de Chagas; Curso de Diagnóstico, Manejo y Tratamiento de la Enfermedad de Chagas; VI Reunión de la Iniciativa Andina para el Control de la Enfermedad de Chagas. Bogotá, D.C.: Ediciones Uniandes; 2005. p. 91-102.<br />41. Zeledón AR, Guardia VM, Zúñiga A, Swartzwelder JC. Biology and ethology of Triatoma dimidiata (Latreille, 1811) II. Life span of adults and fecundity and fertility of females. J Med Entomol.1970;7:462-9.<br />42. Zeledón R. Triatoma dimidiata (Latreille, 1811). En: Carcavallo RU, Rabinovich JE, Tonn RJ, editores. Factores biológicos y ecológicos en la enfermedad de Chagas. Tomo I. Epidemiología-vectores. Washington, D.C.: OPS/OMS; 1985. p. 225-36.<br />43. Zeledón R, Montenegro VM, Zeledón O. Evidence of colonization of man-made ecotopes by Triatoma dimidiata (Latreille,1811) in Costa Rica. Mem Inst Oswaldo Cruz. 2001;96:659-60.
oai:oai.revistabiomedica.org:article/48
2009-12-19T12:04:34Z
biomedica:BREV
Epidemiological analysis of patients coinfected with Chagas disease and cysticercosis
Análisis epidemiológico de pacientes coinfectados con enfermedad de Chagas y cisticercosis
Guimaraes, Ana Carolina
Lino-Junior, Ruy
Lima, Virlanea
Cavellani, Camila
Corrêa, Rosana Rosa
Llaguno, Mauricio
Reis, Marlene
Teixeira, Vicente
enfermedad de Chagas/epidemiología
cisticercosis
infección
supervivencia
autopsia
Chagas disease/epidemiology
cysticercosis
infection
survivorship (Public health)
autopsy
Introduction. Among inhabitants of endemic areas in the developing world, infection with the larva of Taenia solium (cysticercosis) may possibly induce a state of immunosuppression in the host, thereby increasing the risk of multiple infections after exposure to other parasites, such as Trypanosoma cruzi.Objective. Increase in the epidemiological occurrence of infection was assessed for Trypanosoma cruzi (Chagas disease) in patients with cysticercosis.Materials and methods. At the University Hospital in Uberaba, Minas Gerais, Brazil, data were obtained from autopsies performed between 1970-2004 on 1,501 subjects older than 15 years of age. Cases were divided into four groups: (1) no infection, (2) cysticercosis only, (3) Chagas disease only, and (4) cysticercosis coinfected with Chagas disease. Race, gender and age data were analyzed.Results. More than half of the cases showed no infection (848 cases or 56.5%); Chagas disease was found in 611 patients (40.7%); 72 cases (4.8% of the autopsies) had cysticercosis and 30 of them (41.7%) were co-infected with Chagas disease. White race and male gender were predominant in all groups. The youngest median age was found in the non-infected group (46 years), followed by those with Chagas disease without cysticercosis (49 years) and those coinfected with cysticercosis and Chagas disease (57.5 years).Conclusion. Presumably, all patients had a similar exposure to both parasites. However, in this study population, Chagas disease was approximately 10 times more frequent in patients co-infected with cysticercosis.
Introducción. Se ha sugerido que la infección por larvas de Taenia solium (cisticercosis) podría inducir un estado de inmunosupresión en el huésped, aumentando el riesgo de adquirir infecciones múltiples después de estar expuesto a otros parásitos, entre ellos Trypanosoma cruzi, particularmente entre habitantes de áreas endémicas en países en desarrollo.Objetivos. Evaluar un posible aumento en la presentación endémica de infección por T. cruzi (enfermedad de Chagas) en pacientes con cisticercosis.Materiales y métodos. Se estudiaron 1.501 autopsias de individuos mayores de 15 años de edad del Hospital Universitario de Uberaba, Minas Gerais, Brasil, 1970-2004. Se dividieron los casos en cuatro grupos: (1) sin infección, (2) con cisticercosis, (3) con enfermedad de Chagas y (4) coinfectados con cisticercosis y enfermedad de Chagas. Se analizaron las variables de raza, sexo y edad.Resultados. Más de la mitad de todos los casos no presentaban infección (848 casos o 56,5%); 611 pacientes (40,7%) tenían enfermedad de Chagas; 72 casos (4,8% de las autopsias) tenían cisticercosis y 30 (41,7%) presentaron coinfección de cisticercosis con enfermedad de Chagas. La raza blanca y el sexo masculino fueron predominantes en todos los grupos. La mediana de edad más joven fue encontrada en el grupo sin infección (46 años), seguido por aquéllos que presentaban enfermedad de Chagas (49 años) y por aquéllos con coinfección de cisticercosis y enfermedad de Chagas (57,5 años).Conclusión. En teoría, todos los pacientes tuvieron un riesgo similar de exposición para ambos parásitos. Sin embargo, este trabajo demuestra que, en la población estudiada, la enfermedad de Chagas fue, aproximadamente, 10 veces más frecuente en los casos coinfectados con cisticercosis.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/48
10.7705/biomedica.v29i1.48
Biomedica; Vol. 29 No. 1 (2009); 127-132
Biomédica; Vol. 29 Núm. 1 (2009); 127-132
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/48/49
https://revistabiomedica.org/index.php/biomedica/article/view/48/358
/*ref*/Maizels RM, Bundy DA, Selkirk ME, Smith DF, Anderson RM. Immunological modulation and evasion by helminth parasites in human population. Nature. 1993;365:797-805.<br />2. Rodriguez M, Terrazas LI, Márquez R, Bojalil R. Susceptibility to Trypanosoma cruzi is modified by a previous non-related infection. Parasite lmmunol. 1999;21:177-85.<br />3. Muniz-Junqueira MI, Tavares-Neto J, Prata A, Tosta CE. Antibody response to Salmonella typhi in human schistosomiasis mansoni. Rev Soc Bras Med Trop. 1996;29:441-5.<br />4. Booth M, Vennervald BJ, Butterworth AE, Kariuki HC, Amaganga C, Kimani G, et al. Exposure to malaria affects the regression of hepatosplenomegaly after treatment for Schistosoma mansoni infection in Kenyan children. BMC Med. 2004;2:36.<br />5. Nacher M, Gay F, Singhasivanon P, Krudsood S, Treeprasertsuk S, Mazier D, et al. Ascaris lumbricoides infection is associated with protection from cerebral malaria. Parasite Immunol. 2000;22:107-13.<br />6. Fagbeni BO, Christensen NO, Nansen P. Supression of Babesia microti infection in mice concurrently infected with Fasciola hepatica. Vet Parasitol. 1985;17:101-10.<br />7. Del Brutto OH, Castillo PR, Mena IX, Freire AX. Neurocysticercosis among patients with cerebral gliomas. Arch Neurol. 1997;54:1125-8.<br />8. Herrera LA, Benita-Bordes A, Sotelo J, Chávez L, Olvera J, Rascón A, et al. Possible relationship between neurocysticercosis and hematological malignancies. Arch Med Res. 1999;30:154-8.<br />9. Handique SK, Das RR, Saharia B, Das P, Buragohain R, Saikia P. Coinfection of Japanese encephalitis with neurocysticercosis: an imaging study. Am J Neuroradiol. 2008;29:170-5.<br />10. Carod-Artal FJ. Strokes caused by infection in the tropics. Rev Neurol. 2007;44:755-63.<br />11. Santo AH. Cysticercosis-related mortality in the State of São Paulo, Brazil, 1985-2004: a study using multiple causes of death. Cad Saude Publica. 2007;23:2917-27.<br />12. Delobel P, Signate A, El Guedj M, Couppie P, Gueye M, Smadja D, et al. Unusual form of neurocysticercosis associated with HIV infection. Eur J Neurol. 2004;11:55-8.<br />13. Sotelo J, Del Brutto OH. Brain cysticercosis. Arch Med Res. 2000;31:3-14.<br />14. Prata A. Chagas’ disease. Infect Dis Clin North Am. 1994;8:61-76.<br />15. Yoshida N. Molecular basis of mammalian cell invasion by Trypanosoma cruzi. An Acad Bras Ciênc. 2006;78:87-111.<br />16. Cardillo F, Voltarelli JC, Reed SG, Silva JS. Regulation of Trypanosoma cruzi infection in mice by gamma interferon and interleukin 10: role of NK cells. Infect Immun. 1996;64:128-34.<br />17. Del Brutto OH, Wadia NH, Dumas M, Cruz M, Tsang VC, Schantz PM. Proposal of diagnostic criteria for human cysticercosis and neurocysticercosis. J Neurol Sci. 1996;142:1-6.<br />18. Lino RS Jr, Reis MA, Teixeira VP. Occurrence of encephalic and cardiac cysticercosis (Cysticercus cellulosae) in necropsy. Rev Saude Publica. 1999; 33: 495-8.<br />19. Ramirez LE, Machado MI, Maywald PG, Matos A, Chiari E, Silva EL. Primeira evidência de Trypanosoma rangeli no sudeste do Brasil, região endêmica para doença de Chagas. Rev Soc Bras Med Trop. 1998;31:99-102.<br />20. Gobbi H, Adad SJ, Neves RR, Almeida HO. Ocorrência de cisticercose (Cysticercus Cellulosae) em pacientes necropsiados em Uberaba, MG. Rev Patol Trop. 1980;9:51-9.<br />21. Del Brutto OH, Sotelo J. Neurocysticercosis: an update. Rev Infect Dis. 1988;10:1075-87.<br />22. Dias E, Laranja FS, Miranda A, Nobrega G. Chagas’ disease; a clinical epidemiologic and pathologic study. Circulation. 1956;14:1035-60.<br />23. Arechavaleta F, Molinari JL, Tato P. A Taenia solium metacestode factor nonspecifically inhibits cytokine production. Parasitol Res. 1998;84:117-22.<br />24. Sher A, Coffman RL. Regulation of immunity to parasites by T cells and T cell-derived cytokines. Annu Rev Immunol. 1992;10:385-409.<br />25. Belardelli F. Role of interferons and other cytokines in the regulation of the immune response. APMIS. 1995;10:161-79.<br />26. Kierszenbaum F, Sztein MB. Mechanisms underlying immunosuppression induced by Trypanosoma cruzi. Parasitol Today. 1990;6:261-4.<br />27. Kierszenbaum F, Moretti E, Sztein MB. Molecular basis of Trypanosoma cruzi-induced immunosuppression. Altered expression by activated human lymphocytes of molecules which regulate antigen recognition and progression through the cell cycle. Biol Res. 1993;26:197-207.<br />28. Sztein MB, Kierszenbaum F. Mechanisms of development of immunosuppression during Trypanosoma infections. Parasitol Today. 1993;9:424-8.<br />
oai:oai.revistabiomedica.org:article/49
2009-12-19T12:04:34Z
biomedica:BREV
Prevalence of autoantibodies against autonomic receptors in patients with chronic cardiopathies
Prevalencia de autoanticuerpos contra receptores autonómicos en pacientes panameños con cardiopatía chagásica crónica y con otras formas de cardiopatía
Saldaña, Azael
Calzada, José E.
Garisto, Juan
Zebedes, Salomón
Samudio, Franklyn E.
Blandón, Roberto
Avilés, Óscar
enfermedad de Chagas
cardiomiopatía chagásica
autoanticuerpos
receptores beta-adrenérgicos
receptores muscarínicos
Panamá
Chagas disease
Chagas cardiomyopathy
autoantibodies
receptors
adrenergic
beta
muscarinic
Panamá
Introduction. Chagas´ disease is the main cause of chronic myocardiopathy in Central America. The mechanisms proposed for this cardiac pathology during the chronic phase remain controversial. Several studies have detected the presence of circulating autoantibodies against β-adrenergic and cholinergic muscarinic receptors of the myocardium in patients with Chagas disease. These autoantibodies can trigger intracellular signals and modify the cardiac function during the progression of the disease.Objectives. The serological frequency of these autoantibodies was compared among patients with chronic Chagas disease, patients with other cardiopathies and healthy controls.Materials and methods. The prevalence of autoantibodies against β-adrenergic and cholinergic muscarinic receptors was determined in four groups of Panamenian patients: 53 chagasic patients, 25 serologically negative patients with cardiac insufficiency, 25 patients with cardiac arrhythmia and 25 healthy individuals.Results. The antibodies against autonomic receptors were more frequently observed in patients with chronic chagasic cardiomyopathy (24.5%) compared to the cardiac insufficiency group (20.0%) and the cardiac arrhythmia group (16.0%). The proportion of autoantibodies was significantly different between the groups with chronic chagasic cardiomyopathy and healthy controls (24.5% versus 0%; p=0.015). Of the 53 chronically infected chagasic patients, 48 (90%) showed some degree of cardiac dysfunction.Conclusions. The frequency of autoantibodies against autonomic receptors is significantly increased in patients with chronic Chagas disease and in patients with other cardiopathies.
Introducción. La enfermedad de Chagas es la principal causa de cardiomiopatía crónica en Centroamérica. Existe controversia sobre los mecanismos causantes de la patología cardiaca observada durante la fase crónica de esta parasitosis. Varios estudios han detectado la presencia de autoanticuerpos circulantes dirigidos contra receptores beta-adrenérgicos y colinérgicos muscarínicos del miocardio en pacientes chagásicos, que pueden desencadenar señales intracelulares y alterar la función cardiaca durante el curso de la enfermedad.Objetivo. Nuestro objetivo principal fue comparar la frecuencia sérica de estos autoanticuerpos en pacientes chagásicos crónicos con la observada en pacientes con otras formas de cardiopatía y en controles sanos.Materiales y métodos. Se determinó la prevalencia de autoanticuerpos contra receptores beta-adrenérgicos y colinérgicos muscarínicos en cuatro grupos de pacientes panamelos: 53 pacientes chagásicos, 25 pacientes seronegativos con insuficiencia cardiaca, 25 pacientes con diferentes tipos de arritmia cardiaca y 25 controles sanos.Resultados. Los autoanticuerpos contra receptores autonómicos fueron más frecuentes en el grupo de pacientes con cardiopatía chagásica crónica (24,5%) comparados con el grupo de insuficiencia cardiaca (20,0%) y con el grupo con arritmias cardiacas (16,0%). Al comparar la proporción de autoanticuerpos entre el grupo de pacientes con cardiopatía chagásica crónica y los controles sanos, se detectaron diferencias muy significativas (24,5% versus 0%; p=0,0015). De los 53 pacientes con infección crónica, 48 (90,6%) presentaron algún grado de alteración cardiaca.Conclusiones. En comparación con el grupo de controles sanos, la frecuencia de los autoanticuerpos contra receptores autonómicos se encuentra significativamente aumentada en pacientes con enfermedad de Chagas crónica y con otras formas de cardiopatía.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/49
10.7705/biomedica.v29i1.49
Biomedica; Vol. 29 No. 1 (2009); 133-139
Biomédica; Vol. 29 Núm. 1 (2009); 133-139
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/49/50
https://revistabiomedica.org/index.php/biomedica/article/view/49/359
/*ref*/<p>1. Devera R, Fernandes O, Coura JR. Should Trypanosoma cruzi be called “cruzi” complex? A review of the parasite diversity and the potential of selecting population after in vitro culturing and mice infection. Mem Inst Oswaldo Cruz. 2003;98:1-12<br />2. Engman DM, Leon JS. Pathogenesis of Chagas heart disease: role of autoimmunity. Acta Trop. 2002;81:123-32.<br />3. Moncayo A. Chagas disease: current epidemiological trends after the interruption of vectorial and transfusional transmission in the Southern Cone countries. Mem Inst Oswaldo Cruz. 2003;98:577-91.<br />4. Sousa OE. Anotaciones sobre la enfermedad de Chagas en Panamá. Frecuencia y distribución de Trypanosoma cruzi y Trypanosoma rangeli. Rev Biol Trop. 1972;20:167-9.<br />5. Nuñez JM. Enfermedad de Chagas: datos pertinentes y revisión de casos atendidos en el Hospital Santo Tomás 1955 a 1964. Arch Med Panameños. 1966;15:35-47.<br />6. Kierszenbaum F. Chagas’ disease and the autoimmunity hypothesis. Clin Microbiol Rev. 1999;12:210-23.<br />7. Chiale PA, Ferrari I, Mahler E, Vallaza MA, Elizari MV, Rosenbaum MB, et al. Differential profile and biochemical effects of antiautonomic membrane receptor antibodies in ventricular arrhythmias and sinus node dysfunction. Circulation. 2001;103:1765-71.<br />8. Borda E, Pascual J, Cossio P, De La Vega M, Arana R, Sterin Borda LA. Circulating IgG in Chagas´disease which binds to beta-adrenoreceptors of myocardium and modulates their activity. Clin Exp Immunol. 1984;57:679-86.<br />9. Giménez L, Mitelman J, González C, Borda E, Sterin-Borda L. Anticuerpos antirreceptores autonómicos, alteraciones de la variabilidad de la frecuencia cardiaca y arritmias en sujetos con enfermedad de Chagas. Rev Arg Cardio. 2003;71:109-13.<br />10. Saldaña A, Samudio F, Miranda A, Herrera LM, Saavedra SP, Cáceres L, et al. Predominance of Trypanosoma rangeli infection in children from a Chagas’ disease endemic area in the west-shore of the Panama Canal. Mem Inst Oswaldo Cruz. 2005;100:729-31.<br />11. Vasquez JE, Krusnell J, Orn A, Sousa OE, Harris RA. Serological diagnosis of Trypanosoma rangeli infected patients. A comparison of different methods and its implications for the diagnosis of Chagas’ disease. Scand J Immunol. 1997;45:322-30.<br />12. Puigbo JJ, Giordano H, Iosa D. Chagas’ cadioneuropathy: cardiovascular autonomic dysfunction as the first manifestation of the disease. Inter J Angiol. 1998;7:123-9.<br />13. Garcia S, Ramos CO, Senra JF, Vilas-Boas F, Rodrigues MM, Campos-de-Carvalho AC, et al. Treatment with benznidazole during the chronic phase of experimental Chagas’ disease decreases cardiac alterations. Antimicrob Agents Chemother. 2005;49:1521-8.<br />14. Limas CJ, Goldenberg IF, Limas C. Autoantibodies against beta-adrenoreceptors in human idiopathic dilated cardiomiopathy. Circ Res. 1989;64:97-103.<br />15. Jahns R, Boivin V, Siegmund C, Inselmann G, Lohse MJ, Boege F. Autoantibodies activating human β1-adregenic receptors are associated with reduced cardiac function in chronic heart failure. Circulation. 1999;99:649-54.<br />16. Kaplan D, Ferrari I, López-Bergami P, Mahler E, Levitus G, Chiale P, et al. Antibodies to ribosomal P proteins of Trypanosoma cruzi in Chagas’ disease possess functional autoreactivity with heart tissue and differ from anti-P autoanbodies in lupus. Proc Natl Acad Sci USA. 1997;94:10301-6.<br />17. Ferrari I, Levin MJ, Wallukat G, Elies R, Lebegue D, Chiale P, et al. Molecular mimicry between the immunodominant ribosomal protein PO of Trypanosoma cruzi and a functional epitope on the human β1-adrenergic receptor. J Exp Med. 1995;182:59-65.<br />18. Joensen L, Borda E, Kohout T, Perry S, Garcia G, Sterin-Borda L. Trypanosoma cruzi antigen that interacts with the beta1-adrenergic receptor and modifies myocardial contractile activity. Mol Biochem Parasitol. 2003;127:169-77.<br />19. Jahns R, Boivin V, Hein L, Triebel S, Angermann CE, Ertl G, et al. Direct evidence for a β1-adregenic receptor-directed autoimmune attack as a cause of idiopathic dilated cardiomiopathy. J Clin Invest. 2004;113:1419-29.<br />20. Hyland KV, Leon JS, Daniels MD, Giafis N, Woods LM, Bahk TJ, et al. Modulation of autoimmunity by treatment of an infectious disease. Infect Immun. 2007;75:3641-50.<br />21. Talvani A, Rocha MO, Ribeiro AL, Borda E, Sterin-Borda L, Teixeira MM. Levels of anti-M2 and anti-beta1 autoantibodies do not correlate with the degree of heart dysfunction in Chagas’ heart disease. Microbes Infect. 2006;8:2459-64.</p>
oai:oai.revistabiomedica.org:article/50
2009-12-19T12:04:34Z
biomedica:TEMA
Excitation-contraction coupling in skeletal muscle: questions remaining after 50 years of research
El acoplamiento excitación-contracción en el músculo esquelético: preguntas por responder a pesar de 50 años de estudio
Calderón-Vélez, Juan Camilo
Figueroa-Gordon, Lourdes Carolina
músculo esquelético
contracción muscular
relajación muscular
calcio
canal liberador de calcio
canales de calcio tipo L
receptor de rianodina
fatiga muscular
muscle
skeletal
muscle contraction
muscle relaxation
calcium
ryanodine receptor calcium release channel
dihydropyridine receptors
muscle fatigue
The excitation-contraction coupling mechanism was defined as the entire sequence of reactionslinking excitation of plasma membrane to activation of contraction in skeletal muscle. By using different techniques, their regulation and interactions have been studied during the last 50 years, defining until now the importance and origin of the calcium ion as a contractile activator and the main proteins involved in the whole mechanism. Furthermore, the study of the ultrastructural basis and pharmacological regulation of the excitation-contraction coupling phenomenon has begun. The excitation-contraction coupling is thought to be altered in situations as ageing, muscle fatigue and some muscle diseases. However, many questions remain to be answered. For example, (1) How excitation-contraction coupling develops and ages? (2) What role does it play in muscle fatigue and other diseases? (3) What is the nature of the interaction between the proteins believed to be involved? The present review describes excitation-contraction coupling in skeletal muscle and techniques used to better understand it as an introduction for discussing unanswered questions regarding excitation-contraction coupling.
El mecanismo de acoplamiento excitación-contracción fue definido en el músculo esquelético como la secuencia de eventos que ocurre desde la generación del potencial de acción en la fibra muscular hasta que se inicia la generación de tensión. La regulación e interacción de dichos eventos entre sí ha sido estudiada durante los últimos 50 años utilizando diferentes técnicas, con las cuales se estableció la importancia y origen del ion calcio como activador contráctil, se conocen las principales proteínas involucradas y se inició el estudio de la base ultraestructural y de la regulación farmacológica; además, hay evidencias de que el acoplamiento excitación-contracción se altera en diferentes situaciones como en el envejecimiento, en la fatiga muscular y en algunas enfermedades musculares. Sin embargo, aún hay varias preguntas por responder: ¿cómo es el desarrollo y envejecimiento del mecanismo de acoplamiento excitación-contracción?, ¿cuál es su papel en la fatiga muscular y en algunas enfermedades musculares?, ¿cuál es la naturaleza de la interacción entre diferentes proteínas involucradas en el acoplamiento excitación-contracción?La presente revisión describe el acoplamiento excitación-contracción en el músculo esquelético y las técnicas utilizadas para su estudio como introducción para discutir algunas de las preguntas que aún falta por responder al respecto.
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/50
10.7705/biomedica.v29i1.50
Biomedica; Vol. 29 No. 1 (2009); 140-160
Biomédica; Vol. 29 Núm. 1 (2009); 140-160
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/50/51
https://revistabiomedica.org/index.php/biomedica/article/view/50/360
/*ref*/Kahn A, Sandow A. The potentiation of muscular contraction by the nitrate-ion. Science. 1950;112:647-9.<br />2. Sandow A. Excitation-contraction coupling in muscular response. Yale J Biol Med. 1952;XXV:176-201.<br />3. Caputo C. Pharmacological investigations of excitation-contraction coupling. Chapter 14. En: Peachey L, Adrian R, editors. Handbook of physiology. Bethesda: American Physiological Society; 1983.<br />4. Berridge M, Lipp P, Bootman M. The versatility and universality of calcium signaling. Nature Rev Mol Cell Biol. 2000;1:11-21.<br />5. Weber A. On the role of calcium in the activity of adenosine 5´-triphosphate hydrolysis by actomyosin. J Biol Chem. 1959;234:2764-9.<br />6. Niedergerke R. Local muscular shortening by intracellularly applied calcium. J Physiol. 1955;128:12P-3P.<br />7. Hasselbach W. Relaxing factor and the relaxation of muscle. Prog Biophys Mol Biol. 1964;14:167-222.<br />8. Endo M, Tanaka M, Ogawa Y. Calcium induced release of calcium from the sarcoplasmic reticulum of skinned skeletal muscle fibres. Nature. 1970;228:34-6.<br />9. Ebashi S. Calcium ion and contractile proteins. Ann NY Acad Sci USA. 1988;522:51-9.<br />10. Stephenson D, Lamb G, Stephenson G. Events of the excitation-contraction-relaxation (E-C-R) cycle in fast- and slow-twitch mammalian muscle fibres relevant to muscle fatigue. Acta Physiol Scand. 1998;162:229-45.<br />11. Fill M, Copello J. Ryanodine receptor calcium release channels. Physiol Rev. 2002;82:893-922.<br />12. Horowicz P. Influence of ions on the membrane potential of muscle fibres. En: Shanes A, editor. Biophysics of physiological and pharmacological actions. Washington: American Association for the Advancement of Science; 1961. p. 217-34.<br />13. Hodgkin A, Huxley A. A quantitative description of membrane current and its application to conduction and excitation in nerve. J Physiol. 1952;117:500-44.<br />14. González-Serratos H. Inward spread of activation in vertebrate muscle fibres. J Physiol. 1971;212:777-99.<br />15. Bezanilla F, Caputo C, González-Serratos H, Venosa R. Sodium dependence of the inward spread of activation in isolated twitch muscle fibres of the frog. J Physiol. 1972;223:507-23.<br />16. Franzini-Armstrong C, Porter K. Sarcolemmal invaginations constituting the T system in fish muscle fibres. J Cell Biol. 1964;22:675-96.<br />17. Schneider M, Chandler W. Voltage dependent charge movement in skeletal muscle: a possible step in excitation-contraction coupling. Nature. 1973;242:244-6.<br />18. Ríos E, Brum G. Involvement of dihydropyridine receptors in excitation-contraction coupling in skeletal muscle. Nature. 1987;325:717-20.<br />19. Ríos E, Pizarro G. Voltage sensor of excitation-contraction coupling in skeletal muscle. Physiol Rev. 1991;71:849-908.<br />20. Bezanilla F. The voltage sensor in voltage-dependent ion channels. Physiol Rev. 2000;80:555-92.<br />21. Lai F, Erickson H, Rousseau E, Liu Q, Meissner G. Purification and reconstitution of the calcium release channel from skeletal muscle. Nature. 1988; 331:315-9.<br />22. Takeshima H, Nishimura S, Matsumoto T, Ishida H, Kangawa K, Minamino N, et al. Primary structure and expression from complementary DNA of skeletal muscle ryanodine receptor. Nature. 1989;339:439-45.<br />23. Franzini-Armstrong C, Jorgensen A. Structure and development of e-c coupling units in skeletal muscle. Annu Rev Physiol. 1994;56:509-34.<br />24. Franzini-Armstrong C. The sarcoplasmic reticulum and the control of muscle contraction. FASEB J. 1999;13(Suppl):S266-S70.<br />25. Meissner G. Adenine nucleotide stimulation of Ca2+-induced Ca2+ release in sarcoplasmic reticulum. J Biol Chem. 1984;259:2365-74.<br />26. Coronado R, Morrissette J, Sukhareva, Vaughan D. Structure and function of ryanodine receptors. Am J Physiol. 1994;266:C1485-504.<br />27. Wei L, Varsányi M, Dulhunty A, Beard N. The conformation of calsequestrin determines its ability to regulate skeletal ryanodine receptors. Biophys J. 2006;91:1288-301.<br />28. Bleunven C, Treves S, Jinyu X, Leo E, Ronjat M, De Waard M, et al. SRP-27 is a novel component of the supramolecular signaling complex involved in skeletal muscle excitation-contraction coupling. Biochem J. 2008;411:343-49.<br />29. Prosser B, Wright N, Hernández-Ochoa E, Varney K, Liu Y, Olojo R, et al. S100A1 binds to the calmodulin binding site of ryanodine receptor and modulates skeletal muscle coupling. J Biol Chem. 2008;283:5046-57.<br />30. Fabiato A. Dependence of the Ca2+-induced release from the sarcoplasmic reticulum of skinned skeletal muscle fibres from the frog semitendinosus on the rate of change of free Ca2+ concentration at the outer surface of the sarcoplasmic reticulum. J Physiol. 1984;353-6P.<br />31. Baylor S, Hollingwoth S. Sarcoplasmic reticulum calcium release compared in slow-twitch and fast-twitch fibres of mouse muscle. J Physiol. 2003;551:125-38.<br />32. Caputo C, Bolaños P, González A. Inactivation of Ca2+ transients in amphibian and mammalian muscle fibres. J Muscle Res Cell Motil. 2004;25:315-28.<br />33. Miledi R, Parker I, Schalow G. Calcium transients in frog slow muscle fibres. Nature. 1977;268:750-2.<br />34. Klein M, Simon B, Szucs G, Schneider M. Simultaneous recording of calcium transients in skeletal muscle using high and low-affinity calcium indicators. Biophys J. 1988;53:971-88.<br />35. Delbono O, Stefani E. Calcium transients in single mammalian skeletal muscle fibres. J Physiol. 1993; 463: 689-707.<br />36. Shirokova N, García J, Pizarro G, Rios E. Ca2+ release from the sarcoplasmic reticulum compared in amphibian and mammalian skeletal muscle. J Gen Physiol. 1996;107:1-18.<br />37. Ebashi S. Regulatory mechanism of muscle contraction with special reference to the Ca-troponin-tropomyosin system. Essays Biochem. 1974;10:1-36.<br />38. Berchtold M, Brinkmeier H, Müntener M. Calcium ion in skeletal muscle: its crucial role for muscle function, plasticity, and disease. Physiol Rev. 2000;80:1215-65.<br />39. Hasselbach W, Suko J, Stromer M, The R. Mechanism of calcium transport in sarcoplasmic reticulum. Ann NY Acad Sci. 1975;264:335-49.<br />40. Jorgensen A, Jones L. Localization of phospholamban in slow but not fast canine skeletal muscle fibers. J Biol Chem. 1986;261:3775-81.<br />41. Hasselbach W. The Ca2+-ATPase of the sarcoplasmic reticulum in skeletal and cardiac muscle. Ann NY Acad Sci. 1998;853:1-8.<br />42. Odermatt A, Becker S, Khanna V, Kurzydlowski K, Leisner E, Pette D, et al. Sarcolipin regulates the activity of SERCA1, the fast-twitch skeletal muscle sarcplasmic reticulum Ca2+-ATPase. J Biol Chem. 1998;273:12360-9.<br />43. Martonosi A, Pikula S. The structure of the Ca2+-ATPase of sarcoplasmic reticulum. Acta Biochim Pol. 2003;50:337-65.<br />44. Periasamy M, Kalyanasundaram A. Serca pump isoforms: their role in calcium transport and disease. Muscle Nerve. 2007;35:430-42.<br />45. Toyoshima H, Mizutani T. Crystal structure of the calcium pump with a bound ATP analogue. Nature. 2004;430:529-35.<br />46. MacLennan D, Brandl C, Korczak B, Green N. Amino-acid sequence of a Ca2++Mg2+-dependent ATPase from rabbit muscle sarcoplasmic reticulum, deduced from its complementary DNA sequence. Nature. 1985;316:696-700.<br />47. Dulhunty A. Excitation-contraction coupling from the 1950s into the new millennium. Clin Exp Pharmacol Physiol. 2006;33:763-72.<br />48. Bekoff A, Betz W. Physiological properties of dissociated muscle fibres obtained from innervated and denervated adult rat muscle. J Physiol. 1977;271:25-40.<br />49. Lännergren J, Westerblad H. The temperature dependence of isometric contractions of single, intact fibres dissected from a mouse foot muscle. J Physiol. 1987;390:285-93.<br />50. Wood DS, Zollman J, Reuben JP. Human skeletal muscle properties of the “chemically skinned” fiber. Science. 1975;187:1075-6.<br />51. Lamb G, Junankar P, Stephenson D. Raised intracellular Ca2+ abolishes excitation-contraction coupling in skeletal muscle fibres of rat and toad. J Physiol. 1995;489:349-62.<br />52. Lamb G. Excitation-contraction coupling and fatigue mechanisms in skeletal muscle: studies with mecanically skinned fibres. J Muscle Res Cell Motil. 2002;23:81-91.<br />53. Yaffe D, Saxel O. Serial passaging and differentiation of myogenic cells isolated from dystrophic mouse muscle. Nature. 1977;270:725-7.<br />54. Rando TA, Blau HM. Primary mouse myoblast purification, characterization and transplantation for cell-mediated gene therapy. J Cell Biol. 1994;125:1275-87.<br />55. Ridgway E, Ashley C. Calcium transients in single muscle fibres. Biochem Biophys Res Commun. 1967;29:229-34.<br />56. Grynkiewicz G, Poenie M, Tsien R. A new generation of Ca2+ indicators with greatly improved fluorescence properties. J Biol Chem. 1985;260:3440-50.<br />57. Minta A, Kao J, Tsien R. Fluorescent indicators for cytosolic calcium based on rhodamine and fluorescein chromophores. J Biol Chem. 1989;264:8171-8.<br />58. Takahashi A, Camacho P, Lechleiter J, Herman B. Measurement of intracellular calcium. Physiol Rev. 1999;79:1089-125.<br />59. Katerinopoulos H, Foukaraki E. Polycarboxylate fluorescent indicators as ion concentration probes in biological systems. Current Med Chem. 2002;9:275-306.<br />60. Tsien R. A non-disruptive technique for loading calcium buffers and indicators into cells. Nature. 1981;290:527-8.<br />61. Pouvreau S, Collet C, Allard B, Jacquemond V. Whole-cell voltage clamp on skeletal muscle fibers with silicone-clamp technique. Meth Mol Biol. 2007;403:185-94.<br />62. Beam K, Franzini-Armstong C. Functional and structural approaches to the study of excitation-contraction coupling. Methods Cell Biol. 1997;52:283-306.<br />63. Bolaños P, Guillén A, Rojas H, Boncompagni S, Caputo C. The use of CalciumOrange-5N as a specific marker of mitochondrial Ca2+ in mouse skeletal muscle fibers. Pflugers Arch-Eur J Physiol. 2008;455:721-31.<br />64. Cheng H, Lederer W, Cannell M. Calcium sparks: elementary events underlying excitation-contraction coupling in heart muscle. Science. 1993;262:740-4.<br />65. Klein M, Schneider M. Ca2+ sparks in skeletal muscle. Prog Biophys Mol Biol. 2006;92:308-32.<br />66. Papadopoulus S, Leuranguer V, Bannister R, Beam K. Mapping sites of potential proximity between the DHPR and RyR1 in muscle using a cyan fluorescent protein-yellow fluorescent protein tandem as a fluorescent resonance energy transfer probe. J Biol Chem. 2004;279:44046-56.<br />67. Launikonis BS, Zhou J, Royer L, Shannon T, Brum G, Rios E. Confocal imaging of [Ca2+] in cellular organelles by SEER, shifted excitation and emission ratioing of fluorescence. J Physiol. 2005;567:523-43.<br />68. Serysheva I, Chiu W, Ludtke S. Single-particle electron cryomicroscopy of the ion channels in the excitation-contraction coupling junction. Methods Cell Biol. 2007;79:407-35.<br />69. Anderson A, Altafaj X, Zheng Z, Wang Z, Delbono O, Ronjat M, et al. The junctional SR protein JP-45 affects the functional expression of the voltage-dependent Ca2+ channel Cav1.1. J Cell Sci. 2006;119:2145-55.<br />70. DiFranco M, Neco P, Capote J, Meera P, Vergara J. Quantitative evaluation of mammalian skeletal muscle as a heterologous protein expression system. Protein Expr Purif. 2006;47:281-8.<br />71. Flucher B, Franzini-Armstrong C. Formation of junctions involved in excitation-contraction coupling in skeletal and cardiac muscle. Proc Natl Acad Sci USA. 1996;93:8101-6.<br />72. Ríos E, Karhanek M, Ma J, González A. An Allosteric model of the molecular interactions of excitation-contraction coupling in skeletal muscle. J Gen Physiol. 1993;102:449-81.<br />73. Wagenknecht T, Grassucci R, Frank J, Saito A, Inui M, Fleischer S. Three-dimensional architecture of the calcium channel/foot structure of sarcoplasmic reticulum. Nature. 1989;338:167-70.<br />74. Ávila G, Dirksen R. Functional impact of the ryanodine receptor on the skeletal muscle L-type Ca2+ channel. J Gen Physiol. 2000;114: 467-80.<br />75. Wagenknecht T, Hsieh C-E, Rath B, Fleischer S, Marko M. Electron tomography of frozen-hydrated isolated triad junctions. Biophys J. 2002;83:2491-501.<br />76. Paolini C, Fessenden J, Pessah I, Franzini-Armstrong C. Evidence for conformational coupling between two calcium channels. Proc Natl Acad Sci USA. 2004;101:12748-52.<br />77. Tanabe T, Beam K, Adams B, Niidome T, Numa S. Regions of the skeletal dihydropyridine receptor critical for excitation-contraction coupling. Nature. 1990;346:567-9.<br />78. Leong P, MacLennan D. A 37-amino acid sequence in the skeletal muscle ryanodine receptor interacts with the cytoplasmic loop between domains II and III in the skeletal muscle dihydropyridine receptor. J Biol Chem. 1998;273:7791-4.<br />79. Casarotto M, Cui Y, Karunasekara Y, Harvey P, Norris N, Borrad P, et al. Structural and functional characterization of interactions between the dihydropyridine receptor II-III loop and the ryanodine receptor. Clin Exp Pharmacol Physiol. 2006;33:1114-7.<br />80. Protasi F, Paolini C, Nakai J, Beam K, Franzini-Armstrong C, Allen P. Multiple regions of RyR1 mediate functional and structural interactions with α1s-dihidropyridine receptors in skeletal muscle. Biophy J. 2002;83:3220-44.<br />81. Ludtke S, Serysheva I, Hamilton S, Chiu W. The pore structure of the closed RyR1 channel. Structure. 2005;13:1203-11.<br />82. Samsó M, Wagenknecht T, Allen D. Internal structure and visualization of transmembrane domains of the RyR1 calcium release channel by cryo-EM. Nat Struct Mol Biol. 2005;12:539-44.<br />83. Doyle D, Morais Cabral J, Pfuetzner R, Kuo A, Gulbis J, Cohen S, et al. The structure of potassium channel: molecular basis of K+ conduction and selectivity. Science. 1998;280:69-77.<br />84. Jiang Y, Lee A, Chen J, Cadene M, Chalt B, MacKinnon R. The open pore conformation of potassium channels. Nature. 2002;417:523-6.<br />85. Zorzato F, Fujii J, Otsu M, Phillips M, Green N, Lai F, et al. Molecular cloning of cDNA encoding human and rabbit forms of the Ca2+ release channel (ryanodine receptor) of skeletal muscle sarcoplasmic reticulum. J Biol Chem. 1990;265: 2244-56.<br />86. Fitts R. Cellular mechanisms of muscle fatigue. Physiol Rev. 1994;74:49-94.<br />87. Enoka R, Duchateau J. Muscle fatigue: what, why and how it influences muscle function. J Physiol. 2008;586:11-23.<br />88. Allen D, Lamb G, Westerblad. Skeletal muscle fatigue: cellular mechanisms. Physiol Rev. 2008;88:287-332.<br />89. Bigland-Ritchie B, Woods J. Changes in muscle contractile properties and neural control during human muscular fatigue. Muscle Nerve. 1984;7:691-9.<br />90. Abbiss C, Laursen P. Models to explain fatigue during prolonged endurance cycling. Sports Med. 2005;35:865-98.<br />91. Kent-Braun J. Central and peripheral contributions to muscle fatigue in humans during sustained maximal effort. Eur J Appl Physiol. 1999;80:57-63.<br />92. Luttgau H. The effect of metabolic inhibitors on the fatigue of the action potential in single muscle fibres. J Physiol. 1965;178:45-67.<br />93. Grabowski W, Lobsiger E, Luttgau H. The effect of repetitive stimulation at low frequencies upon the electrical and mechanical activity of single muscle fibres. Pflugers Arch. 1972;334:222-39.<br />94. Moussavi R, Carson P, Boska M, Weiner M, Miller R. Nonmetabolic fatigue in exercising human muscle. Neurology. 1989;39:1222-26.<br />95. Nassar-Gentina V, Passonneau J, Vergara J, Rapoport S. Metabolic correlates of fatigue and recovery from fatigue in single frog muscle fibers. J Gen Physiol. 1978;72:593-606.<br />96. Westerblad H, Allen D. Changes of myoplasmic calcium concentration during fatigue in single mouse muscle fibers. J Gen Physiol. 1991;98:615-35.<br />97. Green H. Cation pumps in skeletal muscle: potential role in muscle fatigue. Acta Physiol Scand. 1998;162:201-13.<br />98. Hill A, Kupalov P. Anaerobic and aerobic activity in isolated muscle. Proc R Soc London B. 1929;105:313-22.<br />99. Westerblad H. The role of pH and inorganic phosphate ions in skeletal muscle fatigue. Chapter 12. En: Hargreaves M, Thompson M, editors. Biochemistry of exercise X. Champaign: Human Kinetics; 1999. p. 147-54.<br />100. Westerblad H, Allen D, Lännergren J. Muscle fatigue: lactic acid or inorganic phosphate the major cause? News Physiol Sci. 2002;17:17-21.<br />101. Lamb G, Stephenson D. Lactic acid accumulation is an advantage during muscle activity. J Appl Physiol. 2006;100:1410-2.<br />102. Bangsbo J, Juel C. Lactic acid accumulation is a disadvantage during muscle activity. J Appl Physiol. 2006;100:1412-3.<br />103. McCully K, Clark B, Kent J, Wilson J, Chance B. Biochemical adaptations to training: implications for resisting muscle fatigue. Can J Physiol Pharmacol. 1991;69:274-8.<br />104. Lindinger M, Heigenhauser G. The roles of ion fluxes in skeletal muscle fatigue. Can J Physiol Pharmacol. 1991;69:246-53.<br />105. Kent-Braun J, Miller R, Weiner M. Phases of metabolism during progressive exercise to fatigue in human skeletal muscle. J Appl Physiol. 1993;75:573-80.<br />106. Knuth S, Dave H, Peters J, Fitts R. Low cell pH depresses peak power in rat skeletal muscle fibres at both 30°C and 15°C: implications for muscle fatigue. J Physiol. 2006;575:887-99.<br />107. Rousseau E, Pinkos J. pH modulates conducting and gating behaviour of single calcium release channels. Pflugers Arch-Eur J Physiol. 1990;415:645-7.<br />108. Caputo C, Edman K, Lou F, Sun Y. Variation in myoplasmic Ca concentration during contraction and relaxation studied by the indicator fluo-3 in frog muscle fibres. J Physiol. 1994;478:137-48.<br />109. Verburg E, Murphy R, Stephenson G, Lamb G. Disruption of excitation-contraction coupling and titin by endogenous Ca2+-activated proteases in toad muscle fibres. J Physiol. 2005;564:775-89.<br />110. Gollnick P, Korge P, Karpakka J, Saltin B. Elongation of skeletal muscle relaxation during exercise is linked to reduced calcium uptake by the sarcoplasmic reticulum in man. Acta Physiol Scand. 1991;142:135-6.<br />111. Leppik J, Aughey R, Medved I, Fairweather I, Carey M, McKenna M. Prolongued exercise to fatigue in humans impairs skeletal muscle Na-K ATPase activity, sarcoplasmic reticulum Ca release and Ca uptake. J Appl Physiol. 2004;97:1414-23.<br />112. Verburg E, Dutka T, Lamb G. Long-lasting muscle fatigue: partial disruption of excitation-contraction coupling by elevated cytosolic Ca2+ concentration during contractions. Am J Physiol. 2006;290:C1199-C208.<br />113. Westerblad H, Allen D. Myoplasmic free Mg2+ concentration during repetitive stimulation of single fibres from mouse skeletal muscle. J Physiol. 1992;453:413-34.<br />114. Lamb G, Stephenson D. Effects of intracellular pH and [Mg2+] on excitation-contraction coupling in skeletal muscle fibres of the rat. J Physiol. 1994; 478:331-9.<br />115. Fryer M, Owen V, Lamb G, Stephenson G. Effects of creatine phosphate and Pi on Ca movements and tension development in rat skinned skeletal muscle fibres. J Physiol. 1995;482:123-40.<br />116. Dutka T, Cole L, Lamb G. Calcium phosphate precipitation in the sarcoplasmic reticulum reduces action potential-mediated Ca2+ release in mammalian skeletal muscle. Am J Physiol. 2005;289:C1502-C12.<br />117. Barclay J, Hansel M. Free radicals may contribute to oxidative skeletal muscle fatigue. Can J Physiol Pharmacol. 1991;69:279-84.<br />118. Sen C. Oxidants and antioxidants in exercise. J Appl Physiol. 1995;79:675-86.<br />119. Reid M. Plasticity in skeletal, cardiac, and smooth muscle. Invited review: Redox modulation of skeletal muscle contraction: what we know and what we don’t. J Appl Physiol. 2001;90:724-31.<br />120. Darnley G, Duke A, Steele D, MacFarlane N. Effects of reactive oxygen species on aspects of excitation-contraction coupling in chemically skinned rabbit diaphragm muscle fibres. Exp Physiol. 2001;86:161-8.<br />121. Davies K, Quintanilha A, Brooks G, Packer L. Free radicals and tissue damage produced by exercise. Biochem Biophys Res Commun. 1982;107:1198-205.<br />122. M, Haack K, Kathleen F, Valberg P, Kobzik L, West S. Reactive oxygen in skeletal muscle. I. Intracellular oxidant kinetics and fatigue in vitro. J Appl Physiol. 1992;73:1797-804.<br />123. Kanter M, Nolte L, Holloszy J. Effects of an antioxidant vitamin mixture on lipid peroxidation at rest and postexercise. J Appl Physiol. 1993;74:965-9.<br />124. Jackson M, Pye D, Palomero J. The production of reactive oxygen species by skeletal muscle. J Appl Physiol. 2007;102:1664-70.<br />125. Brotto M, Nosek T. Hydrogen peroxide disrupts Ca2+ release from the sarcoplasmic reticulum of rat skeletal muscle fibers. J Appl Physiol. 1996;81:731-7.<br />126. Oba T, Kurono C, Nakajima R, Takaishi T, Ishida K, Fuller G, et al. H2O2 activates ryanodine receptor but has little effect on recovery of release Ca2+ content after fatigue. J Appl Physiol. 2002;93:1999-2008.<br />127. Hidalgo C. Cross talk between Ca2+ and redox signaling cascades in muscle and neurons through the combined activation of ryanodine receptors/Ca2+ release channels. Phil Trans R Soc B. 2005;360:2237-46.<br />128. Moopanar T, Allen D. Reactive oxygen species reduce myofibrillar Ca2+ sensitivity in fatiguing mouse skeletal muscle at 37°C. J Physiol. 2005;564:189-99.<br />129. Moopanar T, Allen D. The activity-induced reduction of myofibrillar Ca2+ sensitivity in Mouse skeletal muscle is reversed by dithiothreitol. J Physiol. 2006;571:191-200.<br />130. Posterino G, Lamb G. Effects of reducing agents and oxidants on excitation-contraction coupling in skeletal muscle fibres of rat and toad. J Physiol. 1996;496:809-25.<br />131. Andrade F, Reid M, Allen D, Westerblad H. Effects of hydrogen peroxide and dithiotreitol on contractile function of single skeletal muscle fibres from the mouse. J Physiol. 1998;509:565-75.<br />132. Andrade F, Reid M, Allen D, Westerblad H. Effect of nitric oxide on single skeletal muscle fibres from the mouse. J Physiol. 1998;509:577-86.<br />133. Andrade F, Reid M, Westerblad H. Contractile response of skeletal muscle to low peroxide concentrations: myofibrillar calcium sensitivity as a likely target for redox-modulation. FASEB J. 2001;15:309-11.<br />134. Ward K, Wareham A. Changes in membrane potential and potassium and sodium activities during postnatal development of mouse skeletal muscle. Exp Neurol. 1985;89:554-8.<br />135. Brown M, Jansen J, Van Essen D. Polyneural innervation of skeletal muscle in newborn rats and its elimination during maturation. J Physiol. 1976;261:387-422.<br />136. Kjeldsen K, Norgaard A, Clausen T. Age dependent changes in the number of [H3] ouabain binding sites in rat soleus muscle. Biochem Biophys Acta. 1982;686:253-356.<br />137. Harris J, Marshall M. Tetrodotoxin-resistant action potentials in newborn rat muscle. Nature New Biol. 1973;243:191-2.<br />138. Capote J, Bolanos P, Schuhmeier R, Melzer W, Caputo C. Calcium transients in developing mouse skeletal muscle fibres. J Physiol. 2005;564:451-64.<br />139. Kano M, Yamamoto M. Development of spike potentials in skeletal muscle cells differentiated in vitro from chick embryo. J Cell Physiol. 1977;90:439-44.<br />140. Franzini-Armstrong C. Simultaneous maturation of transverse tubules and sarcoplasmic reticulum during muscle differentiation in the mouse. Dev Biol. 1991;146:353-63.<br />141. Bertocchini F, Ovitt C, Conti A, Barone V, Schöler H, Bottinelli R, et al. Requirement for the ryanodine receptor type 3 for efficient contraction in neonatal skeletal muscles. EMBO J. 1997;16:6956-63.<br />142. Chaudhari N, Beam K. mRNA for cardiac calcium channels is expressed during development of skeletal muscle. Dev Biol. 1993;155:507-15.<br />143. Cognard C, Lazdunski M, Romey G. Different types of Ca2+ channels in mammalian skeletal muscle cells in culture. Proc Natl Acad Sci USA. 1986;83:517-21.<br />144. Beam K, Knudson C. Calcium currents in embryonic and neonatal mammalian skeletal muscle. J Gen Physiol. 1988;91:781-98.<br />145. Beam K, Knudson C. Effect of postnatal development on calcium currents and slow charge movement in mammalian skeletal muscle. J Gen Physiol. 1988;91:799-815.<br />146. Romey G, Garcia L, Dimitriadou V, Pincon-Raymond M, Rieger F, Lazdunski M. Ontogenesis and localization of Ca2+ channels in mammalian skeletal muscle in culture and role in excitation-contraction coupling. Proc Natl Acad Sci USA. 1989;86:2933-7.<br />147. Dangain J, Neering I. Effect of caffeine and high potassium on normal and dystrophic mouse EDL muscles at various developmental stages. Muscle Nerve. 1992;16:33-42.<br />148. Ma J, Pan Z. Retrograde activation of store-operated calcium channel. Cell Calcium. 2003;33:375-84.<br />149. Whalen R, Sell S, Butler-Browne G, Schwartz K, Bouveret P, Pinset-Harstom I. Three myosin heavy-chain isozymes appear sequentially in rat muscle development. Nature. 1981;292:805-9.<br />150. Dhoot G, Perry S. The components of the troponin complex and development in skeletal muscle. Exp Cell Res. 1980;127:75-87.<br />151. Roy R, Sreter F, Sarkar S. Changes in tropomyosin subunits and myosin light chains during development of chicken and rabbit striated muscles. Dev Biol. 1979;69:15-30.<br />152. Berchtold M, Means A. The Ca2+-binding protein parvalbumin: molecular cloning and developmental regulation of mRNA abundance. Proc Natl Acad Sci USA. 1985;82:1414-8.<br />153. Figueroa LC, Bolaños P, Guillen A, Caputo C. Efecto del calcio extracelular sobre transitorios de Ca2+ de fibras musculares esqueléticas y miotubos durante el desarrollo. Acta Científica Venezolana. 2006;57:19.<br />154. Sandow A, Taylor S, Preiser H. Role of the action potential in excitation-contraction coupling. Fed Proc. 1965;24:1116-23.<br />155. Marx S, Reiken S, Hisamatsu Y, Jayaraman T, Burkhoff D, Rosemblit N, et al. PKA phosphorylation dissociates FKBP12.6 from the calcium release channel (ryanodine receptor): defective regulation in failing hearts. Cell. 2000;101:365-76.<br />156. Stange M, Xu L, Balshaw D, Yamaguchi N, Meissner G. Characterization of recombinant skeletal muscle (Ser-2843) and cardiac muscle (Ser-2809) ryanodine receptor phosphorylation mutants. J Biol Chem. 2003;278:51693-702.<br />157. Dipolo R, Beaugé L. Sodium/calcium exchanger: influence of metabolic regulation on ion carrier interaction. Physiol Rev. 2006;86:155-203.<br />158. Bruton J, Tavi P, Aydin J, Wasterblad H, Lanergren J. Mitochondrial and myoplasmic [Ca2+] in single fibers from Mouse limb muscles during repeated tetanic contraction. J Physiol. 2003;551:179-90.<br />159. Caputo C, Bolaños P. Effect of mitochondria poisoning by FCCP on Ca2+ signaling in muse skeletal muscle fibers. Pflugers Arch-Eur J Physiol. 2008;455:733-43.<br />160. Caputo C, Bolaños P. Effect of external sodium and calcium on calcium efflux in frog striated muscle. J Membr Biol. 1978;41:1-14.<br />161. Balnave Ch, Allen D. Evidence for Na+/Ca2+ Exchange in intact single skeletal muscle fibers from the mouse. Am J Physiol Cell Physiol. 1998;274:940-6.<br />162. Cifuentes F, Vergara J, Hidalgo C. Sodium/calcium Exchange in amphibian skeletal muscle fibers and isolated transverse tubules. Am J Physiol Cell Physiol. 2000;279:C89-97.
oai:oai.revistabiomedica.org:article/51
2009-12-19T12:04:34Z
biomedica:CART
Cartas al editor
biomedica, biomedica
Instituto Nacional de Salud
2009-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/51
10.7705/biomedica.v29i1.51
Biomedica; Vol. 29 No. 1 (2009); 161-163
Biomédica; Vol. 29 Núm. 1 (2009); 161-163
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/51/52
https://revistabiomedica.org/index.php/biomedica/article/view/51/361
oai:oai.revistabiomedica.org:article/52
2009-12-24T18:03:33Z
biomedica:EDIT
Control del cáncer de cuello uterino en Colombia: triunfos y desafíos de la tamización basada en la citología cérvico-uterina
Murillo, Raúl
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/52
10.7705/biomedica.v28i4.52
Biomedica; Vol. 28 No. 4 (2008); 467-470
Biomédica; Vol. 28 Núm. 4 (2008); 467-470
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/52/53
https://revistabiomedica.org/index.php/biomedica/article/view/52/379
/*ref*/Instituto Nacional de Cancerología. Programa de detección y control del cáncer de cuello uterino: Marco teórico y<br />normativo. Bogotá: Instituto Nacional de Cancerología-Ministerio de Salud; 1990.<br />2. Molano M, Posso H, Méndez F, Murillo R, van den Brule A, Ronderos M, et al. Historia natural de la infección por<br />el virus del papiloma humano en una cohorte de mujeres de Bogotá. Revista Colombiana de Cancerología. 2005;<br />9:192-209.<br />3. Ministerio de Salud. Resolución 412 de 2.000. Bogotá: Ministerio de Salud; 2000.<br />470<br />4. Piñeros M, Hernández G, Bray F. Increasing mortality rates of common malignancies in Colombia: an emerging<br />problem. Cancer. 2004;101:2285-92.<br />5. Murillo R, Piñeros M, Hernández G. Atlas de mortalidad por cáncer en Colombia. Bogotá: Instituto Nacional de<br />Cancerología-Instituto Geográfico Agustín Codazzi; 2004.<br />6. Sankaranarayanan R, Budukh AM, Rajkumar R. Effective screening programmes for cervical cancer in low- and<br />middle-income developing countries. Bull World Health Organ. 2001;79:954-62.<br />7. Murillo R, Almonte M, Pereira A, Ferrer E, Gamboa O, Jerónimo J, et al. Cervical cancer screening programs in<br />Latin America and the Caribbean. Vaccine. 2008;26(Suppl.11):L37-48.<br />8. Piñeros M, Cendales R, Murillo R, Wiesner C, Tovar S. Cobertura de la citología de cuello uterino y factores<br />relacionados en Colombia, 2005. Rev Salud Pública. (Bogotá) 2007;9:327-41.<br />9. Wiesner-Ceballos C, Murillo R, Piñeros M, Tovar-Murillo SL, Cendales R, Gutiérrez MC. El control del cáncer<br />cérvico-uterino en Colombia: percepción de los actores del sistema de salud. Rev Panam Salud Pub. 2008; en imprenta.<br />10. Gamboa OA, Chicaíza L, García-Molina M, Díaz J, González M, Murillo R, et al. Cost-effectiveness of conventional<br />cytology and HPV-DNA testing for cervical-cancer screening in Colombia. Salud Pub Mex. 2008;50:276-85.
oai:oai.revistabiomedica.org:article/53
2009-12-24T18:03:33Z
biomedica:CASO
Report of five cases of severe neonatal Plasmodium vivax malaria in Urabá, Colombia
Reporte de cinco casos de malaria neonatal grave por Plasmodium vivax en Urabá, Colombia
Piñeros, Juan Gabriel
Arboleda, Margarita
Jaramillo, Juan Camilo
Blair, Silvia
Plasmodium vivax
malaria paludismo
recién nacido
estudios de casos
Colombia
Plasmodium vivax
malaria
infant
newborn
case studies
Colombia
Introduction. Neonatal malaria is a type of malaria that occurs during the first month of life. In the last half century, the reports of malaria parasites in neonates generally have been associated with congenital transmission. However, in recent years, cases have appeared with increasing frequency, especially in Africa. In Latin America, the incidence of neonatal malaria is unknown, with only isolated cases reported.Objective. Cases of neonatal malaria were identified and characterized to better recognize the frequency and symptoms of cases as they occur in Colombia. Materials and methods. Between March 2002-March 2004, a search for cases of neonatal malaria was made in the hospitals of the Turbo and Apartadó counties (Urabá, Antioquia Province). The following date were compiled: (1) characteristics of the mother, (2) demographic characteristics of the neonates, (3) clinical characteristics of the disease, and (4) laboratory results.Results. Five cases were discovered of neonatal vivax malaria; however, only one met the criteria for congenital infection. Three patients had institutional delivery and two had a maternal history of gestational malaria, but none underwent a screening test for malaria. One of the four mothers were primaparous and half of them were younger than 20 years. All neonates had fever and presented some sign of severe disease during the first medical examination; each had hemoglobin levels compatible with severe neonatal anemia. No neonate had received the recommended treatment for this type of malaria.Conclusion: Five cases of severe neonatal malaria were reported, caused by infections of P. vivax, which normally does not produce severe disease. Since none of the malaria cases were recognized or treated at the local hospitals, advisories to medical professionals are recommended concerning neonatal malaria, particularly in endemic regions.
Introducción. La malaria neonatal es aquélla que ocurre durante el primer mes de vida. Durante más de medio siglo se reporta la presencia de parásitos de malaria en neonatos, generalmente asociada a transmisión congénita, cuya frecuencia se ha incrementado desde hace algunos años, especialmente en África. En Latinoamérica su situación es desconocida y sólo hayreportes aislados de casos.Objetivos. Describir los casos de paludismo neonatal diagnosticado en los hospitales de la región del Urabá antioqueño entre marzo de 2002 y marzo de 2004.Materiales y métodos. Se hizo una búsqueda de casos en los hospitales de Turbo y Apartadó que cumplieran los criterios de malaria neonatal. Se buscaron y tabularon datos sobre algunas características: maternas, demográficas de los neonatos, clínicas de la enfermedad y hallazgos de laboratorio.Resultados. Se encontraron cinco casos de malaria neonatal, todos por Plasmodium vivax, de los cuales, sólo uno cumplió los criterios de infección congénita. Aunque tres de los pacientes tuvieron parto institucional y dos antecedentes maternos de malaria gestacional, ninguno fue tamizado para malaria; 25% (1 de 4) de las madres eran primíparas y la mitad eran menores de 20 años. Todos los neonatos tuvieron fiebre, algún signo de enfermedad grave al examen físico de ingreso y cifras de hemoglobina compatibles con anemia neonatal grave. Ninguno recibió el esquema antipalúdico recomendado.Conclusión. Se trata de un reporte de cinco casos de malaria neonatal grave por P. vivax, especie que habitualmente no se relaciona con complicaciones, sin que existiera en ningún caso la sospecha clínica y con tratamiento inadecuado.
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/53
10.7705/biomedica.v28i4.53
Biomedica; Vol. 28 No. 4 (2008); 471-479
Biomédica; Vol. 28 Núm. 4 (2008); 471-479
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/53/54
https://revistabiomedica.org/index.php/biomedica/article/view/53/380
/*ref*/Breman JG, Alilio MS, Mills A. Conquering the intolerable burden of malaria: what’s new, what’s needed: a summary. Am J Trop Med Hyg. 2004;71(Suppl 2):1-15.<br />2. Dirección Seccional de Salud de Antioquia. Eventos de salud pública. [Consultado: mayo de 2007]. Disponible en: http://www.dssa.gov.co/htm/event_1.html<br />3. Desai M, ter Kuile FO, Nosten F, McGready R, Asamoa K, Brabin B, et al. Epidemiology and burden of malaria in pregnancy. Lancet Infect Dis. 2007;7:93-104.<br />4. Obiajunwa PO, Owa JA, Adeodu OO. Prevalence of congenital malaria in Ile-Ife, Nigeria. J Trop Pediatr. 2005;51:219-22.<br />5. Orogade AA. Neonatal malaria in a mesoendemic Malaria area of northern Nigeria. Ann Afr Med. 2004;3:170-3.<br />6. Runsewe-Abiodun IT, Ogunfowora OB, Fetuga BM. Neonatal malaria in Nigeria, a 2 year review. BMCPediatr. 2006;6:19-24.<br />7. Alves MJ, Rangel O, Souza SS. Malaria in region of Campinas, Sao Paulo, Brasil, 1980 a 1994. Rev Soc Bras Med Trop. 2000;33:53-60.<br />8. Fernández RD, García Y, Alger J. Malaria y embarazo: observaciones clínico-epidemiológicas en dos zonas geográficas de Honduras. Rev Med Hondur. 2001;69:8-18.<br />9. Marques HH, Vallada MG, Sakane PT, Boulos M. Congenital malaria. case reports and a brief review of literature. J Pediatr (Rio J). 1996;72:103-5.<br />10. Piñeros JG. Malaria congénita. En: Carmona-Fonseca J, editor. Tópicos selectos de infectología. Medellín: Universidad de Antioquia; 2002.<br />11. Reproductive, Maternal and Child Health Erupean Regional Office World Health Organization. Definitions and indicators in family planning, maternal and child health and reproductive health used in the regional office for Europe. Geneve: WHO; 2001.<br />12. Henrys D. A propósito de un caso de paludismo congénito en Thomonde, Haití. Acta Médica Dominicana. 1983;6:216-8.<br />13. Lawn JE, Cousens S, Zupan J. 4 million neonatal deaths: When? Where? Why? Lancet. 2005;365:891- 900.<br />14. Jaramillo-Bustamante JC. Malaria congénita. En: Departamento de Microbiología y Parasitología, editores. Tópicos selectos de infectología. Medellín: Universidad de Antioquia; 2006.<br />15. Hagmann S, Khanna K, Niazi M, Purswani M, Robins EB. Congenital malaria, an important differential diagnosis to consider when evaluating febrile infants of immigrant mothers. Pediatr Emerg Care. 2007;23:326-9.<br />16. Behrman RE, Kliegman R, Jenson HB. Nelson textbook of pediatrics. 16th Edition. Philadelphia: W.B. Saunders; 2000.<br />17 Organización Panamamericana de la Salud. Atención Integrada a las Enfermedades Prevalentes de la Infancia (AIEPI). Curso clínico para profesionales de la salud. Bogotá, D.C.: Ministerio de la Protección Social; 2005.<br />18. Goldstein B, Giroir B, Randolph A. International pediatric sepsis consensus conference: Definitions for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med. 2005;6:2-8. <br />19. World Health Organization. Severe falciparum malaria. Trans Roy Soc Trop Med Hyg. 2000;94 (Suppl.1):s1/2.<br />20. Ministerio de Salud. Guía de atención de la malaria. Diario Oficial. Edición 43956. Santa Fe de Bogotá:Ministerio de Salud; 2000. p.173-84.
oai:oai.revistabiomedica.org:article/54
2009-12-24T18:03:33Z
biomedica:ENSA
La otra transición epidemiológica: hitos en el desarrollo de la epidemiología de los factores de riesgo en Colombia
Idrovo, Álvaro Javier
Eslava, Juan Carlos
Ruiz-Rodríguez, Myriam
Rodríguez, Jorge Martín
transición de la salud
epidemiología/historia
factores de riesgo
Colombia
Este artículo describe la manera como emergió la epidemiología de los factores de riesgo en Colombia y algunos desarrollos posteriores. Los orígenes de la epidemiología de los factores de riesgo se relacionan con la situación sanitaria nacional de mediados del siglo XX, que muestran un cambio en el perfil de presentación de enfermedades infecciosas y nutricionales hacia un perfil con predominio de enfermedades crónicas y traumatismos. Se describen los principales hitos en la historia de la epidemiología de los factores de riesgo nacional: los estudios sobre bocio endémico, cáncer gástrico y cáncer de cuello uterino, y efectos adversos de la desnutrición infantil, y las encuestas de salud locales. El influjo que la Fundación Rockefeller y la Organización Panamericana de la Salud tuvieron sobre la enseñanza de la epidemiología en Colombia es destacado. Finalmente, se describen las principales líneas de investigación actuales y se sugieren algunas pautas de investigación para los futuros historiadores de la salud pública y la epidemiología colombiana.
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/54
10.7705/biomedica.v28i4.54
Biomedica; Vol. 28 No. 4 (2008); 480-496
Biomédica; Vol. 28 Núm. 4 (2008); 480-496
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/54/55
https://revistabiomedica.org/index.php/biomedica/article/view/54/382
/*ref*/Sanmartín C. Epidemiological experiences in overdeveloped sub-countries. Am J Trop Med Hyg. 1973;22:291-5.<br />2. Frenk J. Transiciones: vidas, instituciones, ideas. Salud Pública Mex. 1997;39:144-50.<br />3. Frenk J, Frejka T, Bobadilla JL, Stern C, Lozano R, Sepúlveda J, et al. La transición epidemiológica en América Latina. Bol Of Sanit Panam. 1991;111:485-96.<br />4. Bigelow G, Lombart H. El cáncer y otras enfermedades crónicas en Massachusetts. En: Organización Panamericana de la Salud. El desafío de la epidemiología. Problemas y lecturas seleccionadas. Publicación científica 505. Washington: OPS; 1994. p. 106-14. <br />5. Gordon J. Epidemiología vieja y nueva. En: Organización Panamericana de la Salud. El desafío de la epidemiología. Problemas y lecturas seleccionadas. Publicación científica 505. Washington: OPS; 1994. p. 140-7.<br />6. Terris M. La tradición epidemiológica. En: La revolución epidemiológica y la medicina social. México D.F.: Siglo XXI Editores; 1987. p. 23-38.<br />7. Susser M, Susser E. Choosing a future for epidemiology: I. Eras and paradigms. Am J Public Health. 1996;86:668-73.<br />8. De Almeida-Filho N. Bases históricas da epidemiologia. En: Epidemiología sin números. Washington: OPS/OMS, 1992. p. 3-10.<br />9. Krieger N. Epidemiology and the web of causation: Has anyone seen the spider? Soc Sci Med. 1994;39:887-903.<br />10. Green L. Health education’s contributions to public health in the twentieth century: A glimpse through health promotion’s rear-view mirror. Annu Rev Public Health. 1999;20:67-88.<br />11. Susser M, Susser E. Choosing a future for epidemiology: II. From black box to Chinese boxes and eco-epidemiology. Am J Public Health. 1996;86:674-7. <br />12. Diez-Roux AV. Bringing context back into epidemiology: Variables and fallacies in multilevel analysis. Am J Public Health. 1998;88:216-22. <br />13. Breilh J. La epidemiología entre fuegos. Taller Latinoamericano de Medicina Social. Medellín: ALAMES; 1997. p. 35-59.<br />14. Evans RG. Introducción. En: Evans R, Barer B, Marmor T, editores. ¿Por qué una gente está sana y otra no? Madrid: Ediciones Díaz de Santos; 1994. p. 3-28.<br />15. Zambrano F. Anotaciones sobre el desarrollo de la epidemiología en Colombia en los últimos 20 años. Bol Epidemiol Antioquia. 1992;18:82-4.<br />16. Romero A. Historia de la salud pública y la epidemiología en Colombia. Medellín: OPS/OMS, FNSP, SCE; 1999.<br />17. Estrada V. Comienzos de una epidemiología de terreno en Colombia. En: Márquez J, Casas A, Estrada V, editores. Higienizar, medicar gobernar. Historia, medicina y sociedad en Colombia. Medellín: GIHSA, UN; 2004. p. 127-58.<br />18. Miranda N, Quevedo E, Hernández M. La medicina colombiana de 1867 a 1946. En: Miranda N, Quevedo E, Hernández M. Historia social de la ciencia en Colombia. Bogotá: Colciencias; 1993. p. 15-160.<br />19. Idrovo AJ. Raíces históricas, sociales y epidemiológicas de la tuberculosis en Bogotá, Colombia. Biomédica. 2004;24:356-65.<br />20. Omran AR. The epidemiologic transition. A theory of the epidemiology of population change. Milbank Mem Fund Q. 1971;49:509-38.<br />21. Obregón D. Medicalización de la lepra: una estrategia nacional. An Colomb Hist Soc Cult. 1997;24:139-65.<br />22. Colombia-Ministerio de Salud. Informe al Honorable Congreso de la República 1972-1973. Bogotá; Ministerio de Salud: 1993.<br />23. Ministerio de Salud. Informe al Honorable Congreso de la República 1979-1980. Bogotá; Ministerio de Salud:<br />1980.<br />24. Ministerio de Salud. Diez años de información. Bogotá; Ministerio de Salud; 1992.<br />25. Gast-Galvis A. Una década de labor del Instituto Carlos Finlay de Colombia. Bol Of Sanit Panam. 1961;50:44-58.<br />26. Gast-Galvis A, Renjifo S. Leishmaniasis visceral. Estudio epidemiológico del primer caso diagnosticado en Colombia. Anal Soc Biol Bogotá. 1944;1:1-8.<br />27. Groot H. Estudios sobre virus transmitidos por artrópodos en Colombia. Rev Acad Colomb Cien Exac Fis Nat. 1964;12:3-23.<br />28. Sanmartín C, Arbeláez N. Inmunidad al virus de la encefalitis equina venezolana en la población de la<br />Guajira, Colombia, en abril de 1963. Bol Of Sanit Panam. 1965; 59:516-25.<br />29. Uribe C, Renjifo S, Groot H. Contribución al estudio de trypanosomas humanos y de animales en Colombia. Rev Hig. 1949;34:3-95.<br />30. Boshell J, Bugher JC, Roca M, Osorno E.Epidemiología de la fiebre amarilla selvática en Colombia durante los últimos años. Revista de la Facultad Nacional de Medicina. 1944;13:122-44. <br />31. Corredor A, Kreutzer RD, Tesh RB, Boshell J, Palau MT, Cáceres E, et al. Distribution and etiology of leishmaniasis in Colombia. Am J Trop Med Hyg. 1990;42:206-10. <br />32. Susser M. Epidemiology in the United States after World War II: The evolution of technique. Epidemiol Rev. 1985;7:147-77.<br />33. Quevedo E. Políticas de salud o políticas insalubres? De la higiene a la salud pública en Colombia en la primera mitad del siglo XX. Biomédica. 1996;16:345-60. <br />34. Eslava JC. El influjo norteamericano en el desarrollo de la salud pública en Colombia. Biomédica.1998;18:101-9.<br />35. Maya LH. La epidemiología en Antioquia. Bol Epidemiol Antioquia. 1990;15:379-90. <br />36. Laverde L. Ensayo de contribución al estudio de la etiología ecológica de los cotos. Rev Med Bogotá 1935;45:10-8.<br />37. Góngora Y, López J, Young N, Iregui Borda A. Bocio simple y sal yodada en Colombia. Revista de Higiene (Bogotá). 1950;24:291-329.<br />38. Guzmán MP, Quevedo E. La cooperación técnica norteamericana en salud pública en Colombia durante la Segunda Guerra Mundial. Biomédica. 1999;19:5-17.<br />39. Gaitán E, Merino H, Rodríguez G, Medina P, Meyer JD, DeRouen TA, et al. Epidemiology of endemic goitre in western Colombia. Bull World Health Organ.1978;56:403-16.<br />40. Fierro-Benítez R, Peñafiel W, De Groot LJ, Ramírez I. Endemic goiter and endemic cretinism in the Andean region. N Engl J Med. 1969;280:296-302.<br />41. Horwitz A. La epidemiología en América Latina. Bol Of Sanit Panam. 1961;51:191-4. <br />42. Taussig M. Nutrition, development, and foreign aid: A case study of U.S. directed health care in a Colombian plantation zone. In: Navarro V, editor. Imperialism, health and medicine. Farmingdale, New York: Baywood Publishing Company; 1979. p. 127-46.<br />43. Rockefeller Foundation. The president’s five year review and annual report. New York: Rockefeller Foundation; 1968. p. 62.<br />44. Ministerio de Salud de Colombia. Investigación nacional de morbilidad: evidencia clínica. Bogotá:Ministerio de Salud; 1969.<br />45. Puffer RR, Griffith GW. Patterns of urban mortality. Scientific Publication 151. Washington: PAHO–WHO; 1967.<br />46. Cobo A. Discurso del Dr. Alex Cobo, Decano encargado, Facultad de Medicina, Universidad del Valle, Cali, Colombia. En: Organización Panamericana de la Salud. Seminario sobre registros de cáncer en América Latina. Publicación Científica 215. Washington: OPS; 1970. p. 1-2.<br />47. Cuello C, Correa P, Haenszel W. Trends in cancer incidence in Cali, Colombia. J Natl Cancer Inst. 1983;70:635-41.<br />48. Guzmán N. Leucemias y linfomas en Cali, Colombia. Algunas consideraciones epidemiológicas. Bol Of Sanit Panam. 1971;71:41-9. <br />49. Gail MH. Some of Nathan Mantel’s contributions to epidemiology. Stat Med. 1999;18:3389-400. <br />50. Correa P, Cuello C. Estudio de la etiología del cáncer gástrico. I. Epidemiología de cáncer y lesiones precancerosas. Acta Médica. 1978;9:1-9.<br />51. Cuello C, Correa P, Haenszel W, Gordillo G, Brown C, Archer M, et al. Gastric cancer in Colombia. I.Cancer risk and suspect environmental agents. J Natl Cancer Inst. 1976;57:1015-20.<br />52. Haenszel W, Correa P, Cuello C, Guzmán N, Burbano LC, Lores H, et al. Gastric cancer in Colombia. II. Case-control epidemiologic study of precursor lesions. J Natl Cancer Inst. 1976;57:1021-6.<br />53. Correa P, Cuello C, Duque E, Burbano LC, García FT, Bolaños O, et al. Gastric cancer in Colombia. III. Natural history of precursor lesions. J Natl Cancer Inst. 1976;57:1027-35.<br />54. Correa P, Fox J, Fontham E, Ruiz B, Lin YP, Zavala D, et al. Helicobacter pylori and gastric carcinoma.Serum antibody prevalence in populations with contrasting cancer risks. Cancer. 1990;66:2569-74.<br />55. Nogueira C, Figueiredo C, Carneiro F, Gomes AT, Barreira R, Figueira P, et al. Helicobacter pylorigenotypes may determine gastric histopathology. Am J Pathol. 2001;158:647-54. <br />56. Camargo MC, Yépez MC, Cerón C, Guerrero N, Bravo LE, Correa P, et al. Age at acquisition of Helicobacter pylori infection: Comparison of two areas with contrasting risk of gastric cancer. Helicobacter.2004;9:262-70.<br />57. Correa P, Malcom G, Schmidt B, Fontham E, Ruíz B, Bravo JC, et al. Review article: Antioxidant micronutrients and gastric cancer. Aliment Pharmacol Ther. 1998;12(Suppl.1):73-82.<br />58. Muñoz N, Aristizábal N, Zafra G, Rabson A, Pearson G. Anticuerpos contra virus herpes en pacientes con carcinoma de cuello uterino, condiloma acuminado y controles. Acta Médica. 1975;6:103-6.<br />59. Molano M, van den Brule A, Plummer M, Weiderpass E, Posso H, Arslan A, et al. Determinants of clearance of human papillomavirus infections in Colombian women with normal cytology: A population-based, 5-year followup study. Am J Epidemiol. 2003;158:486-94.<br />60. Muñoz N, Bosch FX, de Sanjose S, Tafur L, Izarzugaza I, Gili M, et al. The causal link between human papillomavirus and invasive cervical cancer: A population-based case-control study in Colombia and Spain. Int J Cancer. 1992; 52:743-9.<br />61. Molano M, Posso H, Weiderpass E, van den Brule AJ, Ronderos M, Franceschi S, et al. Prevalence and determinants of HPV infection among Colombian women with normal cytology. Br J Cancer. 2002;87:324-33.<br />62. Muñoz N. Human papillomavirus and cancer: The epidemiological evidence. J Clin Virol. 2000;19:1-5.<br />63. Smith JS, Bosetti C, Muñoz N, Herrero R, Bosch FX, Eluf-Neto J, et al. IARC multicentric case-control<br />study. Chlamydia trachomatis and invasive cervical cancer: A pooled analysis of the IARC multicentric casecontrol<br />study. Int J Cancer. 2004;111:431-9. <br />64. Muñoz N, Bosch FX. Cervical cancer and human papillomavirus: Epidemiological evidence and perspectives for prevention. Salud Pública Mex. 1997;39:274-82.<br />65. Koutsky LA, Ault KA, Wheeler CM, Brown DR, Barr E, Alvarez FB, et al. A controlled trial of a human papillomavirus type 16 vaccine. N Engl J Med. 2002;347:1645-51.<br />66. Anonymus. Colombian National Cancer Institute. Oncology. 1981;38:126-7.<br />67. Diaz J, García E, Melo M. Historia de la patología en Colombia. [Fecha de consulta: 15 de noviembre de<br />2007]. Disponible en http://www.conganat.org/9congreso/vistaImpresion.asp?id_trabajo= 735&tipo=1<br />68. Mora JO, de Paredes B, de Navarro L, Rodríguez E.Consistent improvement in the nutritional status of Colombian children between 1965 and 1989. Bull Pan Am Health Organ. 1992;26:1-13.<br />69. Mora JO, de Paredes B, Wagner M, de Navarro L, Suescun J, Christiansen N, et al. Nutritional supplementation and the outcome of pregnancy. I. Birth weight. Am J Clin Nutr. 1979;32:455-62.<br />70. Vuori L, Christiansen N, Clement J, Mora JO, Wagner M, Herrera MG. Nutritional supplementation and the outcome of pregnancy. II. Visual habituation at 15 days. Am J Clin Nutr. 1979;32:463-9.<br />71. Vuori L, de Navarro L, Christiansen N, Mora JO, Herrera MG. Food supplementation of pregnant women at risk of malnutrition and their newborns’responsiveness to stimulation. Dev Med Child Neurol.1980;22:61-71.<br />72. Waber DP, Vuori-Christiansen L, Ortíz N, Clement JR, Christiansen NE, Mora JO, et al. Nutritional supplementation, maternal education, and cognitive development of infants at risk of malnutrition. Am J Clin Nut. 1981;34:797-803.<br />73. Mora JO, Herrera MG, Suescun J, de Navarro L, Wagner M. The effects of nutritional supplementation on physical growth of children at risk of malnutrition. Am J Clin Nutr. 1981;34:1885-92.<br />74. Overholt C, Sellers SG, Mora JO, de Paredes B,Herrera MG. The effects of nutritional supplementation on the diets of low-income families at risk of malnutrition. Am J Clin Nutr. 1982;36:1153-61.<br />75. Restrepo M, Muñoz N, Day NE, Parra JE, de Romero L, Nguyen-Dinh X. Prevalence of adverse reproductive outcomes among a population occupationally exposed to pesticides in Colombia. Scand J Work Environ Health.1990;32:232-8.<br />76. Restrepo M, Muñoz N, Day N, Parra JE, Hernández C, Blettner M, et al. Birth defects among children born to a population occupationally exposed to pesticides in Colombia. Scand J Work Environ Health. 1990; 16: 239-46.<br />77. Gautret P, Barreto M, Méndez F, Zorrilla G, Carrasquilla G. High prevalence of malaria in a village<br />of the Colombian Pacific coast. Mem Inst Oswaldo Cruz. 1995;90:559-60.<br />78. González JM, Olano V, Vergara J, Arévalo-Herrera M, Carrasquilla G, Herrera S, et al. Unstable, lowlevel transmission of malaria on the Colombian Pacific Coast. Ann Trop Med Parasitol. 1997;91:349-58.<br />79. Nieto T, Méndez F, Carrasquilla G. Knowledge, beliefs and practices relevant for malaria control in an endemic<br />urban area of the Colombian Pacific. Soc Sci Med.1999;49:601-9.<br />80. Méndez F, Muñoz A, Carrasquilla G, Jurado D, Arévalo-Herrera M, Cortese JF, et al. Determinants of treatment response to sulfadoxine-pyrimethamine and subsequent transmission potential in falciparum malaria. Am J Epidemiol. 2002;156:230-8.<br />81. Méndez F, Barreto M, Arias JF, Rengifo G, Muñoz J, Burbano ME, et al. Human and mosquito infections by dengue viruses during and after epidemics in a dengue-endemic region of Colombia, Am J Trop Med Hyg. 2006;74:678-83.<br />82. Méndez F, Carrasquilla G. Epidemiología de la malaria en el área urbana de Buenaventura: análisis de la ocurrencia en el período 1987-1993. Colombia Médica. 1995;26:77-85.<br />83. Moyano M, Mendez F. Erythrocyte defects and parasitemia density in patients with Plasmodium falciparum malaria in Buenaventura, Colombia. Rev Panam Salud Publica. 2005;18:25-32.<br />84. Carvajal H, de Herrera MA, Quintero J, Alzate A, Herrera S. Anopheles neivai: a vector of malaria in the Pacific lowlands of Colombia. Trans R Soc Trop Med Hyg. 1989;83:609.<br />85. Alvarado BE, Alzate A, Mateus JC, Carvajal R. Effects of an educational and participatory community intervention on malaria control in Buenaventura, Colombia. Biomédica. 2006;26:366-78.<br />86. Klevens J, Roca J. Nonviolent youth in a violent society: Vulnerability and resilience in the country of Colombia.<br />Violence Vict. 1999;14:311-22.<br />87. Klevens J, Bayon MC, Sierra M. Risk factors and context of men who physically abuse in Bogotá, Colombia. Child Abuse Negl. 2000;24:323-32.<br />88. Klevens J, Roca J, Restrepo O, Martínez A. Risk factors for adult male criminality in Colombia. Crim Behav<br />Ment Health. 2001;11:73-85.<br />89. Duque LF, Klevens J, Ramírez C. Cross sectional survey of perpetrators, victims, and witnesses of violence in Bogotá, Colombia. J Epidemiol Community Health. 2003;57:355-60.<br />90. Concha-Eastman A, Violence: a challenge for public health and for all. J Epidemiol Community Health. 2000;55:597-9.<br />91. Reyes C, Vélez LF, Espitía VE, Espinosa R. Lesiones fatales ocasionadas por vehículo motor a personas mayores de 60 años en Cali, 1993-1997. Colombia Médica. 1998;29:129-33.<br />92. Concha-Eastman A, Espitia VE, Espinosa R, Guerrero R. Epidemiología de los homicidios en Cali, Colombia, 1993-1998. Seis años de un modelo poblacional. Rev Panam Salud Pública. 2002;12:230-9.<br />93. Concha-Eastman A, Guerrero R. Epidemiologic surveillance for the prevention and control urban violence. Rev Panam Salud Pública. 1999;5:322-31.<br />94. Concha-Eastman A. Impacto social y económico de la violencia en las Américas. Biomédica. 2002;22:347-61. 95. Instituto de Investigaciones y Desarrollo en Prevención de Violencia y Promoción de la Convivencia Social (Cisalva). Quiénes somos. Origen. [Fecha de consulta: septiembre de 2007]. Disponible en: http://www.cisalva.univalle.edu.co/<br />quienes/quienes.html.<br />96. Dennis RJ, Maldonado D, Norman S, Baena E, Martínez G. Woodsmoke exposure and risk for obstructive airways disease among women. Chest.1996;109:15-9.<br />97. Cepeda MS, Boston R, Farrar JT, Strom BL. Comparison of logistic regression versus propensity score when the number of events is low and there are multiple confounders. Am J Epidemiol. 2003;158:280-7. 98. Pérez A, Dennis RJ, Rodríguez B, Castro AY,<br />Delgado V, Lozano J, et al. An interrupted time series<br />analysis of parental antibiotic use in Colombia. J Clin<br />Epidemiol. 2003;56:1013-20.<br />99. Cepeda MS, Álvarez H, Morales O, Carr DB. Addition of ultralow dose naloxone to postoperative morphine PCA: Unchanged analgesia and opioid requirement but decreased incidence of opioid side effects. Pain. 2004;107:41-6.<br />100. López-Jaramillo P, Casas JP, Bautista L, Serrano NC, Morillo CA. An integrated proposal to explain the epidemic of cardiovascular disease in a developing country. From socioeconomic factors to free radicals. Cardiology. 2001;96:1-6.<br />101. Accini JL, Sotomayor A, Trujillo F, Barrera JG, Bautista L, López-Jaramillo P. Colombian study to assess the use of noninvasive determination of endothelium-mediated vasodilatation (CANDEV). Normal values and factors associated. Endothelium. 2001;8:157-66.<br />102. Bautista LE, Ardila ME, Gamarra G, Vargas CI, Arenas IA. Angiotensin-converting enzyme gene polymorphism and risk of myocardial infarction in Colombia. Med Sci Monit. 2004;10:473-9. 103. Gómez LF, Duperly J, Lucumí DI, Gámez R, Venegas AS. Physical activity levels in adults living in Bogotá-Colombia: prevalence and factors associated. Gac Sanit. 2005;19:206-13.<br />104. Gómez LF, Mateus JC, Cabrera G. Leisure-time physical activity among women in a neighbourhood in Bogotá, Colombia: prevalence and socio-demographic correlates. Cad Saude Publica. 2004;20:1103-9. 105. Lucumí DI, Sarmiento OL, Forero R, Gomez LF, Espinosa G. Community intervention to promote consumption of fruits and vegetables, smoke-free homes, and physical activity among home caregivers in Bogotá, Colombia. Prev Chronic Dis. 2006;3:1-13.<br />106. Gómez LF, Parra DC, Lobelo F, Samper B, Moreno J, Jacoby E, et al. Television viewing and its association with overweight in Colombian children: results from the 2005 National Nutrition Survey: A cross sectional study. Int J Behav Nutr Phys Act. 2007;19:41-8.<br />107. Poveda G, Rojas W, Quiñones ML, Vélez ID, Mantilla RI, Ruiz D, et al. Coupling between annual and ENSO timescales in the malaria-climate association in Colombia. Environ Health Perspect. 2001;109:489-93.<br />108. Velandia M, Fridkin SK, Cárdenas V, Boshell J, Ramírez G, Bland L, et al. Transmission of HIV in dialysis centre. Lancet. 1995;345:417-22.<br />109. Cárdenas V, Sánchez C, De la Hoz F, Jara JH, Velandia M, Martínez M, et al. Colombian field epidemiology training program. Am J Public Health.1998;88:1404-5. <br />110. Guerrero MI, Franco CI, de la Hoz F. The epidemiological evidence for an association between extrapulmonary tuberculosis and AIDS in Colombia. Tuber Lung Dis. 1994;75:160-1.<br />111. De la Hoz F, Higuera AB, Fabio JL, Luna M, Naranjo AG, Valencia Mde L, et al. Effectiveness of Haemophilus influenzae type b vaccination against bacterial pneumonia in Colombia. Vaccine. 2004; 23:36-42.<br />112. Tamayo M, Koblavi S, Grimont F, Castaneda E, Grimont PA. Molecular epidemiology of Vibrio cholerae O1 isolates from Colombia. J Med Microbiol. 1997;46:611-6. <br />113. Gómez AR, Sánches IS, Aires de Sousa M, Castañeda E, de Lencastre H. Molecular epidemiology of methicillin-resistant Staphylococcus aureus in Colombian hospitals: dominance of a single unique multidrug-resistant clone. Microb Drug Resist. 2001; 7:23-32.<br />114. Páez A, Nuñez C, García C, Boshell J. Molecular epidemiology of rabies epizootics in Colombia: Evidence for human and dog rabies associated with bats. J Gen Virol. 2003;84:795-802. <br />115. Villegas MV, Correa A, Pérez F, Miranda MC, Zuluaga T, Quinn JP. Prevalence and characterization of extended-spectrum betalactamases in Klebsiella pneumoniae and Escherichia coli isolates from Colombian hospitals. Diagn Microbiol Infect Dis. 2004;49:217-22.<br />116. Arbeláez MP, Gaviria MB, Franco A, Restrepo R, Hincapié D, Blas E. Tuberculosis control and managed competition in Colombia. Int J Health Plann Manage. 2004;19(Suppl.1):S25-43. <br />117. Arbeláez MP, Ocampo MC, Montoya J, Jaramillo LM, Giraldo PM, Maldonado A, et al. Evaluation of the tuberculin reaction in health occupation students, Rev Panam Salud Pública. 2000;8:272-9.<br />118. Arbeláez MP, Nelson KE, Muñoz A. BCG vaccine effectiveness in preventing tuberculosis and its interaction with human immunodeficiency virus infection. Int J Epidemiol. 2000;29:1085-91. <br />119. Rodríguez JI, Arias M, París SC, Arbeláez MP, Betancur J, García LF. Tuberculin skin test and CD4+/CD8+ T cell counts in adults infected with the human immunodeficiency virus in Medellín, Colombia. Mem Inst Oswaldo Cruz. 1997;92:245-50. <br />120. Vélez ID, Gilchrist K, Arbeláez MP, Rojas CA, Puerta JA, Antunes CM, et al. Failure of a killed Leishmania amazonensis vaccine against American cutaneous leishmaniasis in Colombia, Trans R Soc Trop Med Hyg. 2005;99:593-8. <br />121. Herrera JA, Parra B, Herrera E, Botero JE, Arce RM, Contreras A, et al. Periodontal disease severity is related to high levels of C-reactive protein in preeclampsia. J Hypertens. 2007;25:1459-64.<br />122. Contreras A, Herrera JA, Soto JE, Arce RM, Jaramillo A, Botero JE. Periodontitis is associated with preeclampsia in pregnant women. J Periodontol. 2006;77:182-8. <br />123. Herrera JA, Chaudhuri G, López-Jaramillo P. Is infection a major risk factor for preeclampsia? Med Hypotheses. 2001;57:393-7.<br />124. Becher JC, Garcia JG, Kaplan DW, Gil AR, Li J, Main D, et al. Reproductive health risk behavior survey of Colombian high school students. J Adolesc Health. 1999;24:220-5. <br />125. Herrera JA, Arévalo-Herrera M, Herrera S. Prevention of preeclampsia by linoleic acid and calcium supplementation: a randomized controlled trial. Obstet Gynecol. 1998; 91:585-90. <br />126. Herrera JA, Shahabuddin AK, Ersheng G, Wei Y, García RG, López-Jaramillo P. Calcium plus linoleic acid therapy for pregnancy-induced hypertension, Int J Gynaecol Obstet. 2005;91:221-7. <br />127. Herrera JA, Salmeron B, Hurtado H. Prenatal biopsychosocial risk assessment and low birthweight. Soc Sci Med 1997;44:1107-14.<br />128. Herrera JA, Alvarado JP, Restrepo W. Riesgo biosicosocial prenatal y preeclampsia. Atenc Prim. 1995;16:552-5.<br />129. Herrera JA. Nutritional factors and rest reduce pregnancy-induced hypertension and pre-eclampsia in positive roll-over test primigravidas. Int J Gynaecol Obstet. 1993;41:31-5. <br />130. Charpak N, Ruiz-Pelaez JG, Charpak Y. Rey- Martinez Kangaroo mother program: An alternative way of caring for low birth weight infants? One year mortality in a two cohort study. Pediatrics. 1994;94:804-10. <br />131. Valero MV, Amador R, Aponte JJ, Narváez A, Galindo C, Silva Y, et al. Evaluation of SPf66 malaria vaccine during a 22-month follow-up field trial in the Pacific coast of Colombia. Vaccine. 1996;14:1466-70.<br />132. White ME, McDonnell SM, Werker DH, Cárdenas VM, Thacker SB. Partnerships in international applied epidemiology training and service, 1975-2001. Am J Epidemiol, 2001;154:993-9. 133. Tephinet: Training Programs in Epidemiology and Public Health Interventions Network. [Fecha de consulta: septiembre de 2007]. Disponible en: www.tephinet.org/index.php 134. Organización Panamericana de la Salud. Primer informe sobre la enseñanza de la medicina preventiva y social en las escuelas de medicina de la América Latina. Educ Med Salud. 1969;3:132-55. <br />135. Eslava JC. Buscando el reconocimiento profesional. La salud pública en Colombia, en la primera mitad del siglo XX. Bogotá DC: Instituto de Salud Pública– Universidad Nacional de Colombia; 2004. <br />136. Echeverri EG, Correa F. Memoria sobre la Facultad Nacional de Salud Pública. Medellín: Universidad de Antioquia; 1999. 137. Restrepo HE. La evolución de la epidemiología en la América Ibérica: la enseñanza y la práctica de la epidemiología. Revista de la Facultad Nacional de Salud Pública. 1995;13:54-72. <br />138. Colimon KM. Fundamentos de epidemiología. Medellín: Colimon; 1978. <br />139. Llanos G. La alegría de publicar 1. Revisión por expertos. Colombia Médica. 1996;27:37-8. <br />140. Universidad del Valle. Escuela de Salud Pública. [Fecha de consulta: septiembre de 2007]. Disponible en: http://saludpublica.univalle.edu.co/Presentacion.html. <br />141. Méndez F, Barreto M, Arias JF, Rengifo G, Munoz J, Burbano ME, et al. Human and mosquito infections by dengue viruses during and after epidemics in a dengue-endemic region of Colombia. Am J Trop Med Hyg. 2006;74:678-83. <br />142. Loyola EG, Alzate A, Sánchez A, González A.Epidemiology of a natural focus of Leishmania braziliensis in the Pacific lowlands of Colombia. III. Natural infections in wild mammals. Trans R Soc Trop Med Hyg. 1988;82:406-7. <br />143. Guerrero R, Gonzáles C, Medina E. Epidemiología.Wilmington: Addison Wesley Iberoamericana; 1986. <br />144. International Clinical Epidemiology Network. INCLEN 1997-1998 Annual Report. Philadelphia: INCLEN; 1998. <br />145. Anónimo. Doctor Rodrigo Guerrero miembro del Instituto Nacional de Salud de los Estados Unidos (editorial). Colombia Médica. 1996;27:100. <br />146. Acero H. Reducción de la violencia y la delincuencia en Bogotá, Colombia, 1994-2002. Biomédica. 2002;22:362-72.<br />147. Thomas DC, Clayton DG. Betting odds and genetic associations. J Natl Cancer Inst. 2004;96:421-3. <br />148. Thomas DC. Genetic epidemiology with a capital “E”. Genet Epidemiol. 2000;19:289-300. <br />149. Krieger N. Theories for social epidemiology in the 21st century: An ecosocial perspective. Int J Epidemiol. 2001;30:668-77.
oai:oai.revistabiomedica.org:article/55
2009-12-24T18:03:33Z
biomedica:ARTI
Preliminary evaluation of the Culicoides biting nuisance (Diptera: Ceratopogonidae) in the province of Boyacá, Colombia
Diagnóstico preliminar de la molestia sanitaria causada por Culicoides (Diptera: Ceratopogonidae) en el departamento de Boyacá, Colombia
Santamaría, Erika
Cabrera, Olga Lucía
Zipa, Yaneth
Ferro, Cristina
Ahumada, Martha Liliana
Pardo, Raúl Hernando
Ceratopogonidae
dermatitis
public health
Andean ecosystem
Introduction. Inhabitants in the western border of Boyacá province have reported high nuisance levels and dermatologic problems caused by the intensely irritating bites of the very small flies of the genus Culicoides. Objective. A survey was carried out to locate the affected area, identify the anthropophylic Culicoides species and estimate its abundance in Boyacá. Materials and methods. Nuisance reports and clinical records of dermatologic cases associated with Culicoides bites were requested from health authorities in counties where nuisance reports had been received or which had geographical features apparently favorable for Culicoides infestations. An outdoors entomological survey using human landing catches was undertakenin areas reporting a pest problem.Results. Culicoides infestations were confirmed as a serious nuisance problem in the rural areas of nine counties located in the western foothills of the Eastern Range of the Colombian Andes. Although available epidemiological records were fragmented, it was established that in six counties 11.4% of the dermatitis cases (total=2,472 cases) reported between 2003 and 2005 were attributed to the Culicoides bites. The entomological survey identified Culicoides pachymerus as the dominant species, 99.3% of 3,389 caught females. Biting rates in the most intensely affected areas reach a geometric mean of 52 females/person per 5 minutes. Multivariate analysis indicated that abundance of C. pachymerus had a negative relationship with altitude.Conclusions. Based on its dominance and high biting rates, C. pachymerus is probably the species responsible for the high nuisance levels caused by Culicoides bites and the associated dermatological pathology, within the study area.
Introducción. Los habitantes del occidente del departamento de Boyacá han reportado molestia sanitaria y problemas dermatológicos ocasionados por la constante picadura de insectos del género Culicoides.Objetivo. Identificar el área de Boyacá afectada por Culicoides, determinar las especies antropofílicas involucradas y su abundancia. Materiales y métodos. Se solicitó información sobre la molestia sanitaria y el registro de casos dermatológicos asociados a la picadura de Culicoides a las autoridades de salud de los municipios que por sus reportes previos o por sus características geográficas se consideraron como potencialmente afectados. En los municipios que informaron sufrir la problemática, se realizó un muestreo entomológico con atrayente humano afuera de las viviendas. Resultados. Se confirmó la gravedad de la molestia en el área rural de nueve municipios ubicados en el flanco occidental de la Cordillera Oriental. Aunque los registros epidemiológicos fueron fragmentados, se estableció que en seis municipios el 11,4% de los casos (n=2.472) de dermatitis reportados entre el 2003 y el 2005 fueron atribuidos a la picadura de Culicoides. Los resultados entomológicos mostraron que la especie dominante fue Culicoides pachymerus,99,3% de las 3.389 hembras recolectadas, con tasas de picadura (promedios geométricos) por municipio de hasta 52 hembras/persona en 5 minutos. Mediante análisis multivariado, se encontró que la abundancia de esta especie se relaciona negativamente con la altitud. Conclusiones. Por su dominancia y altas tasas de picadura, C. pachymerus es muy probablemente la especie responsable de la molestia sanitaria y los problemas dermatológicos causados por Culicoides en el departamento de Boyacá.
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/55
10.7705/biomedica.v28i4.55
Biomedica; Vol. 28 No. 4 (2008); 497-509
Biomédica; Vol. 28 Núm. 4 (2008); 497-509
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/55/56
https://revistabiomedica.org/index.php/biomedica/article/view/55/383
/*ref*/Mullen GR. Biting midges (Ceratopogonidae). En: Mullen G, Durden L, editors. Medical and veterinary entomology. San Diego: Academic Press; 2002. p. 163-83. <br />2. Kettle DS. Ceratopogonidae (Biting midges). En: Kettle DS, editor. Medical and veterinary entomology. Second edition. Cambridge: CAB Internacional; 1995. p. 152-76. <br />3. Forattini OP. Culicoides da Regiao Neotropical (Diptera: Ceratopogonidae). Arq Fac Hig Saude Publica Univ Sao Paulo. 1957;11:161-526. <br />4. Sherlock IA, Guitton N. Dermatozoonosis by Culicoides´bite (Diptera: Ceratopogonidae) in Salvador, state of Bahia, Brazil. IV. A clinical study. Mem Inst Oswaldo Cruz. 1965;63:27-37. <br />5. Borkent A. The biting midges, the Ceratopogonidae (Diptera). En: Marquardt WC, editor. Biology of disease vectors. Second edition. Burlington MA: Elsevier Academic Press; 2005. p. 113-26.<br />6. Tesh RB. The emerging epidemiology of Venezuelan hemorrhagic fever and Oropouche fever in tropical South America. Ann NY Acad Sci. 1994;740:129-37. 7. Linley JR, Hoch AL, Pinheiro FP. Biting midges (Diptera: Ceratopogonidae) and human health. J Med Entomol. 1983;20:347-64.<br />8. Leduc JW, Hoch AL, Pinheiro FP, Travassos Da Rosa AP. Epidemic Oropouche virus disease in northern Brazil. Bull Pan Am Health Organ. 1981;15:97-103. 9. Undiano C. Importance and present-day concepts of pathogenicity of Mansonella infections. Rev Fac Ciencias Med Córdoba. 1966;24:183-9.<br />10. Tidwell MA, Tidwell MA. Development of Manzonella ozzardi in Simulium amazonicum, S. argentiscutum and Culicoides insinuatus from Amazonas, Colombia. Am J Trop Med Hyg. 1982;31:1137-41.<br />11. Homan EJ, Taylor WP, De Ruiz L, Yuill TM. Bluetongue virus and epizootic haemorrhagic disease of deer virus serotypes in northern Colombian cattle. J Hyg (Lond). 1985;95:165-72.<br />12. Rodriguez MA, Wirth WW. A new species of manbiting Culicoides from the high Andes of Colombia (Diptera: Ceratopogonidae). Florida Ent. 1986;69:311-4. <br />13. Villarreal LI. Estrategia de control de Culicoides sp., en el departamento de Boyacá. Boletín Epidemiológico de Boyacá. Tunja: Secretaría de Salud de Boyacá. 1998. p. 105-10. <br />14. Barreto P. Catálogo de los Culicoides (Diptera: Ceratopogonidae) de Colombia. Colombia Med. 1986; 17:140-50. <br />15. Browne JE. Light-trap population studies of the Culicoides from three life zones in Colombia with notes on biting habits and larval habitats (Diptera: Ceratopogonidae) (thesis). New Orleans: Tulane University; 1978. p. 134. 16. Hoch AL, Roberts DR, Pinheiro FP. Host-seeking behavior and seasonal abundance of Culicoides paraensis (Diptera: Psychodidae) in Brazil. J Am Mosq Control Assoc. 1990;6:110-4. <br />17. Wirth WW, Dyce AL, Spinelli GR. An atlas of wing photographs, with a summary of the numerical charac ters of the neotropical species of Culicoides (Diptera: Ceratopogonidae). Contrib Am Ent Inst. 1988;25:1-72. <br />18. Spinelli G, Wirth W. Clave para la identificación de las especies del género Culicoides presentes al sur de la Cuenca Amazónica, nuevas citas y notas sinonímicas (Diptera: Ceratopogonidae). Rev Soc Entomol Argentina. 1985;44:49-75.<br />19. Wirth WW, Blanton FS. Biting midges of the genus Culicoides from Panama (Diptera: Heleidae). Proceedings of the United States National Museum. 1959;109:237-482.<br />20. Crawley MJ. GLIM for ecologist. Oxford: Blackwell Scientific Publications: 1993. p. 380.<br />21. Kettle DS, Linley JR. The biting habits of Jamaican sandflies. Preferences for individuals, limbs and site positions. Part I Introduction and Culicoides barbosai Wirth y Blanton. Jamaica: Ministry of Health; 1960.<br />22. Jenkins DW. Ecological observations on the blackflies and punkies of Central Alaska. Mosq News. 1948;8: 148-54. <br />23. Sailer RI, Marks EP, Lienk S. Notes on Culicoides in Alaska (Diptera, Heleidae). Mosq News. 1956;16:270-8. <br />24. Fox I. Notes on Puerto Rican biting midges or Culicoides (Diptera, Ceratopogonidae). Bull Brooklyn Entomol Soc. 1949;44:29-34.<br />25. Carpenter SJ. Studies of Culicoides in the Panama Canal Zone (Diptera, Heleidae). Mosq News. 1951;2:202-8. 26. Blanton FS, Wirth WW. The sand flies (Culicoides) of Florida (Diptera: Ceratopogonidae). Arthropods of Florida 1979;10:1-204.<br />27. Whelan P. Biting midges or “sandflies” in the Northern Territory. The Northern Territory Disease Control Bulletin. 2003;10:1-10. <br />28. Sherlock IA, Guitton N. Dermatozoonosis by Culicoides´bite (Diptera: Ceratopogonidae) in Salvador, State of Bahia, Brazil. III. Epidemiological aspects. Mem Ins Oswaldo Cruz. 1965;63:1-12. <br />29. Agbolade OM, Akinboye DO, Olateju TM, Ayanbiyi OA, Kuloyo OO, Fenuga OO. Biting of anthropophilic Culicoides fulvithorax (Diptera: Ceratopogonidae), a vector of Mansonella perstans in Nigeria. Korean J Parasitol. 2006;44:67-72. <br />30. Conte A, Goffredo M, Ippoliti C, Meiswinkel R. Influence of biotic and abiotic factors on the distribution and abundance of Culicoides imicola and the Obsoletus complex in Italy. Vet Parasitol. 2007;150:333-44.<br />31. Bishop AL, Spohr LJ, Barchia IM. Effects of altitude, distance and waves of movement on the dispersal in Australia of the arbovirus vector, Culicoides brevitarsis Kieffer (Diptera: Ceratopogonidae). Preventive Vet Med. 2004;65:135-45.
oai:oai.revistabiomedica.org:article/56
2009-12-24T18:03:33Z
biomedica:ARTI
Autoimmune syndrome in the tropical spastic paraparesis/myelopathy associated with human T-lymphotropic virus infections
Síndrome autoinmune en la paraparesia tropical espástica/ mielopatía asociada a la infección por el virus linfotrópico humano tipo I de la costa pacífica colombiana
García, Felipe
Domínguez, Martha C.
Torres, Miyerlandi
Tamayo, Óscar
Criollo, William
Quintana, Milton
Sánchez, Adalberto
paraparesia espástica
virus linfotrópico de células T humanas tipo 1
virus 1 T-linfotrópico de los primates
médula espinal
autoanticuerpos
autoinmunidad
imitación molecular
paraparesis
spastic
human T-lymphotropic virus 1
primateT-lymphotropic virus 1
spinal cord
autoantibodies
autoimmunity
molecular mimicry
Introduction. Previous reports have given evidence that in tropical spastic paraparesis (TSP)/ human T-lymphotrophic virus (HTLV-I)-associated myelopathy (HAM), an autoimmune process occurs as part of its pathogenesis.Objective. The roles of autoimmunity and the molecular mimicry was evaluated in TSP/HAMpatients.Materials and methods. Plasma samples were characterized from patients in the Pacific coastal region of Colombia. Thirty-seven were identified as TSP/HAM, 10 were diagnosed with adult Tcell leukemia virus, 22 were asymptomatic carriers but seropositive for HTLV-I and 20 were seronegative and served as negative controls. Plasmatic levels of the following were determined: antinuclear antibody (ANA) levels, anticardiolipine-2 (ACL_2), interferon- (IFN-??) and interleukin- 4 (IL-4). Using Western blot, the crossreactivity of the seropositive and seronegative samples was evaluated against proteins extracted from several central nervous system components of non infected Wistar rats. The HTLV-I seropositive plasmas were crossreacted with a monoclonal tax (LT4 anti-taxp40) from spinal cord neurons of non infected Wistar rats. Results. Of the TSP/HAM patients, 70.2% were reactive against ANA and 83.8% against ACL- 2, in contrast with those ATL and asymptomatic seropositives subjects that were not reactive (P<0.001). Moreover, 70.3% had detectable levels of IFN and 43.2% had detectable IL-4. LT4 anti-taxp40 and plasma of TSP/HAM exhibited cross reactivity with a MW 33-35 kDa protein from the rat spinal cord nuclei. Conclusion. Support was provided for the existence of an autoimmune syndrome mediated by molecular mimicry; the syndrome was responsible for some of the axonal degeneration observed in TSP/HAM patients.
Introducción. Trabajos previos han aportado evidencias de que en la paraparesia espástica tropical/mielopatía asociada con el virus linfotrópico humano tipo I, existe un componente autoinmune asociado a su patogénesis. Objetivo. Evaluar el estado autoinmune y la existencia de mimetismo molecular en pacientes con paraparesia espástica tropical del pacífico colombiano. Materiales y métodos. A partir de muestras de plasma de 37 pacientes con paraparesia espástica tropical/mielopatía asociada al HTLV-I, 10 con leucemia de células T del adulto, 22 individuos portadores asintomáticos y 20 seronegativos para el HTLV-I, se determinaron niveles plasmáticos de anticuerpos antinucleares y anticardiolipina-2 y de interferón-??e interleucina- 4. Se evaluó, por Western blot, la reactividad cruzada de plasmas contra proteínas obtenidas de varias fuentes celulares normales del sistema nervioso. Además, se estudió la reactividad cruzada de plasmas de seropositivos y del anticuerpo monoclonal LT4 anti-taxp40 en secciones de médula espinal de ratas Wistar no infectadas. Resultados. El 70,2% y el 83,8% de los pacientes con paraparesia espástica tropical fueron reactivos para anticuerpos ANA y ACL-2, respectivamente, en contraste con los de leucemia de células T del adulto y los seropositivos asintomáticos (P<0,001). Además, el 70,3% y el 43,2% de los pacientes con paraparesia espástica tropical tuvieron niveles detectables de IFN-?? e IL-4, respectivamente. El anticuerpo LT4 anti tax-p40 y los plasmas de paraparesia espástica tropical/mielopatía asociada al HTLV-I mostraron una reacción cruzada con una proteína de PMr 33-35 kDa, obtenida del núcleo de neuronas de la médula espinal de ratas Wistar no infectadas. Conclusión. Se obtuvieron evidencias que apoyan la existencia de un síndrome autoinmune mediado por mimetismo molecular como parte de la etiopatogénesis de la degeneración axonal observada en la paraparesia espástica tropical en pacientes colombianos de la costa pacífica.
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/56
10.7705/biomedica.v28i4.56
Biomedica; Vol. 28 No. 4 (2008); 510-522
Biomédica; Vol. 28 Núm. 4 (2008); 510-522
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/56/57
https://revistabiomedica.org/index.php/biomedica/article/view/56/385
/*ref*/Shuh M, Beilke M. The human T-cell leukemia virus type 1 (HTLV-1): new insights into the clinical aspects and molecular pathogenesis of adult T-cell leukemia/ lymphoma (ATLL) and tropical spastic paraparesis/ HTLV-associated myelopathy (TSP/HAM). Microsc Res Tech. 2005;68:176-96. <br />2. Vernant JC, Maurs L, Gessain A, Barin F, Gout O, Delaporte JM, et al. Endemic tropical spastic paraparesis associated with human T-lymphotropic virus type I: a clinical and seroepidemiological study of 25 cases. Ann Neurol. 1987;21:123-30. <br />3. Osame M, Matsumoto M, Usuku K, Izumo S, Ijichi N, Amitani H, et al. Chronic progressive myelophathy associated with elevated antibodies to human Tlymphotropic virus type I and adult T-cell leukemia like cells. Ann Neurol. 1987;21:117-22. <br />4. Zaninovic V, Galindo J, Blank A. Paraparesia espástica tropical en Colombia. En: Enfermedades asociadas con el virus HTLV-I. Cali: Fundación MAR; 1992. p. 77-86. <br />5. Bartholomew C, Jack N, Edwards J, Charles W, Corbin D, Cleghorn FR, et al. HTLV-I serostatus of mothers of patients with adult T-cell leukemia and HTLVI- associated myelopathy/tropical spastic paraparesis. J Hum Virol. 1998;1:302-5. <br />6. Chávez M, Domínguez MC, Blank A, Quintana M, Eizuru Y, García-Vallejo F. Reconstrucción de la evolución molecular de la infección actual por el virus linfotrópico humano tipo I en Colombia. Biomédica. 2004;24:65-72. <br />7. Balcázar N, Sánchez G, García-Vallejo F. Sequence and phylogenetic analysis of Human T-Lymphotropic Virus type 1 from Tumaco, Colombia. Mem Inst Oswaldo Cruz. 2003 98:641-8 <br />8. Trujillo JM, Concha M, Muñoz A, Bergonzoli G, Mora C, Borrero I, et al. Seroprevalence and cofactors of HTLV-I infection in Tumaco, Colombia. AIDS Res Hum Retroviruses. 1992;8:651-7. <br />9. Nakamura H, Kawakami A, Tominaga M, Hida A, Yamasaki S, Migita K, et al. Relationship between Sjögren’s syndrome and human T-lymphotropic virus type I infection: follow-up study of 83 patients. J Lab Clin Med. 2000;135:139-44. <br />10. Fox RI, Stern M, Michelson P. Update in Sjögren syndrome. Curr Opin Rheumatol. 2000;12:391-8. <br />11. Beger E, Deocharan E, Edelman M, Erblich B, Gu Y, Putterman C. A peptide DNA surrogate accelerates autoimmune manifestations and nephritis in lupus-prone mice. J Immunol. 2002;168:3617-26. <br />12. Bangham CR. HTLV-1 infections. J Clin Pathol. 2000;53:581-6. <br />13. Asquith B, Zhang Y, Mosley AJ, de Lara CM, Wallace DL, Worth A, et al. In vivo T lymphocyte dynamics in humans and the impact of human T-lymphotropic virus 1 infection. Proc Natl Acad Sci USA. 2007; 104:8035-40. <br />14. Verdonck K, González E, van Dooren S, Vandamme AM, Vanham G, Gotuzzo E. Human T-lymphotropic virus 1: recent knowledge about an ancient infection. Lancet Infect Dis. 2007;7:266-81. <br />15. Trujillo JR, Mclane MF, Lee TH, Essex M. Molecular mimicry between the human immunodeficiency virus type 1 gp120 V3 loop and human brain proteins. J Virol. 1993;67:7711-5. <br />16. Levin MC, Krikavsky M, Berck J, Foley S, Rosenfeld M, Dalmau J, et al. Neuronal molecular mimicry in immune-mediated neurologic disease. Ann Neurol. 1998;44:87-98. <br />17. Levin MC, Lee SM, Kalume F, Morcos Y, Dohan FC Jr, Hasty KA, et al. Autoimmunity due to molecular mimicry as a cause of neurological disease. Nat Med. 2002;8:509-13. <br />18. García-Vallejo F, Domínguez MC, Tamayo O. Autoimmunity and molecular mimicry in tropical spastic paraparesis/human T-lymphotropic virus-associated myelopathy. Braz J Med Biol Res. 2005;38:241-50. <br />19. Tanaka Y, Zeng L, Shiraki H, Shida H, Tozawa H. Identification of a neutralization epitope on the envelope gp46 antigen of human T cell leukemia virus type I and induction of neutralizing antibody by peptide immunization. J Immunol. 1991;147:354-60. <br />20. Lee B, Tanaka Y, Tozawa H. Monoclonal antibody defining tax protein of human T-cell leukemia virus type- I. Tohoku J Exp Med.1989;157:1-11. <br />21. Burnette WN. “Western blotting”: Electroforetic transfer of proteins from sodium dodecyl sulfate-polyacrilamide gels to unmodified nitrocellulose and radiographic detection with antibody and radiodinated protein. Anal Biochem. 1981;112:195-203. <br />22. Barin F, M’Boup S, Denis F, Kanki P, Allan JS, Lee TH, et al. Serological evidence for virus related to simian T-lymphotropic retrovirus III in residents of West Africa. Lancet. 1985;2:1387-9. <br />23. Hsu S, Raine L, Fanger H. Use of avidine-biotineperoxidase complex (ABC) in immnuperoxidase techniques: A comparison between ABC and unlabeled antibody (PAP) procedure. J. Histochem Cytochem. 1981;29:577. <br />24. Shi SR, Iman A, Young L, Cote R, Taylor CR. Antigen retrieval immunohistochemistry under the influenza of using monoclonal antibodies. J Histochem Cytochem. 1995; 43:193-201. <br />25. Ochi H, Wu XM, Osoegawa M, Horiuchi I, Minohara M, Murai H, et al. Tc1/Tc2 and Th1/Th2 balance in Asian and Western types of multiple sclerosis, HTLV-Iassociated myelopathy/tropical spastic paraparesis and hyper-IgEaemic myelitis. J Neuroimmunol. 2001; 119: 297-305. <br />26. Wu X, Osoegawa M, Yamasaki K, Kawano Y, Ochi H, Horiuchi I, et al. Flow cytometric differentiation of Asian and Western types of multiple sclerosis, HTLV- 1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and hyperIgEaemic myelitis by analyses of memory CD4 positive T cell subsets and NK cell subsets. J Neurol Sci. 2000;177:24-31. <br />27. Horiuchi I, Kawano Y, Yamasaki K, Minohara M, Furue M, Taniwaki T, et al. Th1 dominance in HAM/ TSP and the optico-spinal form of multiple sclerosis versus Th2 dominance in mite antigen-specific IgE myelitis. J Neurol Sci. 2000;172:17-24. <br />28. Azran I, Schavinsky-Khrapunsky Y, Aboud M. Role of Tax protein in human T-cell leukemia virus type-I leukemogenicity. Retrovirology. 2004;1:20-43 <br />29. Barmak K, Harhaj E, Grant C, Alefantis T, Wigdahl B. Human T cell leukemia virus type I-induced disease: pathways to cancer and neurodegeneration. Virology. 2003;308:1-12. <br />30. Levin MC, Lee SM, Morcos Y, Brady J, Stuart J. Cross-reactivity between immunodominant human T lymphotropic virus type I tax and neurons: implications for molecular mimicry. J Infect Dis. 2002;186:1514-7 <br />31. Lee SM, Dunnavant FD, Jang H, Zunt J, Levin MC. Autoantibodies that recognize functional domains of hnRNPA1 implicate molecular mimicry in the pathogenesis of neurological disease. Neurosci Lett. 2006;401:188-93. <br />32. Caporali R, Bugatti S, Bruschi E, Cavagna L, Montecucco C. Autoantibodies to heterogeneous nuclear ribonucleoproteins. Autoimmunity. 2005; 38: 25-32. <br />33. Princler GL, Julias JG, Hughes SH, Derse D. Roles of viral and cellular proteins in the expression of alternatively spliced HTLV-1 pX mRNAs. Virology. 2003;317:136-45. <br />34. Kress E, Hachem BH, Bex F, Gazzolo L, Duc M. Critical role of hnRNP A1 in HTLV-1 replication in human transformed T lymphocytes. Retrovirology. 2005;2:1-8.
oai:oai.revistabiomedica.org:article/57
2009-12-24T18:09:11Z
biomedica:ARTI
Alta frecuencia de mutaciones puntuales en pfcrt de Plasmodium falciparum y emergencia de nuevos haplotipos mutantes en Colombia
Alta frecuencia de mutaciones puntuales en pfcrt de Plasmodium falciparum y emergencia de nuevos haplotipos mutantes en Colombia
Maestre, Amanda
Carmona-Fonseca, Jaime
Maestre, Amanda
Plasmodium falciparum
malaria
antimalarials
chloroquine
mutation
Colombia
Plasmodium falciparum
malaria
antimaláricos
cloroquina
Colombia
mutación
Introduction. Studies on the molecular epidemiology of antimalarial resistance constitute a useful tool to understand the events underlying treatment failure and resistance in falciparum malaria in Colombia. Several authors have reported on the efficacy of some molecular markers to predict drug resistance in Plasmodium falciparum. The P. falciparum pfcrt gene has been widely characterized in this context. Objective. The frequency of pfcrt gene mutations in P. falciparum were associated with treatment failure to the antimalarials chloroquine, mefloquine, amodiaquine and sulfadoxine/ pyrimethamine. Materials and methods. A representative sample of 172 patients with non-complicated falciparum malaria was selected from two highly malaria-endemic areas of northeastern Colombia, the Turbo and Bajo Cauca regions. These patients were assessed for treatment response together with the status of codons 72, 74, 75 and 76 in the pfcrt gene using a PCRRFLP approach. Results. A high frequency of treatment failure to chloroquine (82%) and to amodiaquine (29%) was confirmed, whereas mefloquine and combined therapy remained effective. The presence of the T76 mutation in pfcrt was confirmed in all samples. The most common haplotype was CMNT (67%). Conclusions. No significant association was confirmed between specific haplotypes and the treatment response in any of the treatment groups. Two haplotypes, SMET and SMNT, were reported for the first time in Colombia. Twelve percent of the samples carried both mixed mutant and wild-type alleles.
Introducción. Los estudios en epidemiología molecular de resistencia a antipalúdicos constituyen una herramienta útil para comprender eventos involucrados en la falla al tratamiento y la resistencia en paludismo por Plasmodium falciparum en Colombia. Diversos autores han informado sobre la eficacia de algunos marcadores moleculares para predecir resistencia a fármacos en P. falciparum y el gen pfcrt ha sido ampliamente caracterizado en este contexto. Objetivo. Estudiar la frecuencia de mutaciones en el gen pfcrt de P. falciparum y su asociación con falla al tratamiento con cloroquina, mefloquina, amodiaquina y sulfadoxina/pirimetamina, en dos regiones muy endémicas para paludismo del noroeste de Colombia: Turbo y Bajo Cauca. Materiales y métodos. Una muestra representativa de pacientes con paludismo por P. falciparum no complicado fue seleccionada de cada localidad para la evaluación de la respuesta al tratamiento y la determinación del estado de los codones 72, 74, 75 y 76 de pfcrt, usando una aproximación basada en PCR-RFLP. Resultados. Se confirmó una alta frecuencia de falla al tratamiento con cloroquina (82%) y amodiaquina (29%), mientras que la mefloquina y la terapia combinada fueron eficaces para eliminar la infección. La presencia de la mutación T76 en pfcrt fue confirmada en todas las 172 muestras; el haplotipo más común fue CMNT (67%). Conclusiones. No se observó asociación significativa entre un haplotipo particular y la respuesta al tratamiento en cualquiera de los grupos. Se reporta por primera vez en Colombia la presencia de dos haplotipos, SMET y SMNT; se encontraron alelos mutantes y silvestres simultáneamente en 12% de las muestras.
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/57
10.7705/biomedica.v28i4.57
Biomedica; Vol. 28 No. 4 (2008); 523-530
Biomédica; Vol. 28 Núm. 4 (2008); 523-530
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/57/58
https://revistabiomedica.org/index.php/biomedica/article/view/57/386
/*ref*/Lopes D, Rungsihirunrat K, Nogueira F, Seugorn A, Gil JP, do Rosário VE, et al. Molecular characterisation of drug-resistant Plasmodium falciparum from Thailand. Malar J. 2002;14:1-12. <br />2. White NJ. Drug resistance in malaria. Br Med Bull. 1998;54:703-15. <br />3. Peters W. Drug resistance in malaria parasites of animals and man. Adv Parasitol. 1998;41:1-62. <br />4. Holmgren G, Gil JP, Ferreira PM, Veiga MI, Obonyo CO, Björkman A. Amodiaquine resistant Plasmodium falciparum malaria in vivo is associated with selection of pfcrt 76T and pfmdr1 86Y. Infect Gen Evol. 2006;6:309-14. <br />5. Ochong EO, van den Broek, Keus K, Nzila A. Association between chloroquine and amodiaquine resistance and allelic variation in the Plasmodium falciparum multiple drug resistance 1 gene and the chloroquine resistance transporter gene in isolates from the upper Nile in southern Sudan. Am J Trop Hyg. 2003;69:184-7. <br />6. Le Bras J, Durand R. The mechanisms of resistance to antimalarial drugs in Plasmodium falciparum. Fundament Clin Pharmacol. 2003;17:147-53. <br />7. Congpuong K, Bangchang KN, Mungthin M, Bualombai P, Wernsdorfer WH. Molecular epidemiology of drug resistance markers of Plasmodium falciparum malaria in Thailand. Trop Med Int Health. 2005;10:717-22. <br />8. Mayengue PI, Ndounga M, Davy MM, Tandou N, Ntoumi F. In vivo chloroquine resistance and prevalence of the pfcrt codon 76 mutation in Plasmodium falciparum isolates from the Republic of Congo. Acta Trop. 2005;95:219-25. <br />9. Sidhu AB, Verdier-Pinard D, Fidock DA. Chloroquine resistance in Plasmodium falciparum malaria parasites conferred by pfcrt mutations. Science. 2002;298:210-3. <br />10. Fidock DA, Nomura T, Talley AK, Cooper RA, Dzekunov SM, Ferdig MT, et al. Mutations in the P. falciparum digestive vacuole transmembrane protein PfCRT and evidence for their role in chloroquine resistance. Mol Cell. 2000;6:861-71. <br />11. Djimde A, Doumbo OK, Steketee RW, Plowe CV. Application of a molecular marker for surveillance of chloroquine-resistant falciparum malaria. Lancet. 2001;358:890-1. <br />12. Howard EM, Zhang H, Roepe PD. A novel transporter, Pfcrt, confers antimalarial drug resistance. J Membr Biol. 2002;190:1-8. <br />13. Wernsdorfer WH, Noedl H. Molecular markers for drug resistance in malaria: use in treatment, diagnosis and epidemiology. Curr Opin Infect Dis. 2003;16:553-8. <br />14. OMS/OPS. Evaluación de la eficacia terapéutica de los medicamentos para el tratamiento del paludismo por Plasmodium falciparum sin complicaciones en las Américas. Washington D.C.: OPS/HCP/HCT/113/98; 1998. <br />15. Singh B, Cox-Singh J, Miller AO, Abdullah MS, Snounou G, Rahman HA. Detection of malaria in Malaysia by nested polymerase chain reaction amplification of dried blood spots on filter papers. Trans R Soc Trop Med Hyg. 1996;90:519-21. <br />16. Blair S, Lopez ML, Piñeros JG, Alvarez T, Tobon A, Carmona J. Eficacia terapéutica de tres esquemas de tratamiento de malaria no complicada por Plasmodium falciparum, Antioquia, Colombia, 2002. Biomédica. 2003;23:318-27. <br />17. Dittrich S, Alifrangis M, Stohrer JM, Thongpaseuth V, Vanisaveth V, Phetsouvanh R, et al. Falciparum malaria in the north of Laos: the occurrence and implications of the Plasmodium falciparum chloroquine resistance transporter (pfcrt) gene haplotype SVMNT. Trop Med Int Health. 2005;10:1267-70. <br />18. Nsimba B, Jafari-Guemouri S, Malonga DA, Mouata AM, Kiori J, Louya F, et al. Epidemiology of drug resistant malaria in Republic of Congo: using molecular evidence for monitoring antimalarial drug resistance combined with assessment of antimalarial drug use. Trop Med Int Health. 2005;10:1030-7. <br />19. Basco LK, Le Bras J, Rhoades Z, Wilson CM. Analysis of pfmdr1 and drug susceptibility in fresh isolates of Plasmodium falciparum from subSaharan Africa. Mol Biochem Parasitol. 1995;74:157-66. <br />20. Duraisingh MT, Drakeley CJ, Muller O,Bailey R, Snounou G, Targett GA, et al. Evidence for selection for the tyrosine-86 allele of the pfmdr 1 gene of Plasmodium falciparum by chloroquine and amodiaquine. Parasitology. 1997;114:205-11. <br />21. Foote SJ, Kyle DE, Martin RK, Oduola AM, Forsyth K, Kemp DJ, et al. Several alleles of the multidrugresistance gene are closely linked to chloroquine resistance in Plasmodium falciparum. Nature. 1990; 345:255-8. <br />22. Grobusch MP, Adagu IS, Kremsner PG, Warhurst DC. Plasmodium falciparum: in vitro chloroquine susceptibility and allele-specific PCR detection of Pfmdr1 Asn86Tyr polymorphism in Lambarene, Gabon. Parasitology. 1998;116:211-7.<br />23. von Seidlein L, Duraisingh MT, Drakeley CJ, Bailey R, Greenwood BM, Pinder M. Polymorphism of the Pfmdr1 gene and chloroquine resistance in Plasmodium falciparum in The Gambia.Trans R Soc Trop Med Hyg. 1997;91:450-3. <br />24. Gomez-Saladin E, Fryauff DJ, Taylor WR, Laksana BS, Susanti AI, Purnomo, et al. Plasmodium falciparum mdr1 mutations and in vivo chloroquine resistance in Indonesia. Am J Trop Med Hyg. 1999;61:240-4. <br />25. Nagesha HS, Din-Syafruddin, Casey GJ, Susanti AI, Fryauff DJ, Reeder JC, et al. Mutations in the pfmdr1, dhfr and dhps genes of Plasmodium falciparum are associated with in-vivo drug resistance in West Papua, Indonesia. Trans R Soc Trop Med Hyg. 2001;95:43-9. <br />26. Reed MB, Saliba KJ, Caruana SR, Kirk K, Cowman AF. Pgh1 modulates sensitivity and resistance to multiple antimalarials in Plasmodium falciparum. Nature. 2000;403:906-9. <br />27. Mita T, Kaneko A, Hombhanje F, Hwaihwanje I, Takahashi N, Osawa H, et al. Role of pfmdr1 mutations on chloroquine resistance in Plasmodium falciparum isolates with pfcrt K76T from Papua New Guinea. Acta Trop. 2006;98:137-44. <br />28. Montoya P, Tobón A, Blair S, Carmona J, Maestre A. Polimorfismos del gen pfmdr1 en muestras clínicas de Plasmodium falciparum y su relación con la respuesta terapéutica a antipalúdicos y paludismo grave en Colombia. Biomédica. 2007;27:204-15. <br />29. Kublin JG, Cortese JF, Njunju EM, Mukadam RA, Wirima JJ, Kazembe PN, et al. Reemergence of chloroquine- sensitive Plasmodium falciparum malaria after cessation of chloroquine use in Malawi. J Infect Dis. 2003;187:1870-5. <br />30. Mita T, Kaneko A, Lum JK, Bwijo B, Takechi M, Zungu IL, et al. Recovery of chloroquine sensitivity and low prevalence of the Plasmodium falciparum chloroquine resistance transporter gene mutation K76T following the discontinuance of chloroquine use in Malawi. Am J Trop Med Hyg. 2003;68:413-5. <br />31. Gonzalez IJ, Varela RE, Murillo C, Ferro BE, Salas J, Giraldo LE, et al. Polymorphisms in cg2 and pfcrt genes and resistance to chloroquine and other antimalarials in vitro in Plasmodium falciparum isolates from Colombia. Trans R Soc Trop Med Hyg. 2003;97:318-24. <br />32. Echeverry DF, Holmgren G, Murillo C, Higuita JC, Björkman A, Gil JP, et al. Polymorphisms in the pfcrt and pfmdr1 genes of Plasmodium falciparum and in vitro susceptibility to amodiaquine and desethylamodiaquine. Am J Trop Med Hyg. 2007;77:1034-8. <br />33. Vieira PP, Ferreira MU, Alecrim MG, Alecrim WD, da Silva LH, Sihuincha MM, et al. pfcrt polymorphism and the spread of chloroquine resistance in Plasmodium falciparum populations across the Amazon Basin. J Infect Dis. 2004;190:417-24. <br />34. Wootton JC. Genetic diversity and chloroquine selective sweeps in Plasmodium falciparum. Nature. 2002;418:320-3.<br />
oai:oai.revistabiomedica.org:article/58
2009-12-24T18:03:33Z
biomedica:ARTI
Clinical evolution of dengue in hospitalized patients
Evolución clínica de pacientes hospitalizados por dengue en una institución de salud de Bucaramanga, Colombia
González, Andrés Leonardo
Martínez, Ruth Aralí
Villar, Luis Ángel
fiebre dengue hemorrágica
hospitalización
pronóstico
adulto
niño
estudios de cohortes
Dengue hemorrhagic fever
hospitalization
prognosis
adult
child
adolescent
cohort studies
Introduction. Dengue hemorrhagic fever has extended to every tropical and subtropical area of the world, resulting in a half million hospitalizations every year. This disease appears to affect increasing numbers of adolescents and young adults. Objective. The clinical characteristics were described for adult and pediatric dengue inpatients to establish risk factors associated with bad prognosis. Materials and methods. A cohort of dengue inpatients of years 2006 and 2007 was evaluated retrospectively at “Clínica Chicamocha”, a high level hospital in Bucaramanga, Colombia. Results. Of 328 patients evaluated, 165 were female and 163 were male with a median age of 25 years. Dengue hemorrhagic fever was diagnosed in 116 patients, of which 113 were classified grade II. Of the 212 patients with dengue fever, 156 developed signs of plasma leakage, bleeding or thrombocytopenia. A positive serology was indicated in 82.4% of the patients. Inpatients with dengue hemorrhagic fever were younger (20.1 vs. 25.7 years, p<0.0054). Both lowest level of platelets and highest hematocrit were reached at the sixth day of illness. Children presented the typical symptoms of dengue less frequently, but demonstrated a greater proportion of ascites, pleural effusion and bleeding, and a higher risk of developing respiratory distress (RR=3.59, 95%CI 1.3-9.9, p<0.014) and hypotension (RR=10.77, 95%CI 5.56-20.86, p<0.001). Conclusions. Age was the most determinant factor of severity in dengue inpatients. In addition, a combination of particular symptoms and laboratory data at the day of admission may predict the development of complications.
Introducción. El dengue hemorrágico abarca todas las áreas tropicales y subtropicales del planeta, y causa medio millón de hospitalizaciones al año en el mundo. Se ha descrito que esta enfermedad afecta a un grupo cada vez mayor de adolescentes y adultos jóvenes. Objetivo. Describir las características clínicas de la población, tanto adulta como pediátrica, hospitalizada por dengue durante un periodo endémico y determinar los factores de riesgo asociados a mal pronóstico. Materiales y métodos. Cohorte retrospectiva de pacientes hospitalizados por dengue en los años 2006 y 2007 en la Clínica Chicamocha. Resultados. Se evaluaron 328 pacientes, 165 mujeres y 163 hombres, con mediana de edad de 25 años. Se encontraron 116 casos de dengue hemorrágico, de los cuales, 113 eran de grado II. De los 212 pacientes con dengue clásico, 156 presentaron extravasación, sangrado o trombocitopenia. El 82,4% tuvieron serología positiva. Los pacientes con dengue hemorrágico eran más jóvenes (20,1 contra 25,7 años, p=0,0054). El número mínimo de plaquetas y el valor máximo del hematocrito se alcanzaron alrededor del sexto día de enfermedad. Los menores de 13 años presentaron con menor frecuencia los síntomas típicos de dengue, aunque con un mayor porcentaje de ascitis, derrame y sangrado; además, tuvieron mayor riesgo de desarrollar dificultad respiratoria (riesgo relativo (RR)=3,59, IC95% 1,3-9,9, p=0,014) e hipotensión (RR=10,77, IC95% 5,56-20,86, p<0,001). Conclusiones. La edad continúa siendo el factor predominante en la gravedad intrahospitalaria del dengue. Independientemente de ésta, un grupo de signos, síntomas y hallazgos de laboratorio al ingreso permite predecir la aparición de complicaciones.
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/58
10.7705/biomedica.v28i4.58
Biomedica; Vol. 28 No. 4 (2008); 531-543
Biomédica; Vol. 28 Núm. 4 (2008); 531-543
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/58/59
https://revistabiomedica.org/index.php/biomedica/article/view/58/389
/*ref*/World Health Organization. Dengue and dengue haemorrhagic fever. Geneva: WHO; 2008. [Fecha de consulta: 18 de agosto de 2008]. Disponible en: http:// www.who.int/mediacentre/factsheets/fs117/en/ <br />2. Kurane I. Dengue hemorrhagic fever with special emphasis on immunopathogenesis. Comp Immunol Microbiol Infect Dis. 2007;30:329-40. <br />3. World Health Organization. Dengue and dengue haemorrhagic fever. In: WHO Report on Global Surveillance of Epidemic-prone Infectious Diseases. First edition. Geneva: WHO; 2000. p. 75-8. [Fecha de consulta: 30 de enero de 2008]. Disponible en: http:// www.who.int/entity/csr/resources/publications/surveillance/ dengue.pdf <br />4. Pan American Health Organization. Number of reported cases of dengue and dengue hemorrhagic fever (DHF), Region of the Americas (by country and subregion). Washington D.C.: PAHO; 2008. [Consultada: 5 de marzo de 2008]. Disponible en: http:/ /www.paho.org/English/AD/DPC/CD/dengue-cases- 2008.pdf. <br />5. Pan American Health Organization. The history of dengue and dengue hemorrhagic fever (DHF) in the Region of the Americas, 1635-2001. Washington D.C.: PAHO; 2001. [Fecha de consulta: 30 de enero de 2008]. Disponible en: http://www.ops-oms.org/English/AD/ DPC/CD/dengue_history.htm <br />6. Instituto Nacional de Salud. Casos totales en la semana epidemiológica 52 y acumulados del año. Bogotá D.C.: INS; 2006. [Fecha de consulta: 18 de agosto de 2008]. Disponible en: http://www.ins.gov.co/ pdf/vcsp/Tablas/2006/2006_semana_52.pdf <br />7. Instituto Nacional de Salud. Casos totales en la semana epidemiológica 50 y acumulados del año. Bogotá D.C.: INS; 2007. [Fecha de consulta: 18 de agosto de 2008]. Disponible en: http://www.ins.gov.co/ pdf/vcsp/Tablas/2007/2007_semana_50.pdf <br />8. World Health Organization. Guidelines for treatment of dengue fever/dengue haemorrhagic fever in small hospitals. Geneva: WHO; 1999. p. 28. [Fecha de consulta: 30 de enero de 2008]. Disponible en: http:// www.searo.who.int/LinkFiles/Dengue_Guidelinedengue. pdf <br />9. Méndez A, Bárcenas C, González G, Villar LA, Sepúlveda JW, Rey JJ, et al. Protocolo para la atención del dengue y dengue hemorrágico en el municipio de Bucaramanga. Bucaramanga: Secretaría de Salud y del Ambiente; 2003. p. 48. [Fecha de consulta: 30 de enero de 2008]. Disponible en: http://www. bucaramanga. gov. co/docs/Protocolo% 20manejo% 20dengue.pdf <br />10. Martínez-Vega RA, Díaz-Quijano FA, Villar-Centeno LA. Low concordance between early clinical suspicion of dengue and its serological confirmation. Rev Med Chil. 2006;134:1153-60. <br />11. Khan NA, Azhar EI, El-Fiky S, Madani HH, Abuljadial MA, Ashshi AM, et al. Clinical profile and outcome of hospitalized patients during first outbreak of dengue in Makkah, Saudi Arabia. Acta Trop. 2008;105:39-44. <br />12. Malavige GN, Velathanthiri VG, Wijewickrama ES, Fernando S, Jayaratne SD, Aaskov J, et al. Patterns of disease among adults hospitalized with dengue infections. QJM. 2006;99:299-305. <br />13. Kularatne SA, Gawarammana IB, Kumarasiri PR. Epidemiology, clinical features, laboratory investigations and early diagnosis of dengue fever in adults: a descriptive study in Sri Lanka. Southeast Asian J Trop Med Public Health. 2005;36:686-92. <br />14. Shah I, Deshpande GC, Tardeja PN. Outbreak of dengue in Mumbai and predictive markers for dengue shock syndrome. J Trop Pediatr. 2004;50:301-5. <br />15. Murgue B, Deparis X, Chungue E, Cassar O, Roche C. Dengue: an evaluation of dengue severity in French Polynesia based on an analysis of 403 laboratory-confirmed cases. Trop Med Int Health. 1999;4:765-73. <br />16. Tai DY, Chee YC, Chan KW. The natural history of dengue illness based on a study of hospitalised patients in Singapore. Singapore Med J. 1999;40:238-42. <br />17. Malavige GN, Ranatunga PK, Velathanthiri VG, Fernando S, Karunatilaka DH, Aaskov J, et al. Patterns of disease in Sri Lankan dengue patients. Arch Dis Child. 2006;91:396-400. <br />18. Lee VJ, Lye DC, Sun Y, Fernandez G, Ong A, Leo YS. Predictive value of simple clinical and laboratory variables for dengue hemorrhagic fever in adults. J Clin Virol. 2008;42:34-9. <br />19. Rosso F, Restrepo M, Alzate A, Muñoz J, Moreno C. Dengue hemorrágico en el Hospital Universitario del Valle, 1990-1992. Colomb Med. 1994;25:10-4. <br />20. Salgado D, Rodríguez A, Vega R. Dengue hemorrágico: emergencia pediátrica en el Huila. Pediatría (Bogotá). 1999;34:78-83. <br />21. Méndez A, González G. Dengue hemorrágico en niños: diez años de experiencia clínica. Biomédica. 2003;23:180-93. <br />22. Arboleda M, Campuzano M, Restrepo BN, Cartagena G. Caracterización clínica de los casos de dengue hospitalizados en la E.S.E. "Antonio Roldán Betancur" Apartadó, Antioquia, 2000. Biomédica. 2006;26:286-94. <br />23. Salgado DM, Rodríguez JA, Garzón M, Cifuentes G, Ibarra M, Vega MR, et al. Clinical and epidemiological characterisation of dengue haemorrhagic fever in Neiva, Colombia, 2004. Rev Salud Pública (Bogotá). 2007;9:53-63. 24. Guha-Sapir D, Schimmer B. Dengue fever: new paradigms for a changing epidemiology. Emerg Themes Epidemiol. 2005;2:1. <br />25. Park MK, Menard SW, Schoolfield J. Oscillometric blood pressure standards for children. Pediatr Cardiol. 2005;26:601-7. <br />26. World Health Organization. Clinical diagnosis. In: Dengue haemorrhagic fever: diagnosis, treatment, prevention and control. Second edition. Geneva: WHO; 1997. p. 12-23. [Fecha de consulta: 30 de enero de 2008]. Disponible en: http://www.who.int/entity/csr/resources/ publications/dengue/012-23.pdf <br />27. McPhee SJ, Papadakis MA, Tierney LM. Appendix, therapeutic drug monitoring & laboratory reference ranges. In: Current medical diagnosis & treatment. 46th edition. New York: McGraw-Hill; 2007. p. 1768-77. <br />28. Hay W, Levin M, Sondheimer J, Deterding R. Chemistry & hematology reference intervals. In: Current diagnosis & treatment in pediatrics. 18th edition. New York: McGraw-Hill; 2007. p. 1294-306. <br />29. Deen JL, Harris E, Wills B, Balmaseda A, Hammond SN, Rocha C, et al. The WHO dengue classification and case definitions: time for a reassessment. Lancet. 2006;368:170-3. <br />30. Balmaseda A, Hammond SN, Perez MA, Cuadra R, Solano S, Rocha J, et al. Short report: assessment of the World Health Organization scheme for classification of dengue severity in Nicaragua. Am J Trop Med Hyg. 2005;73:1059-62. <br />31. Avila-Aguero ML, Avila-Aguero CR, Um SL, Soriano-Fallas A, Canas-Coto A, Yan SB. Systemic host inflammatory and coagulation response in the dengue virus primo-infection. Cytokine. 2004;27:173-9. <br />32. Venkata Sai PM, Dev B, Krishnan R. Role of ultrasound in dengue fever. Br J Radiol. 2005;78:416-8. <br />33. Srikiatkhachorn A, Krautrachue A, Ratanaprakarn W, Wongtapradit L, Nithipanya N, Kalayanarooj S, et al. Natural history of plasma leakage in dengue hemorrhagic fever: a serial ultrasonographic study. Pediatr Infect Dis J. 2007;26:283-90. <br />34. Díaz FA, Martínez RA, Villar LA. Criterios clínicos para diagnosticar el dengue en los primeros días de enfermedad. Biomédica. 2006;26:22-30. <br />35. Lee VJ, Lye DC, Sun Y, Fernandez G, Ong A, Leo YS. Predictive value of simple clinical and laboratory variables for dengue hemorrhagic fever in adults. J Clin Virol. 2008;42:34-9. <br />36. Tanner L, Schreiber M, Low JG, Ong A, Tolfvensta T, Lai YL et al. Decision tree algorithms predict the diagnosis and outcome of dengue fever in the early phase of illness. PLoS Negl Trop Dis. 2008;2:e196.<br />
oai:oai.revistabiomedica.org:article/59
2009-12-24T18:03:34Z
biomedica:ARTI
Reliability and reproducibility of the Fitzpatrick phototype scale for skin sensitivity to ultraviolet light
Confiabilidad y reproducibilidad de la escala de fototipos de Fitzpatrick antes y después de un ejercicio de estandarización clínica
Sánchez, Guillermo
Nova, John
reproducibilidad de resultados
dermatología
piel
pigmentación de la piel
neoplasias cutáneas
radiación solar/efectos adversos
reproducibility of results
dermatology
skin
skin pigmentation
skin neoplasm
solar radiation/adverse effects
<!-- /* Font Definitions */ @font-face {font-family:Helvetica; panose-1:2 11 6 4 2 2 2 2 2 4; mso-font-charset:0; mso-generic-font-family:swiss; mso-font-pitch:variable; mso-font-signature:-536855809 -1073711037 9 0 511 0;} /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-parent:""; margin:0cm; margin-bottom:.0001pt; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-fareast-font-family:"Times New Roman";} @page Section1 {size:595.3pt 841.9pt; margin:70.85pt 3.0cm 70.85pt 3.0cm; mso-header-margin:35.4pt; mso-footer-margin:35.4pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> Introduction. The Fitzpatrick phototype scale has been used to determine skin sensitivity to ultraviolet light. The reliability of this scale in estimating sensitivity permits risk evaluation of skin cancer based on phototype. Objective. Reliability and changes in intra and inter-observer concordance was determined for the Fitzpatrick phototype scale after the assessment methods for establishing the phototype were standardized. Materials and methods. An analytical study of intra and inter-observer concordance was performed. The Fitzpatrick phototype scale was standardized using focus group methodology. To determine intra and inter-observer agreement, the weighted kappa statistical method was applied. The standardization effect was measured using the equal kappa contrast hypothesis and Wald test for dependent measurements. The phototype scale was applied to 155 patients over 15 years of age who were assessed four times by two independent observers. The sample was drawn from patients of the Centro Dermatológico Federico Lleras Acosta. Results. During the pre-standardization phase, the baseline and six-week inter-observer weighted kappa were 0.31 and 0.40, respectively. The intra-observer kappa values for observers A and B were 0.47 and 0.51, respectively. After the standardization process, the baseline and six-week inter-observer weighted kappa values were 0.77, and 0.82, respectively. Intra-observer kappa coefficients for observers A and B were 0.78 and 0.82. Statistically significant differences were found between coefficients before and after standardization (p<0.001) in all comparisons. Conclusion. Following a standardization exercise, the Fitzpatrick phototype scale yielded reliable, reproducible and consistent results.
Introducción. La escala de fototipos de Fitzpatrick permite conocer la sensibilidad de la piel frente a la luz ultravioleta; una estimación confiable del fototipo permite establecer el verdadero riesgo de cáncer de piel de acuerdo con esta característica. Objetivo. Establecer si existen diferencias en la concordancia intraobservador e interobservador de dos dermatólogos que evalúan el fototipo utilizando la escala de Fitzpatrick, antes y después de un proceso de estandarización clínica. Materiales y métodos. Se realizó un estudio analítico de concordancia intraobservador e interobservador. La escala de fototipos de Fitzpatrick se estandarizó mediante la metodología de grupos focales. Para conocer el acuerdo intra e interobservador se utilizó el estadístico kappa ponderado. El efecto de la estandarización se midió mediante un contraste de hipótesis de igualdad de coeficientes kappa utilizando el estadístico de Wald, a través de la metodología de mínimos cuadrados ponderados. Resultados. Se incluyeron 155 pacientes mayores de 15 años evaluados en cuatro oportunidades, por dos observadores independientes. En la fase de pre-estandarización, el kappa ponderado interobservador basal fue de 0,31 y de 0,40 a las seis semanas. El kappa intraobservador A fue de 0,47 y el intraobservador B fue de 0,51. Después del proceso de estandarización, se obtuvo un kappa ponderado interobservador basal de 0,77, y de 0,82 a las seis semanas. Los coeficientes kappa intraobservador A y B fueron 0,78 y 0,82, respectivamente. Se establecieron diferencias estadísticamente significativas entre los coeficientes antes y después de la estandarización (p=0,000 en todas las comparaciones). Conclusiones. La escala de fototipos de Fitzpatrick posterior a un ejercicio de estandarización arroja resultados confiables, reproducibles y estables en el tiempo.
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/59
10.7705/biomedica.v28i4.59
Biomedica; Vol. 28 No. 4 (2008); 544-550
Biomédica; Vol. 28 Núm. 4 (2008); 544-550
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/59/60
https://revistabiomedica.org/index.php/biomedica/article/view/59/392
/*ref*/Fitzpatrick TB. Soleil et peau. J Med Esthet. 1975;2: 33-4. <br />2. Walter U, Kron M, Sander S, Sebastian G, Sander R, Peter RU, et al. Risk and protective factors for sporadic basal cell carcinoma: results of a two centre case control study in southern Germany. Clinical actinic elastosis may be a protective factor. Br J Dermatol. 2004;151:170-8. <br />3. Lear JT, Tan BB, Smith AG, Bowers W, Jones PW, Heagerty AH, et al. Risk factors for basal cell carci noma in the UK: case control study in 806 patients. J R Soc Med. 1997;90:371-4. <br />4. Loria D, Matos E. Risk factors for cutaneous melanoma: a case-control study in Argentina. Int J Dermatol. 2001;40:108-14. <br />5. Youn JI, Oh JK, Kim BK, Suh DH, Chung JH, Oh SJ, et al. Relationship between skin phototype and MED in Korean, brown skin. Photodermatol Photoimmunol Photomed. 1997;13:208-11. <br />6. Machin D, Campbell M, Fayers P, Pinol A. Sample size tables for clinical studies. Second edition. Oxford: Blackwell Science; 1997. <br />7. Streiner DL, Norman GR. Health measurement scales. A practical guide to their development and use. Second edition. Oxford: Oxford University Press; 2000. p. 104-27. <br />8. Strauss A, Corbin J. Basics of qualitative research. Techniques and procedures for developing grounded theory. London: Sage; 1998. <br />9. Walker D, Myrick F. Grounded theory: An exploration of process and procedure. Qual Health Res. 2006;16:547-59. 10. Shaw VN. Research with participants in problem experience: challenge and strategies. Qual Health Res. 2005;15:841-54. <br />11. Sim J, Wright CC. The kappa statistic in reliability studies: use, interpretation, and sample size requirements. Phys Ther. 2005;85:257-68. <br />12. Kramer MS, Feinstein AR. Clinical biostatistics. LIV. The biostatistics of concordance. Clin Pharmacol Ther. 1981;29:111-23. <br />13. Landis JR, Koch GG. The measurement of observer agreement for categorical data. Biometrics. 1977;33:159-74 14. Barnhart H, Williamson J. Weighted least squares approach for comparing correlated kappa. Biometrics. 2002;58:1012-9. <br />15. Venkataram MN, Haitham AA. Correlating skin phototype and minimum erythema dose in Arab skin. Int J Dermatol. 2003;42:191-2. <br />16. Stern RS, Momtaz K. Skin typing for assessment of skin cancer risk and acute response to UV-B and oral methoxalen photochemotherapy. Arch Dermatol. 1984;120:869-73.
oai:oai.revistabiomedica.org:article/60
2009-12-24T18:03:34Z
biomedica:ARTI
Concordance between two methods of bronchoalveolar lavage for the microbiological diagnosis of pneumonia in mechanically ventilated patients
Evaluación de la concordancia entre dos métodos de lavado broncoalveolar para el diagnóstico microbiológico de la neumonía en pacientes con asistencia respiratoria mecánica
Vélez, Lázaro
Loaiza, Natalia
Gaviria, Lina María
Maya, María Angélica
Rueda, Zulma Vanessa
Correa, Luz Teresita
Ortega, Jorge
Ortega, Héctor
neumonía/etiología
respiración artificial
técnicas y procedimientos diagnósticos
técnicas microbiológicas
lavado broncoalveolar
pneumonia/etiology
respiration
artificial
diagnostic techniques and procedures
microbiological techniques
bronchoalveolar lavage
Introduction. Microbiological diagnosis of pneumonia allows the optimal use of antibiotics in mechanically ventilated patients. That is why samples of bronchoscopic bronchoalveolar lavage had been quantitatively cultivated, but this procedure is not always possible. Objective. To evaluate the microbiological concordance between respiratory samples obtained by non-bronchoscopic protected bronchoalveolar lavage compared to the bronchoscopic ones, and to find out whether concordance was affected by previous use of antibiotics or the time of pneumonia Honest Materials and methods. Prospective study conducted at Hospital Universitario San Vicente de Paúl, in 38 patients with suspected pneumonia in mechanical ventilation. Bronchoalveolar lavage specimens were taken by two methods, the traditional one and non-bronchoscopic bronchoalveolar lavage, using a telescoping preformed tip catheter (Balcath®). All samples were processed using conventional microbiologic protocols. Results. Considering flexible bronchoscopy with bronchoalveolar lavage as the gold standard, cultures allowed the identification of at least one respiratory pathogen in 60.5% of cases. Diagnostic agreement was achieved in 82% of patients and 79% of microbiologic isolates. Using the Cohen´s kappa coefficient, general concordance between both methods was 0.76 [0.60-0.93]; but in those who received previously antibiotics was 0.26 [0.05-0.48], versus 1.0 in those who did not (p<0.0001). Concordance did not differ significantly when cases of early or late pneumonia were compared. Conclusions. Concordance between non-bronchoscopic and bronchoscopic bronchoalveolar lavage is good in mechanically ventilated patients with pneumonia. However, the use of antibiotics previously, but not the time of pneumonia presentation, significantly decreases that concordance.
Introducción. El diagnóstico microbiológico de la neumonía permite optimizar el uso de antibióticos en pacientes con asistencia respiratoria mecánica. Para ello se han cultivado cuantitativamente las muestras del lavado broncoalveolar broncoscópico, procedimiento que no siempre es posible. Objetivo. Evaluar la concordancia microbiológica entre muestras respiratorias tomadas por lavado broncoalveolar broncoscópico y no broncoscópico, y establecer si el uso previo de antibióticos y el momento de presentación de la neumonía pueden afectarla. Materiales y métodos. Estudio prospectivo realizado en el Hospital Universitario San Vicente de Paúl, en 38 pacientes con sospecha de neumonía y con asistencia respiratoria mecánica. En todos se practicó el lavado broncoalveolar por fibrobroncoscopia y el lavado no broncoscópico usando un catéter telescopado de punta preformada (Balcath®). Todas las muestras fueron procesadas siguiendo protocolos microbiológicos convencionales. Resultados. Considerando el lavado broncoalveolar por fibrobroncoscopia como patrón de referencia, los cultivos permitieron identificar el agente en 60,5% de los casos. El acuerdo diagnóstico se logró en 82% de los pacientes y 79% de los aislamientos. Utilizando el índice kappa de Cohen, la concordancia general entre los dos métodos fue 0,76 [0,60-0,93]; pero en quienes habían recibido antibióticos previos fue 0,26 [0,05-0,48], versus 1,0 en quienes no lo habían hecho (p<0,0001). La concordancia no difirió significativamente cuando se compararon los casos de neumonía temprana y tardía. Conclusiones. La concordancia general entre los dos métodos de lavado broncoalveolar es buena en pacientes con neumonía y respiración asistida mecánicamente. Sin embargo, el uso previo de antibióticos y no el momento de aparición de la neumonía, disminuye ésta significativamente.
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/60
10.7705/biomedica.v28i4.60
Biomedica; Vol. 28 No. 4 (2008); 551-561
Biomédica; Vol. 28 Núm. 4 (2008); 551-561
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/60/61
https://revistabiomedica.org/index.php/biomedica/article/view/60/395
/*ref*/Heyland DK, Cook DJ, Griffith L, Keenan SP, Brun- Buisson C. The attributable morbidity and mortality of ventilator-associated pneumonia in the critically ill patient. The Canadian Critical Trials Group. Am J Respir Crit Care Med. 1999;159:1249-56. <br />2. Bercault N, BoulainT. Mortality rate attributable to ventilator-associated nosocomial pneumonia in an adult intensive care unit: a prospective casecontrol study. Crit Care Med. 2001;29:2303-9. <br />3. Fagon JY, Chastre AJ, Hance AJ, Montravers P, Novara A, Gilbert C. Nosocomial pneumonia in ventilated patients: a cohort study evaluating attributable mortality and hospital stay. Am J Med. 1993;94:281-8. <br />4. Chastre J, Fagon JY. Ventilator-associated pneumonia. Am J Respir Crit Care Med. 2002;165:867-903. <br />5. Fagon JY, Chastre J, Wolff M, Gervais C, Parer- Aubas S, Stéphan F, et al. Invasive and non-invasive strategies for management of suspected ventilator associated pneumonia: a randomized trial. Ann Intern Med. 2000;132:621-30. 6. The Canadian Critical Care Trials Group. A randomized trial of diagnostic techniques for ventilator-associated pneumonia. N Engl J Med. 2006;21:2619-30. <br />7. Torres A, El-Ebiary M, Padró L, González J, de la Bellacasa JP, Ramírez J. Validation of different techniques for the diagnosis of ventilator-associated pneumonia. Comparison with immediate postmortem pulmonary biopsy. Am J Respir Crit Care Med.1994; 149:324-31. <br />8. Marik P, Brown W. A comparison of bronchoscopic Vs. blind protected specimen brush sampling in patients with suspected ventilator-associated pneumonia. Chest. 1995;108:203-7. <br />9. Torres A, El-Ebiary M. Invasive diagnostic techniques for pneumonia: protected specimen brush, bronchoalveolar lavage and lung biopsy methods. Infect Dis Clin North Am. 1998;12;701-22. <br />10. Pittet D, Harbarth S. What techniques for diagnosis of ventilator-associated pneumonia? Lancet. 1998; 352:83-4. 11. Casetta M, Blot F, Antoun S, Leclercq B, Tancrède C, Doyon F, et al. Diagnosis of nosocomial pneumonia in cancer patients undergoing mechanical ventilation: a prospective comparison of the plugged telescoping catheter with the protected specimen brush. Chest. 1999;115:1641-5. <br />12. Heyland DK, Cook DJ, Marshall J, Heule M, Guslits B, Lang J, et al. The clinical utility of invasive diagnostic techniques in the setting of ventilator-associated pneumonia. Canadian Care Trials Group. Chest. 1999;115:1076-84. 13. Grossman R, Fein A. Evidence-based assessment of diagnostic test for ventilator associated pneumonia: executive summary. Chest. 2000;117:177S-81. <br />14. American Thoracic Society. Clinical role of bronchoalveolar lavage in adults with pulmonary disease. Am J Respir Crit Care Med. 1990;142:481-86. <br />15. Kahn FW, Jones JM. Analysis of bronchoalveolar lavage specimens from immunocompromised patients with a protocol applicable in the microbiology laboratory. J Clin Microbiol. 1988;26:1150-5. <br />16. Mayhall CG. Ventilator-associated pneumonia or not? Contemporary diagnosis. Emerg Infect Dis. 2001;7:200-4. <br />17. Souweine B, Veber B, Bedos JP, Gachot B, Dombret MC, Regnier B, et al. Diagnostic accuracy of protected specimen brush and bronchoalveolar lavage in nosocomial pneumonia: Impact of previous antimicrobial treatments. Crit Care Med. 1998;26:236-44. <br />18. Campbell GD. Blinded invasive diagnostic procedures in ventilator-associated pneumonia. Chest. 2000;117:207S-11. <br />19. Woske HG, Röding T, Schulz I, Lode H. Ventilatorassociated pneumonia in a surgical intensive care unit: epidemiology, etiology and comparison of three bronchoscopic methods for microbiological specimen sampling. Crit Care. 2001;5:167-73. <br />20. Chastre J, Fagon JY, Bornet-Lecso M, Calvat S, Dombret MC, al Khani R, et al. Evaluation of bronchoscopic techniques for the diagnosis of nosocomial pneumonia. Am J Respir Crit Care Med. 1995;152:231-40. <br />21. Pham LH, Brun-Buisson C, Legrand P, Rauss A, Verra F, Brochard L, et al. Diagnosis of nosocomial pneumonia in mechanically ventilated patients. Comparison of a plugged telescoping catheter with the protected specimen brush. Am Rev Respir Dis. 1991;143:1055-61. <br />22. Wearden PD, Chendrasekhar A, Timberlake GA. Comparison of nonbronchoscopic techniques with bronchoscopic brushing in the diagnosis of ventilatorassociated pneumonia. J Trauma. 1996;41:703-7. <br />23. Bello S, Tejada A, Chacón E, Villuendas MC, Senar A, Gascon M, et al. “Blind” protected specimen brush ing versus bronchoscopic techniques in the aetiolological diagnosis of ventilator-associated pneumonia. Eur Respir J. 1996;9:1494-9. <br />24. Jordá R, Parras F, Ibañez J, Reina J, Bregada J, Raurich JM. Diagnosis of nosocomial pneumonia in mechanically ventilated patients by the blind protected telescoping catheter. Intensive Care Med. 1993; 19: 377-82. <br />25. Papazian L, Martin C, Meric B, Dumon JF, Gouin F. A reappraisal of blind bronchial sampling in the microbiologic diagnosis of nosocomial bronchopneumonia. A comparative study in ventilated patients. Chest. 1993;103:236-42. <br />26. Middleton RM III, Huff W, Brickey DA, Kirkpatrick MB. Comparison of quantitative cultures to semiquantitative loop cultures of bronchoscopic protected specimen brush samples. Chest. 1996; 109:1204-9. <br />27. Leal-Noval SR, Alfaro-Rodríguez E, Murillo-Cabeza F, Garnacho-Montero J, Rey-Pérez J, Muñoz- Sánchez MA. Diagnostic value of the blind brush in mechanically ventilated patients with nosocomial pneumonia. Intensive Care Med. 1992;18:410-4. <br />28. Wood AY, Davit AJ II, Ciraulo DL, Arp NW, Richart CM, Maxwell RA, et al. A prospective assessment of diagnostic efficacy of blind protective bronchial brushings compared with bronchoscope-assisted lavage, bronchoscope-directed brushings, and blind endotracheal aspirates in ventilator-associated pneumonia. J Trauma. 2003; 55:825-34. <br />29. Torres A, Puig de la Bellacasa J, Rodríguez-Roisin R, Jiménez deAnta MT, Agusti-Vidal A. Diagnostic value of telescoping plugged catheters in mechanically ventilated patients with bacterial pneumonia using the Metras catheter. Am Rev Respir Dis.1988;138:117-20. <br />30. Kollef MH, Bock KR, Richards RD, Hearns ML. The safety and diagnostic accuracy of minibronchoalveolar lavage in patients suspected of ventilator-associated pneumonia. Ann Intern Med. 1995;122:743-8. <br />31. Levy H. Comparison of Ballard catheter bronchoalveolar lavage with bronchoscopic bronchoalveolar lavage. Chest. 1994;106:1753-8. <br />32. Timsit JF, Misset B, Renaud B, Goldstein FW, Carlet J. Effect of previous antimicrobial therapy on the accuracy of the main procedures used to diagnose nosocomial pneumonia in patients who are using ventilation. Chest. 1995;108:1036-40. <br />33. Solé Violán J, Rodríguez de Castro F, Caminero J, Bordes A, Manzano JL. Comparative efficacy of broncoalveolar lavage and telescoping plugged catheter in the diagnosis of pneumonia in mechanically ventilated patients. Chest. 1993;103:386-90. <br />34. Torres A, Martos A, Puig de la Bellacasa J, Ferrer M, el-Ebiary M, González J, et al. Specificity of endotracheal aspiration, protected specimen brush, and broncoalveolar lavage in mechanically ventilated patients. Am Rev Respir Dis. 1993;147:952-7. <br />35. Marik PE, Careau P. A comparison of minibronchoalveolar lavage and blind-protected specimen brush sampling in ventilated patients with suspected pneumonia. J Crit Care. 1998;13:67-72. <br />36. Sirvent JM, Vidaur L, González S, Castro P, de Batle J, Castro A, et al. Microscopic examination of intracellular organisms in protected bronchoalveolar mini-lavage fluid for the diagnosis of ventilator-associated pneumonia. Chest. 2003;123:518-23. <br />37. De Jaeger A, Litalien C, Lacroix J, Guertin MC, Infante-Rivard C. Protected specimen brush or bronchoalveolar lavage to diagnose bacterial nosocomial pneumonia in ventilated adults: a meta-analysis. Crit Care Med. 1999;27:2548-60. <br />38. Dotson RG, Pingleton SK. The effect of antibiotic therapy on recovery of intracellular bacteria from bronchoalveolar lavage in suspected ventilator-associated nosocomial pneumonia. Chest. 1993;103:541-6. <br />39. Trouillet JL, Chastre J, Vuagnat A, Joly-Guillou ML, Combaux D, Dombret MC, et al. Ventilator-associated pneumonia caused by potentially drug-resistant bacteria. Am J Respir Crit Care Med. 1998; 157:531-9. <br />40. Fridkin SK, Lawton R, Edwards JR, Tenover FC, McGowan JE, Gaynes RP, et al. Monitoring antimicrobial use and resistance: comparison with a national benchmark on reducing vancomycin use and vancomycin- resistant enterococci. Emerg Infect Dis. 2002;8:702-7. <br />41. Chastre J. Evolving problems with resistant pathogens. Clin Microbiol Infect. 2008;14:3-14. <br />42. Rello J, Ausina V, Ricart M, Castella J, Prats G. Impact of previous antimicrobial therapy on the etiology and outcome of ventilator-associated pneumonia. Chest. 1993;104:1230-5. <br />43. Lynch JP. Hospital-acquired pneumonia. Risk factors, microbiology, and treatment. Chest. 2001;119:373S-84. <br />44. Ewig S, Bauer T, Torres A. The pulmonary physician in critical care. Nosocomial pneumonia. Thorax. 2002;57:366-71.
oai:oai.revistabiomedica.org:article/61
2009-12-24T18:03:34Z
biomedica:ARTI
Distribution of Paragonimus (Digenea: Troglotrematidae) in Antioquia Province, Colombia, based on metacercariae counts in freshwater crabs
Distribución parcial de Paragonimus (Digenea: Troglotrematidae) en Antioquia, por presencia de metacercarias en cangrejos dulciacuícolas
Velásquez, Luz Elena
Uruburu, Mónica
Granada, Mabel
braquiuros
Colombia
interacciones huésped-parásitos
localización geográfica de riesgo
Paragonimus
trematodos
Brachyura
Colombia
geographical localization of risk
host-parasite interactions
Trematoda
Paragonimus
Introduction. Paragonimosis or lung fluke disease courses with signs similar to those seen in tuberculosis. The causative agent is a parasite of the genus Paragonimus (Digenea: Troglotrematidae). People become infected by ingesting raw or partially cooked crabs containing metacercariae. The first focus of human paragonimosis in Colombia was recorded in the county of Urrao, where two species of crabs infected with Paragonimus were found. In 2005, crabs with Paragonimus’ metacercariae were captured near Medellín, western Colombia. This prompted a search for the parasite in other locations through its presence in the crabs. Objective. To establish the distribution of Paragonimus in Antioquia, we evaluated the presence of metacercaria in freshwater brachyuran crabs. Materials and methods. From 2005 to 2007, crabs were captured in 13 counties of Antioquia. The crabs were relaxed and dissected to determine presence of trematodes and then to make the taxonomic identifications. Results. From 52 crabs captured in 9 counties, 42 (80.8%) were found with Paragonimus metacercariae. The crabs were identified as Pseudothelphusidae in 2 genera—Hypolobocera and Strengeriana— and were assigned to four species. Three of the species were recorded for the first time as hosts of Paragonimus. Conclusions. A Paragonimus’ distribution map was constructed for Antioquia; for the first time urban zones were included. Because of the high rate of infection, the handling and consumption of raw and poorly cooked crabs pose risk factors for human infection. Because crabs are affordable and provide means of easy diagnosis, crabs are targeted as primary agents of and diagnostic tools for paragonmosis.
Introducción. La paragonimosis, o distomatosis pulmonar, es una enfermedad con sintomatología similar a la observada en la tuberculosis. Es causada por parásitos del género Paragonimus (Digenea: Troglotrematidae). Las personas se infectan al consumir cangrejos crudos o mal cocidos, con metacercarias del parásito. El primer foco de paragonimosis humana en Colombia se registró durante 1995 en Urrao, Antioquia, donde se hallaron dos especies de cangrejos que hospedaban el parásito. En el 2005 se capturaron cangrejos con metacercarias de Paragonimus en Medellín, lo que motivó la búsqueda del parásito en otras localidades, mediante su presencia en estos crustáceos. Objetivo. Establecer la distribución de Paragonimus en Antioquia, evaluando la presencia de metacercarias en macrocrustáceos braquiuros, dulciacuícolas. Materiales y métodos. Desde 2005 hasta 2007 se capturaron cangrejos en 13 municipios antioqueños. Se relajaron y sacrificaron para la búsqueda del digeneo y la identificación taxonómica. Resultados. En nueve municipios se capturaron 52 cangrejos, 42 (80,76%) con metacercarias de Paragonimus. Todos los crustáceos se determinaron como Pseudothelphusidae, de los géneros Hypolobocera y Strengeriana, y se asignaron a cuatro especies. Tres se registran por primera vez como huéspedes del parásito. Conclusión. Se inicia la construcción de un mapa con la distribución de Paragonimus en Antioquia que incluye por primera vez zonas urbanizadas. Se ratifican el consumo y la manipulación de los cangrejos crudos y mal cocidos como factores de riesgo para la infección humana. Se propone a los cangrejos como agentes focalizadores de paragonimosis por ser asequibles y de fácil diagnóstico.
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/61
10.7705/biomedica.v28i4.61
Biomedica; Vol. 28 No. 4 (2008); 562-568
Biomédica; Vol. 28 Núm. 4 (2008); 562-568
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/61/62
https://revistabiomedica.org/index.php/biomedica/article/view/61/394
/*ref*/Nabakumar ST, Rebachandra SH, Sulochana Dk, Brajachand SN, Ibotomba SY. Pulmonary Paragonimiasis. Indian J Chest Dis Allied Sci. 2004;46:225-27. <br />2. OMS. Serie de informes técnicos. Lucha contra las trematodiasis de transmisión alimentaria. Ginebra: Organización Mundial de la Salud; 1995. <br />3. Keiser J, Utzinger J. Emerging foodborne trematodiasis. Emerg Infect Dis. 2005;11:1507-14. <br />4. Vélez ID, Velásquez LE. Paragonimosis una investigación multidisciplinaria en salud, biología y cultura en Colombia. Medellín: Editorial Universidad de Antioquia; 2002. <br />5. Alvarado L, Pariona R, Beltrán M. Casos de paragonimiasis (Paragonimiosis) en el Hospital Nacional Sergio E. Bernales (Lima, Perú). Rev Peru Med Exp Salud Pública. 2004;21:107-10. <br />6. Rumbea GJ. Paragonimiasis. Enfermedades infecciosas y parasitarias. Sao Paulo; 1982. <br />7. Little MD. Paragonimus caliensis sp. and paragonimiasis en Colombia. J Parasitol. 1968;54:738-46. <br />8. Buitrago B, Rodríguez G, Gómez G, Abril A. Paragonimiasis humana. Primera descripción de un caso colombiano. Biomédica. 1981;1:142-51. <br />9. Vélez ID, Ortega J, Hurtado M, Salazar AL. La paragonimosis en la comunidad indígena Embera de Colombia. Biomédica. 1995;27:51-4. <br />10. Vélez ID, Ortega J, Hurtado MI, Salazar AL, Robledo SM, Jiménez JN, et al. Epidemiology of paragonimiasis in Colombia. Trans R Soc Trop Med Hyg. 2000;94:1-3. <br />11. Velásquez LE, Restrepo S, Gómez MI, Velez I. Aspectos epidemiológicos del caracol Aroapyrgus sp. Rev Asoc Col Cienc Biol. 1999;11:7-15. <br />12. Campos RM, Rodríguez G. Three new species of Strengeriana from Colombia (Crustacea: Decápoda: Pseudothelphusidae). Proc Biol Soc Wash. 1993;106:508-13. <br />13. Campos RM, Rodríguez G. Two new species of freshwater crabs of genus Hypolobocera from Colombia (Crustacea: Decápoda: Pseudothelphusidae). Proc Biol Soc Wash. 1995;108:649-55. <br />14. Campos RM. A review of the freshwater crabs of the genus Hypolobocera Ortmann, 1897 (Crustacea: Decapoda: Brachyura: Pseudothelphusidae), from Colombia. Proc Biol Soc Wash. 2003;116:754-802. <br />15. Campos RM. Freshwater crabs from Colombia. A taxonomic and distributional study. Bogotá, D.C.: Editorial Guadalupe Ltda.; 2005. <br />16. Vélez I, Velásquez LE, Vélez ID. Morphological description and life cycle of Paragonimus sp. (Trematoda: Troglotrematidae): causal agent of human paragonimiasis in Colombia. J Parasitol. 2003;89:749-55. <br />17. Gómez C, Valencia E, Velásquez LE. Estudio de foco de Paragonimus en Fuente Clara, Robledo área periurbana de Medellín, Antioquia (tesis). Medellín: Universidad de Antioquia; 2007. <br />18. Lamothe-Argumedo R. La paragonimosis en el continente americano. Salud Pública Mex. 1985;27:514- 23. <br />19. Rodríguez G, Magalhaes C. Recent advances in the biology of the Neotropical freshwater crab family Pseudothelphusidae (Crustacea, Decapoda, Brachiura). Rev Bras Zool. 2005;22:354-65. <br />20. Ikeda T. Cystatin capture enzyme-linked immunosorbent assay for immunodiagnosis of human paragonimiasis and fascioliasis. Am J Trop Med Hyg. 1998;59:286-90. <br />21. Sugiyama H, Morishima Y, Kameoka Y, Kawanaka M. Polymerase chain reaction (PCR)-based molecular discrimination between Paragonimus westermani and P. miyazakii at the metacercarial stage. Mol Cell Probes. 2002;16:231-6. <br />22. Narain K, Rekha DK, Mahanta J. Development of enzyme-linked immunosorbent assay for serodiagnosis of human paragonimiasis. Indian J Med Res. 2005;121:739-46. <br />23. Rekha Dk, Narain K, Bhattacharya S, Negmu K, Agatsuma T, Blair D, et al. Pleuropulmonary paragonimiasis due to Paragonimus heterotremus: molecular diagnosis, prevalence of infection and clinicoradiological features in an endemic area of northeastern India. Trans R Soc Trop Med Hyg. 2007;101:786-92.
oai:oai.revistabiomedica.org:article/62
2009-12-24T18:03:34Z
biomedica:ARTI
Análisis de ADN mitocondrial en una muestra de restos óseos arcaicos del periodo Herrera en la sabana de Bogotá
Silva, Alejandro
Briceño, Ignacio
Burgos, Javier
Torres, Diana
Villegas, Victoria
Gómez, Alberto
Bernal, Jaime Eduardo
ADN mitocondrial/análisis
polimorfismo de nucleótido simple
haplotipos
arqueología
población indígena
Colombia
Introducción. Los restos óseos arcaicos son fuente privilegiada de información biológica y su caracterización genética permite confirmar o descartar filiaciones propuestas por otras aproximaciones científicas. La historia precolombina de los Andes orientales se divide en tres periodos principales: i) un poblamiento temprano por parte de grupos cazadores-recolectores; ii) un periodo intermedio (Herrera) de pueblos con agricultura incipiente, y iii) un periodo tardío de pueblos chibchas, agrícolas y alfareros (agroalfarero). Objetivo. Analizar el ADN mitocondrial de restos óseos del periodo Herrera. Materiales y métodos. Se analizaron 11 individuos pertenecientes al yacimiento arqueológico Madrid 2-41, con una edad aproximada de 2.000 años. Un fragmento (192 pb) del segmento hipervariable I fue amplificado y secuenciado, siguiendo criterios estrictos de autenticidad de ADN arcaico. Las secuencias se compararon con las existentes en bases de datos de Norteamérica y Europa usando herramientas bioinformáticas. Resultados. Todas las secuencias resultaron idénticas y fueron clasificadas como haplogrupo B. Esto puede relacionarse con el tipo de entierro ritual practicado en Madrid 2-41, es decir, probablemente los individuos analizados hagan parte de una familia jerárquicamente importante en la antigua sociedad Herrera. La búsqueda de secuencias homólogas en las bases de datos estadounidense y europea no arrojó coincidencias exactas, aunque existe el reporte de un individuo amazónico de ~4.000 años de antigüedad (Brasil) cuya secuencia coincide con la hallada en Madrid 2-41. Conclusión. Los individuos del yacimiento arqueológico Madrid 2-41 están estrechamente emparentados entre sí por línea materna y presentan una secuencia aparentemente ausente en poblaciones actuales.
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/62
10.7705/biomedica.v28i4.62
Biomedica; Vol. 28 No. 4 (2008); 569-577
Biomédica; Vol. 28 Núm. 4 (2008); 569-577
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/62/63
https://revistabiomedica.org/index.php/biomedica/article/view/62/393
/*ref*/Horai S, Kondo R, Nakagawa-Hattori Y, Hayashi S, Sonoda S, Tajima K. Peopling of the Americas, founded by four major lineages of mitochondrial DNA. Mol Biol Evol. 1993;10:23-47. <br />2. Schurr TG, Ballinger SW, Gan YY, Hodge JA, Merriwether DA, Lawrence DN, et al. Amerindian mitochondrial DNAs have rare Asian mutations at high frequencies, suggesting they derived from four primary maternal lineages. Am J Hum Genet. 1990;46:613-23. <br />3. Schurr TG. The peopling of the new world: Perspectives from molecular anthropology. Annu Rev Anthropol. 2004;33:551-83. <br />4. Torroni A, Schurr TG, Yang CC, Szathmary EJ, Williams RC, Schanfield MS, et al. Native American mitochondrial DNA analysis indicates that the Amerind and the Nadene populations were founded by two independent migrations. Genetics. 1992;130:153-62. <br />5. Melton PE, Briceño I, Gómez A, Devor EJ, Bernal JE, Crawford MH. Biological relationship between Central and South American Chibchan speaking populations: evidence from DNA. Am J Phys Anthropol. 2007;133:753-70. <br />6. Wallace DC, Garrison K y Knowler WC. Dramatic founder effects in Amerindian mitochondrial DNA. Am J Phys Anthropol. 1985;68:149-55. <br />7. Bailliet G, Rothhammer F, Carnese FR, Bravi CM, Bianchi NO. Founder mitochondrial haplotypes in Amerindian populations. Am J Hum Genet. 1994; 55: 27-33. <br />8. Macaulay V, Richards M, Hickey E, Vega E, Cruciani F, Guida V, et al. The emerging tree of West Eurasian mtDNAs: A synthesis of control-region sequences and RFLPs. Am J Hum Genet. 1999;64:232-49. <br />9. Rondón-González F, Cifuentes L, Cárdenas H, Barreto G. Evaluación de la diversidad genética mediante el análisis de mtDNA en poblaciones aisladas del centro y suroccidente colombiano. Salud Uninorte. 2004;18:74. <br />10. Rondón-González F, Torres AM, Barreto G. Relaciones filéticas de comunidades indígenas colombianas a partir de la comparación de secuencias de mtDNA y sus implicaciones en el poblamiento del continente americano. Salud Uninorte. 2004;18:88. <br />11. Briceño I, Umaña A, Bernal JE, Torres DM. Estudios moleculares en poblaciones amerindias. Salud Uninorte. 2004;18:76. <br />12. Acosta MA, Salas A, Álvarez V, Lareu MV, Carracedo A. El ADN mitocondrial revela la condición multiétnica de las poblaciones del Cauca (Colombia). Salud Uninorte. 2004;18:78. <br />13. Roa M. Polimorfismos de la región control del ADN mitocondrial humano en una muestra de población mestiza del altiplano cundiboyacense colombiano. (tesis). Bogotá, D.C.: Universidad Nacional de Colombia; 2005. p. 140. <br />14. Torroni A, Schurr TG, Cabell MF, Brown MD, Neel JV, Larsen M, et al. Asian affinities and continental radiation of the four founding native American mtDNAs. Am J Hum Genet. 1993;53:563-90. <br />15. Keyeux G, Rodas C, Gelvez N, Carter D. Possible migration routes into South America deduced from mitochondrial DNA studies in Colombian Amerindian populations. Hum Biol. 2002;74:211-33. <br />16. Jones M. Ancient DNA in pre-Columbian archaeology: a review. J Archaeol Sci. 2003;30:629-35. <br />17. Lleonart R, Riego E, Rodríguez R, Travieso R, de la Fuente J. Analyses of DNA from ancient bones of a pre-columbian Cuban woman and a child. Genet Mol Biol. 1999;22:285-89. <br />18. Stone A, Stoneking M. mtDNA analysis of a prehistoric Oneota population: implications for the peopling of the New World. Am J Hum Genet. 1998;62:1153-70. <br />19. Lalueza C, Perez-Perez A, Prats E, Cornudella L, Turbon D. Lack of founding American mitochondrial DNA lineages in extinct aborigines from Tierra del Fuego-Patagonia. Hum Mol Genet. 1997;6:41-6. <br />20. Lalueza-Fox C, Luna Calderon F, Calafell F, Morera B, Bertranpetit J. MtDNA from extinct Tainos and the peopling of the Caribbean. Ann Hum Genet. 2001;65:137-51. <br />21. García-Bour J, Pérez-Pérez A, Álvarez S, Fernández E, López-Parra AM, Arroyo-Pardo E, et al. Early population differentiation in extinct aborigines from Tierra del Fuego-Patagonia: Ancient mtDNA sequences and Y-chromosome STR characterization. Am J Phys Anthropol. 2004;123:361-70. <br />22. Luciani S, Fornaciari G, Rickards O, Martínez C, Rollo F. Molecular characterization of a Pre-Columbian mummy and in situ coprolite. Am J Phys Anthropol. 2006;129:620-9. <br />23. Ribeiro-Dos-Santos AK, Santos SE, Machado AL, Guapindaia V, Zago M. Heterogeneity of mitochondrial DNA haplotypes in Pre-Columbian natives of the Amazon region. Am J Phys Anthropol. 1996;101:29-37. <br />24. Shimada I, Shinoda K, Farnum J, Corruccini R, Watanabe H. An integrated analysis of Pre-Hispanic mortuary practices: A middle Sicán case study. Curr Anthropol. 2004;45:369-402. <br />25. Shinoda K, Adachi N, Guillen S, Shimada I. Mitochondrial DNA analysis of ancient Peruvian highlanders. Am J Phys Anthropol. 2006;131:98-107. <br />26. Moraga M, Santoro CM, Standen VG, Carvallo P, Rothhammer F. Microevolution in prehistoric Andean populations: Chronologic mtDNA variation in the desert valleys of northern Chile. Am J Phys Anthropol. 2005; 127:170-81. <br />27. Monsalve MV, Cárdenas F, Guhl F, Delaney AD, Devine DV. Phylogenetic analysis of mtDNA lineages in South American mummies. Ann Hum Genet. 1996;60:293-303. <br />28. Fernández C. La arqueología molecular aplicada a la solución de problemas prehistóricos: análisis de ADN mitocondrial en momias y restos óseos prehispánicos (tesis). Bogotá: Universidad Nacional de Colombia; 1999. <br />29. Rodríguez JV, Cifuentes A. Un yacimiento formativo ritual en el entorno de la antigua laguna de La Herrera, Madrid, Cundinamarca. Maguaré. 2005;19:103-31. <br />30. Kalmár T, Bachrati CZ, Marcsik A, Raskó I. A simple and efficient method for PCR amplifiable DNA extraction from ancient bones. Nucleic Acids Res. 2000;28:e67. <br />31. Kemp BM, Smith DG. Use of bleach to eliminate contaminating DNA from the surface of bones and teeth. Forensic Sci Int. 2005;154:53-61. <br />32. Vigilant L, Pennington R, Harpending H, Kocher TD, Wilson AC. Mitochondrial DNA sequences in single hairs from a southern African population. Proc Natl Acad Sci USA. 1989;86:9350-4. <br />33. Cooper A, Poinar HN. Ancient DNA: Do it right or not at all. Science. 2000;289:1139. <br />34. Monson KL, Miller KW, Wilson MR, DiZinno JA, Budowle B. The mtDNA population database: An integrated software and database resource for forensic comparison. Forensic Sci Commun. 2002;4. [Fecha de consulta: agosto de 2007]. Disponible en: http:// www.fbi.gov/hq/lab/fsc/backissu/april2002/miller1.htm <br />35. Horai S, Hayasaka K. Intraspecific nucleotide sequence differences in the major noncoding region of human mitochondrial DNA. Am J Hum Genet. 1990;46:828-42. <br />36. Correa F. El sol del poder. Bogotá D.C.: Unibiblos, Universidad Nacional de Colombia; 2004. <br />37. Langebaek CH. Regional archaeology in the Muisca territory: a study or the Fúquene and Susa Valleys. Memoirs in Latin American Archaeology No. 9, Bogotá, University of Pittsburgh Latin American Archaeology Publications and Universidad de los Andes; 1995.<br />
oai:oai.revistabiomedica.org:article/64
2009-12-24T18:03:35Z
biomedica:BREV
Use of the function semivariogram and kriging estimation in the spacial analysis of Aedes aegypti (Diptera: Culicidae) distributions
Uso de la función semivariograma y estimación kriging en el análisis espacial de un indicador entomológico de Aedes aegypti (Diptera: Culicidae)
Niño, Larry
Aedes aegypti
modelos estadísticos
vigilancia epidemiológica
vectores de enfermedades
mapa de riesgo
Colombia
Aedes aegypti
models
statistical
epidemiological surveillance
disease vectors
risk map
Colombia
Introduction. Aedes aegypti is the main vector of dengue in the Americas. The prevention and control of this disease require new monitoring techniques for this mosquito. Knowledge of the spatial and temporal distributions of A. aegypti populations allow the planning and evaluation of measures to decrease the vector-human contact. Objective. The spatial variation pattern of the A. aegypti container index (defined as the percentage of artificial containers infested with A. aegypti larva) was analyzed for the purpose of developing a graphical representation. Materials and methods. Larval surveys were undertaken in every household of La Independencia neighborhood in May 2007 (Acacías-Meta). Spatial statistics employing the semivariogram function and kriging estimations were applied to these data. Results. The experimental semivariogram output was adjusted to the gaussian mathematical model, whose sill was calculated to be 5.1, the range as 57.1 meters and the nugget as 0.01. A bidimensional graph of the kriging estimation was built, allowing the identification of the urban areas with highest container index. Conclusion. The analysis of the container index and distribution map provided a useful tool in monitoring, evaluating and making control decisions concerning A. aegypti infestations.
Introducción. Aedes aegypti es el principal vector del dengue en América. La prevención y control de esta enfermedad requieren de nuevas técnicas de vigilancia para este mosquito. El análisis de la distribución espacial de estas poblaciones puede llegar a jugar un papel importante en la planificación y evaluación de medidas orientadas a la disminución del contacto vector-hombre. Objetivo. Analizar y representar gráficamente el patrón de variación espacial del indicador aédico correspondiente al índice de recipientes, definido como el porcentaje de depósitos con agua infestados con larvas de A. aegypti. Materiales y métodos. Se realizaron encuestas sobre larvas en la totalidad de las viviendas del barrio La Independencia (Acacías, Meta) en mayo de 2007, con las cuales se calcularon los índices de recipientes en cada manzana. La metodología empleada en el análisis de este indicador correspondió a la estadística espacial, concretamente a la función semivariograma junto con estimaciones kriging. Resultados. El semivariograma experimental obtenido se ajustó al modelo matemático de Gauss, cuya meseta se calculó en 5,1, el rango en 57,1 m y la pepita en 0,09. Se construyó una gráfica bidimensional de la estimación kriging que permitió identificar las manzanas con mayores índices de recipientes. Conclusión. El análisis y la representación gráfica de la distribución del índice de recipientes pueden ser útiles en la vigilancia, la toma y la evaluación de acciones contra la infestación de A. aegypti.
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/64
10.7705/biomedica.v28i4.64
Biomedica; Vol. 28 No. 4 (2008); 578-586
Biomédica; Vol. 28 Núm. 4 (2008); 578-586
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/64/64
https://revistabiomedica.org/index.php/biomedica/article/view/64/391
/*ref*/Schatzmayr H. Viroses emergentes e remergentes. Cad Saúde Publica. 2001;7(Suppl.):209-13. <br />2. Tinker M, Olano V. Ecología del Aedes aegypti en un pueblo de Colombia, Sur América. Biomédica. 1993;13:5-14. <br />3. Fernández W, Iannacone J, Rodríguez E, Salazar N, Valderrama B, Morales A. Comportamiento poblacional de larvas de Aedes aegypti para estimar los casos de Dengue en Yurimaguas, Perú, 2000- 2004. Rev Peru Med Exp Salud Pública. 2005;22:175-82. <br />4. Taylor L. Assessing and interpreting the spatial distributions of insect populations. Annu Rev Entomol. 1984;29:321-57. <br />5. Niño L. Características de las comunidades de Diptera (Arthropoda: Insecta) y su relación con el paisaje en la altillanura de la Orinoquia (Meta, Colombia) (trabajo de grado). Bogotá D.C.: Universidad Nacional de Colombia; 2005. 6. Liebhold AM, Rossi RE, Kemp WP. Geostatistics and geographic information systems in applied insect ecology. Annu Rev Entomol. 1993;38:303-27. <br />7. Burrough P, MacDonell R. Principles of geographical information systems. New York: Oxford University Press; 1998. <br />8. Moral F. Aplicación de la geoestadística en las ciencias ambientales. Ecosistemas. 2004;13:78-86. <br />9. Isaaks E, Srivastava R. An introduction to applied geostatistics. New York: Oxford University Press; 1989. <br />10. Dale M, Dixon P, Fortin M, Legendre P, Myers D, Rosemberg M. Conceptual and mathematical relationships among methods for spatial analysis. Ecography. 2002;25:558-77. <br />11. Journel A, Huijbregts C. Mining geostatistics. New York: Academic Press; 1978. <br />12. Kyle J, Harris E. Global spread and persistence of dengue. Annu Rev Microbiol. 2008;62:71-92. <br />13. Regis L, Monterior AM, Varial MA, Silveira JC Jr, Furtado AF, Acioli RV, et al. Developing new approaches for detecting and preventing Aedes aegypti population outbreaks: basis for surveillance, alert and control system. Mem Inst Oswaldo Cruz. 2008;103:50-9 <br />14. Lagrotta M, Silva W, Souza-Santos R. Identification of key areas for Aedes aegypti control through geoprocessing in Nova Iguaçu, Rio de Janeiro State, Brazil. Cad. Saúde Pública. 2008;24:70-80. <br />15. Fantinatti E, Duque J, Silva A, Navarro-Silva M. Abundância e agregação de ovos de Aedes aegypti L. e Aedes albopictus (Skuse) (Diptera: Culicidae) no Norte e Noroeste do Paraná. Neotrop Entomol. 2007;36:960-5.<br />
oai:oai.revistabiomedica.org:article/65
2009-12-24T18:03:35Z
biomedica:BREV
Hallazgo de Aedes aegypti (Linnaeus 1762), en el casco urbano del corregimiento de La Pedrera, Amazonas, Colombia
Rojas, Yesika del Carmen
Brochero, Helena
Aedes aegypti
vigilancia
dengue
fiebre amarilla
Colombia
Introducción. Hasta el año 2005 no se había registrado la especie Aedes aegypti en el departamento de Amazonas en Colombia. En el marco de la vigilancia entomológica para enfermedades transmitidas por vectores realizada por la Secretaría de Salud Departamental, se registra en abril de 2006 la presencia de este mosquito en el casco urbano del corregimiento de La Pedrera, Amazonas. Objetivo. Registrar el hallazgo de Ae. aegypti en el departamento de Amazonas. Materiales y métodos. Se realizaron levantamientos de índices de infestación larvaria para Ae. aegypti y se calcularon los valores clásicos de índice de vivienda (IV) (porcentaje de casas que presentaron criaderos con larvas), índice de depósito (ID) (porcentaje de depósitos con larvas con respecto al total de depósitos inspeccionados) y el índice de Breteau (IB) (número de depósitos con larvas de la especie en 100 viviendas inspeccionadas). Se indagó a la comunidad sobre la percepción de la presencia del insecto en sus viviendas. Se realizaron actividades de control tendientes a reducir la infestación del mosquito. Resultados. Se registró Ae. aegypti en el casco urbano del corregimiento de La Pedrera.Durante la primera inspección los valores de los índices correspondieron a: IV=29,6%; ID=9,0%; IB=40,8%. Se observó disminución de estos valores luego de las actividades de control de vectores realizadas. Sin embargo, no se eliminó la infestación de la especie en esta área geográfica. La comunidad reconoce las larvas del mosquito en los recipientes de su domicilio y, en general, lo asocia como transmisor de diversas enfermedades. Conclusión. Este estudio evidenció el hallazgo de Ae. aegypti en el departamento de Amazonas. En el casco urbano de La Pedrera no se encontró Ae. albopictus.
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/65
10.7705/biomedica.v28i4.65
Biomedica; Vol. 28 No. 4 (2008); 587-596
Biomédica; Vol. 28 Núm. 4 (2008); 587-596
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/65/65
https://revistabiomedica.org/index.php/biomedica/article/view/65/390
/*ref*/Instituto Geográfico Agustín Codazzi. Diccionario geográfico de Colombia. Bogotá, D.C.: IGAC; 1996. <br />2. Departamento Nacional de Estadística DANE. Boletín Censo General 2005. Perfil La Pedrera Amazonas. [Fecha de consulta: 30 de noviembre de 2007]. Disponible en: http://www.dane.gov.co/files/ censo2005/perfiles/amazonas/la_pedrera.pdf <br />3. Pérez L, Suárez M, Murcia L, de la Hoz F, Olano V, Brochero H, et al. La malaria en el Amazonas: conocimientos, prácticas, prevalencia de parasitemia y evaluación entomológica en mayo de 1997. Biomédica. 1999;19:93-102. <br />4. Castillo O, Chaparro P, García I, Idárraga I, Izquierdo V, Otálvaro J, et al. Situación de las enfermedades transmisibles objeto de vigilancia intensificada en salud pública, Colombia, 2002. Inf Quinc Epidemiol Nac. 2002;7:463-74. <br />5. Gualdrón L, Brochero H, Arévalo C, Pérez L, Suárez M, Olano V. Hallazgo de algunos vectores de la enfermedad de Chagas en el departamento del Amazonas y sus implicaciones en salud pública. Revista Colombiana de Entomología. 2001;27:121-7. <br />6. Molina J, Gualdrón L, Brochero H, Olano V, Guhl F. Distribución actual e importancia epidemiológica de las especies de triatominos (Reduviidae: Triatominae) en Colombia. Biomédica. 2000;20:344-60. <br />7. Vélez I, Quiñones M, Suárez M, Olano V, Murcia LM, Correa E, et al. Presencia de Aedes albopictus en Leticia, Amazonas, Colombia. Biomédica. 1998;18:192-8. <br />8. Pan American Health Organization PAHO/WHO. Second Meeting to Establish a Surveillance Network QQ1)2)for Emerging Infectious Diseases in the Amazon Region. Documento técnico. Tarapoto (Perú): PAHO/HCP/ HCT/143/99; 1999. p. 56. <br />9. Olano V, Padilla J, Sáenz R, Morales A, Pinzón E, Ferro C, et al. Distribución de Aedes aegypti en Colombia, 1997. Inf Quinc Epidemiol Nac. 1998;3:94-6. <br />10. Fé NF, Barbosa M, Alecrim W, Guerra M. Registro da ocorrência de Aedes albopictus em área urbana do município de Manaus, Amazonas. Revista de Saúde Pública. 2003;37:674-5. <br />11. Gast-Galvis A. Historia de la fiebre amarilla en Colombia. Bogotá: Instituto Nacional de Salud; 1978. <br />12. Instituto Nacional de Salud. Sistema Nacional de Vigilancia en Salud Pública, SIVIGILA 2005-2007. Bogotá, D.C.: Instituto Nacional de Salud; 2007. <br />13. Instituto Geográfico Agustín Codazzi. Zonificación ambiental para el plan modelo colombo-brasilero (Eje Apaporis-Tabatinga: PAT). Santafé de Bogotá, D.C.: Linotipia Bolívar; 1997. p. 45. <br />14. Universidad Nacional de Colombia. La Amazonia colombiana y sus recursos, proyecto radargramétrico del Amazonas. Bogotá: Universidad Nacional de Colombia; 1979. p. 590. <br />15. Martínez I. Técnicas básicas de anatomía microscópica y de morfometría para estudiar los insectos. Boletín SEA. 2002;30:187-95. [Fecha de consulta: 14 de abril de 2008]. Disponible en: http:// entomologia.rediris.es/aracnet/9/metodologias/ tecnicas/index.htm <br />16. Cova-García P, Sutil E, Rausseo JA. Mosquitos de Venezuela. Volumen II. Caracas: Publicaciones del Ministerio de Sanidad y Asistencia Social; 1966. <br />17. Forattini O. Culicidología médica. Volumen 2. Identificación, biología y epidemiología. São Paulo: Universidad de São Paulo; 2002. p. 860. <br />18. Rueda L. Pictorial keys for the identification of mosquitoes (Diptera: Culicidae) associated with dengue virus transmisión. Zootaxa. 2004;589:1-60. <br />19. Salvatella R. Aedes aegypti, Aedes albopictus (Diptera, Culicidae) y su papel como vectores en las Américas. La situación de Uruguay. Rev Med Uruguay. 1996; 12: 28-36. <br />20. Marquetti, M, Suárez S, Bisset J, Leyva M. Reporte de hábitats utilizados por Aedes aegypti en Ciudad de La Habana, Cuba. Rev Cubana Med Trop. 2005;57:159-61. <br />21. Tun-Lin W, Kay B, Barnes A, Forsyth S. Critical examination of Aedes aegypti indices: correlations with abundance. Am J Trop Med Hyg. 1996;54:543-7. <br />22. Sánchez L, Vanlerberghe V, Alonso L, Marquetti M, Guzman M, Bisset J, et al. Aedes aegypti larval indices and risk for dengue epidemics. Emerg Infect Dis. 2006;12:800-6. <br />23. Focks D, Chadee D. Pupal survey: an epidemiologically significant surveillance method for Aedes aegypti: an example using data from Trinidad. Am J Trop Med Hyg. 1997;56:159-67. <br />24. Barrera R, Amador M, Clark G. Use of the pupal survey technique for measuring Aedes aegypti (Diptera: Culicidae) productivity in Puerto Rico. Am J Trop Med Hyg. 2006;74:290-302. <br />25. Morrison A, Gray K, Getis A, Astete H, Sihuincha M, Focks D, et al. Temporal and geographic patterns of Aedes aegypti (Diptera: Culicidae) in Iquitos, Perú. J Med Entomol. 2004;41:1123-42. <br />26. Guzmán M, Kouri G. Dengue: an update. Lancent Infect Dis. 2002;2:33-42. <br />27. Ooi E, Goh K, Gubler D. Dengue prevention and 35 years of vector control in Singapore. Emerg Infect Dis. 2006;12:887-93. <br />28. Kay B, Vu S. New strategy against Aedes aegypti in Vietnam. Lancet. 2005;365:613-7. <br />29. Ole Nielsen N. Enfoques ecosistémicos para la salud humana. Reports in Public Health. 2001;17:69-75. <br />30. Navarrete-Espinosa J, Acevedo-Vales J, Huerta- Hernández E, Torres-Barranca J, Gavaldón-Rosas D. Prevalencia de anticuerpos contra dengue y leptospira en la población de Jáltipan, Veracruz. Salud Pública Mex. 2006;48:220-8. <br />31. Benítez-Leite S, Machi ML, Gibert E, Rivarola K. Conocimientos, actitudes y prácticas acerca del dengue en un barrio de Asunción. Rev Chil Pediatr. 2002;73:64-72. <br />32. Toledo-Romaní ME, Baly-Gil A, Ceballos-Ursula E, Boelaert M, van der Stuyft P. Participación comunitaria en la prevención del dengue: un abordaje desde la perspectiva de los diferentes actores sociales. Salud Pública Mex. 2006;48:39-44. <br />33. Toledo ME, Vanlerberghe V, Baly A, Ceballos E, Valdes L, Searret M, et al. Towards active community participation in dengue vector control: results from action research in Santiago de Cuba, Cuba. Trans R Soc Trop Med Hyg. 2007;101:56-63. <br />34. Castro M, Quintana N, Quiñones M. Evaluating two pyrethroids in dengue vector control in Putumayo, Colombia. Rev Salud Pública. 2007;9:106-16<br />
oai:oai.revistabiomedica.org:article/66
2009-12-24T18:03:35Z
biomedica:NOTA
PCR-RFLP and RAPD for typing neotropical Leishmania
PCR-RFLP y RAPD para la tipificación de Leishmania neotropical
Montalvo, Ana Margarita
Monzote, Lianet
Fraga, Jorge
Montano, Ivón
Muskus, Carlos
Marín, Marcel
De Donck, Simonne
Vélez, Iván Darío
Dujardin, Jean Claude
Leishmania
leishmaniasis/diagnóstico
reacción en cadena de la polimerasa
polimorfismo de longitud del fragmento de restricción
Leishmania
leishmaniasis/diagnosis
polymerase chain reaction
polymorphism
restriction fragment length
Introduction. The analysis of the PCR-restriction fragment length polymorphism and random amplified polymorphic DNA have been useful tools for Leishmania identification. Objectives. Molecular procedures were demonstrated for identification and typing of reference strains of New World Leishmania and their applicability was validated for clinical samples. Materials and methods. DNA was extracted from 16 reference strains of Latin American Leishmania as well as from clinical samples of leishmaniasis patients. A sequence coding for cysteine proteinase B was amplified by PCR and subjected to restriction fragment length polymorphism analysis. The enzyme used was Taq1. For eight of the reference strains, the random amplified polymorphic desoxyribonucleic acid technique (RAPD) was applied. Band patterns for Leishmania species differentiation were established each each method. The sample size of the clinical sample was of 5. Results. PCR products of the cysteine proteinase B gene were obtained for L. braziliensis, L. peruviana, L. panamensis and L. guyanensis. For the other species, L. mexicana, L. amazonensis, L. garnhami, L. lainsoni, L. chagasi, L. naiffi, no amplification occurred. The patterns of restriction fragments revealed band patterns in common for L. peruviana, L. guyanensis and L. panamensis, whereas L. braziliensis had a distinctive pattern. When human samples were examined, amplification occurred for all cases, and the profiles corresponded to the common profile of L. peruviana, L. guyanensis and L. panamensis. The RAPD technique demonstrated reproducible and distinctive patterns for each of the 8 reference strains, L. mexicana, L. amazonensis, L. garnhami, L. lainsoni, L. chagasi, L. naiffi, making possible to differentiate all them. The advantages and limitations of each procedure are discussed. Conclusions. The combination of RFP and RAPD methodologies provide useful tools to identify medical important species of Leishmania by recognizing DNA sequences characteristic of each species.
Introducción. El análisis de la longitud de los fragmentos de restricción del producto amplificado y el estudio del ADN polimórfico amplificado al azar han demostrado ser herramientas útiles para la tipificación de Leishmania. Objetivos. Estudiar la utilidad de las técnicas moleculares para la identificación y tipificación de cepas de referencia de Leishmania spp. del Nuevo Mundo y valorar su aplicabilidad a muestras clínicas. Materiales y métodos. Se aplicó PCR para amplificar el gen que codifica la cisteíno-proteinasa B, y el análisis de la longitud de los fragmentos de restricción del producto amplificado utilizando ácido desoxirribonucleico de 16 cepas de referencia de Latinoamérica y de muestras clínicas de pacientes colombianos con leishmaniasis, y la técnica del ácido desoxirribonucleico polimórfico amplificado al azar utilizando ocho cepas de referencia. Se establecieron los patrones de bandas en cada caso. Resultados. Se obtuvo producto de amplificación en la PCR para Leishmania braziliensis, L. peruviana, L. panamensis y L. guyanensis. Para el resto, no fue posible amplificar el gen con los cebadores utilizados. La restricción mostró un patrón de bandas común para L. peruviana, L. guyanensis y L. panamensis, mientras L. braziliensis, presentaba un perfil individual único. El análisis de restricción del producto amplificado generó un patrón de bandas similar en los cinco pacientes estudiados, que se correspondía con el patrón generado por L. peruviana, L. guyanensis o L. panamensis. Mediante la amplificación al azar se obtuvieron patrones de bandas reproducibles con todas las cepas estudiadas, que posibilitaron la diferenciación. Se discuten las ventajas y limitaciones de ambos procederes. Conclusiones. El combinar ambas metodologías resultaría útil para identificar especies de importancia médica, tomando en cuenta sus ventajas y desventajas.
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/66
10.7705/biomedica.v28i4.66
Biomedica; Vol. 28 No. 4 (2008); 597-606
Biomédica; Vol. 28 Núm. 4 (2008); 597-606
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/66/66
https://revistabiomedica.org/index.php/biomedica/article/view/66/388
/*ref*/García AL, Kindt A, Quispe-Tintaya KW, Bermúdez H, Llanos A, Arévalo J, et al. American tegumentary leishmaniasis: antigen gene polymorphism, taxonomy and clinical pleomorphism. Inf Genet Evol. 2005;5:109-16. <br />2. World Health Organization. Tropical disease research. Progress 1975-94, highlights 1993-94. Twelfth Programme Report of the UNDP/World Bank/ WHO Special Programme for Research and Training in Tropical Disease (TDR). Geneva: WHO; 1995. p.135-46. <br />3. Rotureau B, Ravel C, Couppie P, Pratlong F, Nacher M, Dedet JP, et al. Use of PCR-restriction fragment length polymorphism analysis to identify the main New World Leishmania species and analyze their taxonomic properties and polymorphism by application of the assay to clinical samples. J Clin Microbiol. 2006;44:459-67. <br />4. Victoir K, De Doncker S, Cabrera L, Álvarez E, Arévalo J, Llanos-Cuentas A, et al. Direct identification of Leishmania species in biopsies from patients with American tegumentary leishmaniasis. Trans R Soc Trop Med Hyg. 2003;97:80-7. <br />5. Serin MS, Daglioglu K, Bagirova M, Allahverdiyev A, Uzun S, Vural Z, et al. Rapid diagnosis and genotyping of Leishmania isolates from cutaneous and visceral leishmaniasis by microcapillary cultivation and polymerase chain reaction-restriction fragment length polymorphism of miniexon region. Diagn Microbiol Infect Dis. 2005; 53:209-14. <br />6. Noyes HA, Belli AA, Maingon R. Appraisal of various random amplified polymorphic DNA polymerase Chain reaction primers for Leishmania identification. Am J Trop Med Hyg. 1996;55:98-105. <br />7. Sambrook J, Fritsch EF, Maniatis T. Molecular cloning. A laboratory manual. Second edition. Cold Spring Harbor: Cold Spring Harbor Laboratory; 1989. <br />8. Ordeñana-Pilotos R. Optimización de la técnica del ADN polimórfico amplificado al azar (RAPD), para la identificación de especies de Leishmania (tesis). Ciudad de La Habana: Instituto Pedro Kourí; 2005. <br />9. Sneath PH, Sokal RR. Numerical taxonomy. San Francisco: Freeman WH & Co.; 1973. <br />10. Pavlícèk A, Hrdá S, Flegr J. Free tree-freeware program for construction of phylogenetic trees on the basis of distance data and for bootstrap/jackknife analysis of the threes robustness. Application in the RAPD analysis of genus Frenkelina. Folia Biol (Praha). 1999;45:97-9. <br />11. Reithinger R, Dujardin JC. Molecular diagnosis of leishmaniasis: Current status and future applications. J Clin Microbiol. 2007;45:21-5.<br />12. Croft SL, Yardley V, Kendrick H. Drug sensitivity of Leishmania species: some unresolved problems. Trans R Soc Trop Med Hyg. 2002;96(Suppl.1):127-9. <br />13. Berman JD. Human leishmaniasis: clinical, diagnostic, and chemotherapeutic developments in the last 10 years. Clin Infect Dis. 1997;24:684-703. <br />14. Singh S, Sivakumar R. Recent advances in the diagnosis of leishmaniasis. J Postgrad Med. 2003; 49:55-60. <br />15. Tavares CA, Fernandes AP, Melo MN. Molecular diagnosis of leishmaniasis. Expert Rev Mol Diagn. 2003;3:657-67. <br />16. Cupolillo E, Grimaldi G Jr, Momen H, Beverly SM. Intergenic region typing (IRT):a rapid molecular approach to the characterization and evolution of Leishmania. Mol Biochem Parasitol. 1995;73:145-55. <br />17. Bañuls AL, Jonquieres R, Guerrini F, LePont F, Barrera C, Espinel I, et al. Genetic analysis of Leishmania parasites in Ecuador: are Leishmania (Viannia) panamensis and Leishmania (V) guyanensis distinct taxa? Am J Trop Med Hyg. 1999;61:828-45. <br />18. Montalvo AM, Fraga J, Romero JA, Monzote L, Montano I, Dujardin JC. PCR-RFLP/HsP70 para identificar y tipificar Leishmania de la región neotropical. Rev Cub Med Trop. 2006;58(3). [Fecha de consulta: 24 de octubre de 2008]. Disponible en: http:// scielo.sld.cu/scielo.php?script=sci_arttext&pid=S0375- 07602006000300009&lng=es&nrm=iso. <br />19. Bhattacharyya R, Singh R, Hazra TK, Majumder HK. Application of polymerase chain reaction with specific and arbitrary primers to identification and differentiation of Leishmania parasites. FEMS Microbiol Lett. 1993;114:99-104. <br />20. Tibayrenc M, Neubauer K, Barnabe C, Guerrini F, Skarechy D, Ayala FJ. Genetic characterization of six parasitic protozoa: a parity between random-primer DNA typing and multilocus enzyme electrophoresis. Proc Natl Acad Sci USA. 1993;90:1335-9. <br />21. Diakou A, Dovas CI. Optimization of random amplified polymorphic DNA producing amplicons of 8500 bp and revealing intraspecies polymorphism in Leishmania infantum isolates. Anal Biochem. 2001;288:195-200. <br />22. Hanafi R, Barhoumi M, Ali SB, Guizani I. Molecular analyses of Old World Leishmania RAPD markers and development of a PCR assay selective for parasites of the L. donovani species complex. Exp Parasitol. 2001;98:90-9. 23. Zemanova E, Jirku M, Mauruicio IL, Miles MA, Lukes J. Genetic polymorphism within the Leishmania donovani complex: correlation with geographic origin. Am J Trop Med Hyg. 2004;70:613-7. <br />24. Martínez E, Alonso V, Quispe A, Thomas MC, Alonso R, Pinero JE, et al. RAPD method useful for distinguishing Leishmania species: design of specific primers for L. braziliensis. Parasitology. 2003;127:513-7. <br />25- Rodríguez-Bonfante C, Bonfante-Garrido R, Grimaldi G Jr, Momen H, Cupolillo E. Genotypically distinct Leishmania colombiensis isolates from Venezuela cause both cutaneous and visceral Leishmaniasis in humans. Infect Genet Evol. 2003;3:119-24. <br />26- García L, Kindt A, Bermúdez H, Llanos-Cuentas A, De Doncker S, Arévalo J, et al. Culture- independent species typing of neotropical Leishmania for clinical validation of a PCR-based assay targeting heat shock protein 70 genes. J Clin Microbiol. 2004;42:2294-7.<br />
oai:oai.revistabiomedica.org:article/67
2009-12-24T18:03:35Z
biomedica:NOTA
Successful in vitro culture of Plasmodium falciparum gametocytes
Exitoso cultivo in vitro de gametocitos de Plasmodium falciparum
Blair, Silvia
Rada, Ana Mercedes
Moreno, Carolina
Plasmodium falciparum
in vitro
paludismo
Anopheles
Plasmodium falciparum
in vitro
malaria
Anopheles
Introduction. The sexual stages of Plasmodium falciparum have not been studied in as much detail as the asexual stages due to the lack of standardized in vitro cultures as well as difficulties in identifying the sexual development stages of the parasite. These difficulties hamper the studies on biology, metabolism, gene expression and protein synthesis during sexual stages. Each of these facets are important targets in antimalarial drug research, particularly the identification of potential therapeutic agents against Plasmodium (derived mainly from plants). Objectives. An in vitro culture of P. falciparum gametocytes was established to standardize the identification of its five developmental stages and ensure their continuous production. Materials and methods. The in vitro gametocyte culture was established from the P. falciparum NF54 strain in RPMI culture medium, with assessment of the asexual and sexual parasitaemia. The medium was supplemented with type A Rh+ red blood cells only on the first day of culture. Subsequently, the medium was changed daily, together with addition of gas mixture (90% N2, 5% O2, 5% CO2) and maintenance of the culture temperature at 37 °C. When asexual parasitaemia reached 3 to 5%, the medium was changed by doubling its volume. Conclusions. We standardized an in vitro culture for sexual stages of P. falciparum that can be used for future studies about evaluation of compounds of synthetic or natural origen against the sexual stage, which may permit to develop new control strategies against malaria.
Introducción. Los estadios sexuales de Plasmodium falciparum han sido menos estudiados que los estadios asexuales. Al parecer, esto se debe a la carencia de cultivos estandarizados in vitro y a la dificultad de reconocer sus estadios de desarrollo. Estos hechos no permiten el estudio de aspectos biológicos, aspectos metabólicos, expresión de genes y síntesis de proteínas durante los estadios sexuales, temas de interés en la investigación de nuevos medicamentos antipalúdicos, principalmente los aislados de plantas, y la identificación de un potencial blanco contra Plasmodium. Objetivos. Establecer un cultivo in vitro de gametocitos, con la identificación de sus cinco estadios de desarrollo, y asegurar su continua producción. Materiales y métodos. El cultivo in vitro de gametocitos se realizó a partir de la cepa NF54 de P. falciparum en medio RPMI, con determinación de la parasitemia asexual y sexual, adición de glóbulos rojos A-Rh+ sólo el primer día de cultivo y cambio diario del medio con adición de mezcla de gases (90% N2, 5% O2; 5% CO2), asegurándose que el cultivo se mantuviera a 37 °C. Cuando la parasitemia asexual estuvo entre 3% y 5%, se comenzó a agregar el doble de volumen de medio. Resultados. Se obtuvieron gametocitos en estadios I, II y III a partir del día 11 de cultivo y estadios IV y V a partir del día 14 de cultivo. Conclusiones. Se estandarizó un cultivo in vitro para estadios sexuales de P. falciparum que puede usarse para futuros estudios de evaluación de compuestos, naturales o sintéticos, que actúen sobre los gametocitos, lo cual podría permitir el desarrollo de nuevas estrategias de control contra el paludismo.
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/67
10.7705/biomedica.v28i4.67
Biomedica; Vol. 28 No. 4 (2008); 607-615
Biomédica; Vol. 28 Núm. 4 (2008); 607-615
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/67/67
https://revistabiomedica.org/index.php/biomedica/article/view/67/384
/*ref*/Schneider P, Schoone G, Schallig H, Verhage D, Telgt D, Eling W, et al. Quantification of Plasmodium falciparum gametocytes in differential stages of development by quantitative nucleic acid sequence-based amplification. Mol Biochem Parasitol. 2004;137:35-41. <br />2. Shute PG, Maryon M. A study of gametocytes in a West African strain of Plasmodium falciparum. Trans R Soc Trop Med Hyg. 1951;44:421-38. <br />3. Eichner M, Diebner HH, Molineaux L, Collins WE, Jeffery GM, Dietz K. Genesis, sequestration and survival of Plasmodium falciparum gametocytes: parameter estimates from fitting a model to malaria therapy data. Trans R Soc Trop Med Hyg. 2001;95:497-501. <br />4. Sinden RE. Sexual development of malaria parasite. Adv Parasitol. 1983;22:153-216. <br />5. Kitchen SF, Putnam P. Observations on the mechanism of the parasite cycle in falciparum malaria. Am J Trop Med. 1942; 22:361-86. <br />6. Kitchen SF. Falciparum malaria. En: Boyd MF, editor. Malariology. Philadelphia: WB Saunders; 1949. p. 995- 1016. <br />7. Carter R, Graves PM. Gametocytes. En: Wernsdorfer WH, McGregor SI, editors. Malaria: principles and practice of malariology. First edition. Edinburgh, Scotland: Churchill Livingstone; 1988. p. 1-59. <br />8. Talman AM, Domarle O, Mckenzie FE, Ariey F, Robert V. Gametocytogenesis: the puberty of Plasmodium falciparum. Malar J. 2004;3:24. <br />9. Hawking F, Wilson ME, Gammage K. Evidence for cyclic short-lived maturity in the gametocytes of Plasmodium falciparum. Trans R Soc Trop Med Hyg. 1971;65:549-59. <br />10. Field JW, Shute PG. The microscopic diagnosis of human malaria. A morphological study of erythrocytic parasites. Kuala Lumpur, Malaysia: Institute for Medical Research, Government Press; 1956. p. 142. <br />11. Lobo CA, Kumar N. Sexual differentiation and development in the malaria parasite. Parasitol Today. 1998;14:146-50. <br />12. Row R. On some observation on the malarial parasites grow aerobically in simple cultures with special reference to the evolution and degeneration of the crescents. Indian J Med Res. 1929;16:120-7. <br />13. Trager W, Jensen JB. Human malaria parasite in continuous culture. Science. 1976;193:673-5. <br />14. Smalley ME. Plasmodium falciparum gametocytogenesis in vitro. Nature. 1976;264:271-2. <br />15. Ifediba T, Vanderberg JP. Complete in vitro maturation of Plasmodium falciparum gametocytes. Nature. 1981;294:364-6. <br />16. Ponnudurai T, Meuwissen JH, Leeuwenberg AD, Verhave JP, Lensen AH. The production of mature gametocytes of Plasmodium falciparum in continuous cultures of different isolates infective to mosquitoes. Trans R Soc Trop Med Hyg. 1982;76:242-50. <br />17. Freese JA, Sharp BL, Ridl FC, Markus MB. In vitro cultivation of southern African strains of Plasmodium falciparum and gametocytogenesis. S Afr Med J .1988;73:720-2. <br />18. Ponnudurai T, Lensen AH, Meuwissen JH. An automated large – scale culture system of Plasmodium falciparum using tangential flow filtration for medium change. Parasitology. 1983;87:439-45. <br />19. Ponnudurai T, Lensen AH, Meis JF, Meuwissen JH. Synchronization of Plasmodium falciparum gametocytes using an automated suspension culture system. Parasitology. 1986;93:263-74. <br />20. Kanti BM, Kumar N. Plasmodium falciparum gametocyte culture, purification, and gametogenesis. In: Ljungström I, Perlmann H, Schlichtherle M, Scherf A, Wahlgren M, editors. Methods in malaria research. Fourth edition. Manassas, Virginia; MR4/ATCC; 2004. p. 93-4. <br />21. Instituto Nacional de Salud. Protocolos para el manejo de la cepa de P. falciparum in vitro. Bogotá. Instituto Nacional de Salud; 1989. p. 28. <br />22. Ali E, Mackinnon MJ, Abdel-Muhsin AM, Ahmed S, Walliker D, Babiker HA. Increased density but not prevalence of gametocytes following drug treatment of Plasmodium falciparum. Trans R Soc Trop Med Hyg. 2006;100:176-83. <br />23. Sutherland CJ, Alloueche A, Curtis J, Drakeley CJ, Ord R, Duraisingh M, et al. Gambian children successfully treated with chloroquine can harbor and transmit Plasmodium falciparum gametocytes carrying resistance genes. Am J Trop Med Hyg. 2000;67:578-85. <br />24. Sinden RE, Ponnudurai T, Smits MA, Simm AM, Meuwissen JH. Gametocytogenesis of Plasmodium falciparum in vitro: a simple technique for the routine culture of pure capacitated gametocytes en masse. Parasitology. 1984;88:239-47. <br />25. Chutmongkonkul M, Maier WA, Seitz HM. A new model for testing gametocytocidal effects of some antimalarial drugs on Plasmodium falciparum in vitro. Ann Trop Med Parasitol. 1992;86:207-15. <br />26. Saul A, Graves P, Edser L. Refractoriness of erythrocytes infected with Plasmodium falciparum gametocytes to lysis by sorbitol. Int J Parasitol. 1990;20:1095-7. <br />27. Kariuki MM, Kiaira JK, Mulaa FK, Mwangi JK, Wasunna MK, Martin SK. Plasmodium falciparum: Purification of the various gametocyte developmental stages from in vitro–cultivated parasites. Am J Trop Med Hyg. 1998;59:505-8. <br />28. Jensen JB. Observations on gametogenesis in Plasmodium falciparum from continuous culture. J Protozool. 1979;26:129-32. <br />29. Phillips RS, Wilson RJ, Pasvol G. Differentiation of gametocytes in microcultures of human blood infected with Plasmodium falciparum. J Protozool. 1978;25:394-8.<br />
oai:oai.revistabiomedica.org:article/68
2009-12-24T18:03:35Z
biomedica:NOTA
Evaluation of TcH2AF-R and S35-S36 primers in PCR tests for the detection of Trypanosoma cruzi in mouse cardiac tissue
Evaluación de las pruebas de PCR TcH2AF-R y S35-S36 para la detección de Trypanosoma cruzi en tejido cardiaco de ratón
Puerta, Concepción Judith
Guevara, Johana María
Pavía, Paula Ximena
Montilla, Marleny
Nicholls, Rubén Santiago
Parra, Edgar
Barrera, Yuli Katherine
Trypanosoma cruzi
enfermedad de Chagas
cardiomiopatía chagásica
reacción en cadena de la polimerasa
Trypanosoma cruzi
Chagas disease
Chagas cardiomyopathy
polymerase chain reaction
Introduction. Heart transplant is a therapeutic option in the treatment of chagasic cardiomyopathy. For early detection of Chagas reactivation cases, the use of PCR tests using endomyocardial biopsies has been proposed. Development of an animal model will be the first step in evaluating the applicability of this approach. Objective. PCR tests based on the TcH2AF-R and S35-S36 primers were evaluated for the detection of T. cruzi in heart tissue of mice experimentally infected with the parasite. Materials and methods. Two groups of ICR mice of 15 and 10 individuals were infected by intraperitoneal injection with 0.3 ml of PBS containing 1x106 trypomastigotes of the MHOM/CO/ 2001/D.A. (T. cruzi I) strain or 1x104 trypomastigotes of MHOM/BR/00/Y (T. cruzi II) strain. Parasitemia and cardiac parasitic infection were determined at 30, 60 (acute model), 100 and 150 (chronic model) days by means of histopathological examination and by PCR, using the TcH2AF-R and S35-S36 primers. Results. The histopathological findings revealed alterations in the heart and the presence of intracellular amastigotes in acute and chronic models. In contrast to parasitemia levels and histopathological analyses, S35-S36 PCR detected infections in mice that were infected with either parasite strain. TcH2AF-R PCR detected T. cruzi I-infected mice earlier and more frequently than inspection for parasitemia or histopathological examination. Conclusions. Applying PCR tests with both primers proved superior for Chagas disease confirmation over currently standard detection methods.
Introducción. El trasplante es una opción terapéutica en la cardiomiopatía chagásica. Para la detección temprana de una posible reactivación de la infección, se propone el uso de pruebas de reacción en cadena de la polimerasa (PCR) a partir de biopsias endomiocárdicas; el modelo de ratón es una aproximación preliminar para evaluar la aplicación de éstas. Objetivo. Evaluar la aplicación de las pruebas de PCR basadas en los iniciadores TcH2AF-R y S35-S36 para la detección de T. cruzi en tejido cardiaco de ratones infectados con el parásito. Materiales y métodos. Se infectaron por vía intraperitoneal dos grupos de ratones ICR de 15 y 10 individuos con 0,3 ml de PBS que contenían 1x106 tripomastigotes de la cepa MHOM/CO/ 2001/D.A. (T. cruzi I) o 1x104 tripomastigotes de la cepa MHOM/BR/00/Y (T. cruzi II), respectivamente. El seguimiento de la parasitemia se realizó mediante microhematocrito y presencia de parásitos en el corazón a los 30, 60 (modelo agudo), 100 y 150 (modelo crónico) días por medio de histopatología y de las PCR TcH2AF-R y S35-S36. Resultados. La histopatología mostró alteraciones en el miocardio y presencia de amastigotes en los modelos agudo y crónico. En contraste al microhematocrito y al análisis histopatológico, la PCR S35-S36 permitió la detección de ambas cepas del parásito. La PCR TcH2AF-R detectó la cepa T. cruzi I con un desempeño superior al microhematocrito y al análisis histopatológico. Conclusiones. El uso de ambas pruebas de PCR puede ser útil en la confirmación de la reactivación de la infección postrasplante.
Instituto Nacional de Salud
2008-12-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/68
10.7705/biomedica.v28i4.68
Biomedica; Vol. 28 No. 4 (2008); 616-626
Biomédica; Vol. 28 Núm. 4 (2008); 616-626
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/68/68
https://revistabiomedica.org/index.php/biomedica/article/view/68/387
/*ref*/World Health Organization. Control of Chagas disease. Second report of the WHO Expert Committee. Technical report 2002, series 905. Geneva: WHO; 2002. p. 39-40. <br />2. Moncayo A, Ortiz MI. An update on Chagas disease (Human American trypanosomiasis). Ann Trop Med Parasitol. 2006;100:663-77. <br />3. Urinovsky FM, Salomone OA, Córdoba R, Zazu AJ, Martínez A, Zlocowsky JC, et al. Morbimortalidad de los pacientes con cardiomiopatía chagásica y trasplante cardiaco. Experiencia inicial. Rev Arg Cardiol. 2003;71:325-31. <br />4. Castro AM, Luquetti AO, Rassi A, Rassi GG, Chiari E, Galvao LM. Blood culture and polymerase chain reaction for the diagnosis of the chronic phase of human infection with Trypanosoma cruzi. Parasitol Res. 2002;88:894-900. <br />5. Teixeira AR, Nitz N, Guimaro MC, Gomes C, Santos- Buch CA. Chagas disease. Postgrad Med J. 2006;82:788-98. <br />6. Bértoli M, Andó MH, De Ornelas Toledo MJ, De Araújo SM, Gomes ML. Infectivity for mice of Trypanosoma cruzi I and II strains isolated from different hosts. Parasitol Res. 2006;99:7-13. <br />7. Schijman AG, Vigliano CA, Viotti RJ, Burgos JM, Brandariz S, Lococo BE, et al. Trypanosoma cruzi DNA in cardiac lesions of Argentinian patients with endstage chronic Chagas heart disease. Am J Trop Med Hyg. 2004;70:210-20. <br />8. Andrade Z, Andrade S. Chagas disease, pathology and pathogenesis. En: Gilles HM, editor. Protozoal diseases. New York, USA: Arnold Publishers; 1999. p. 323-35. <br />9. Kirchhoff LV, Votava JR, Ochs DE, Moser DR. Comparison of PCR and microscopic methods for detecting Trypanosoma cruzi. J Clin Microbiol. 1996;34:1171-5. <br />10. Pavía P, Cuervo C, Montilla M, Nicholls S, Puerta C. Estandarización de una prueba de PCR específica para la detección de Trypanosoma cruzi. Infectio. 2003;7:129-35. <br />11. Pavia PX, Vallejo GA, Montilla M, Nicholls RS, Puerta CJ. Detection of Trypanosoma cruzi and Trypanosoma rangeli infection in triatomine vectors by amplification of the histone H2A/SIRE and the sno-RNA-C11 genes. Rev Inst Med Trop Sao Paulo. 2007;49:23-30. <br />12. Gil J, Pavía P, Montilla M, Florez AC, Quintero C, Mercado M, et al. Comparación de una prueba de PCR basada en los genes codificantes para la histona H2A/SIRE con pruebas serológicas convencionales para el diagnóstico de la enfermedad de Chagas crónica en pacientes colombianos. Biomédica. 2007;27(Suppl.1):83-91. <br />13. Sturm NR, Degrave W, Morel C, Simpson L. Sensitive detection and schizodeme classification of Trypanosoma cruzi cells by amplification of kinetoplast minicircle DNA sequences: use in diagnosis of Chagas’ disease. Mol Biochem Parasitol. 1989;33:205-14. <br />14. Montilla MM, Guhl F, Jaramillo C, Nicholls S, Barnabe C, Bosseno MF, et al. Isoenzyme clustering of Trypanosomatidae Colombian populations. Am J Trop Med Hyg. 2002;66:394-400. <br />15. Vallejo GA, Guhl F, Chiari E, Macedo AM. Species specific detection of Trypanosoma cruzi and Trypano soma rangeli in vector and mammalian hosts by polymerase chain reaction amplification of kinetoplast minicircle DNA. Acta Trop. 1999;72:203-12. <br />16. de Arias AR, Ferro EA. Quantification of Trypanosoma cruzi parasitemia by direct micromethod. Trans R Soc Trop Med Hyg. 1988;82:248. <br />17. Martin DL, Postan M, Lucas P, Gress R, Tarleton RL. TGF-beta regulates pathology but not tissue CD8+ T cell dysfunction during experimental Trypanosoma cruzi infection. Eur J Immunol. 2007;37:2764-71. <br />18. Freitas JM, Lages-Silva E, Crema E, Pena SD, Macedo AM. Real time PCR strategy for the identification of major lineages of Trypanosoma cruzi directly in chronically infected human tissues. Int J Parasitol. 2005;35:411-7. <br />19. Puerta C, Urueña C. Electroforesis en geles de agarosa. En: Puerta CJ, editor. Prácticas de biología molecular. Colección Biblioteca del Profesional. Bogotá D.C.: Editorial Pontificia Universidad Javeriana; 2005. p. 24-30. <br />20. Vallejo GA. Estudios comparativos entre las secuencias de kDNA de Trypanosoma cruzi y Trypanosoma rangeli y su aplicación en el diagnóstico molecular de la tripanosomiasis americana. Actual Biol. 1998;20:43-56. <br />21. Guarner J, Bartlett J, Zaki SR, Colley DG, Grijalva MJ, Powell MR. Mouse model for Chagas disease: inmunohistochemical distribution of different stages of Trypanosoma cruzi in tissues throughout infection. Am J Trop Med Hyg. 2001;65:152-8. <br />22. Marinho CR, Bucci DZ, Dagli ML, Bastos KR, Grisotto MG, Sardinha LR, et al. Pathology affects different organs in two mouse strains chronically infected by a Trypanosoma cruzi clone: a model for genetic studies of Chagas’ disease. Infect Immun. 2004;72:2350-7. <br />23. Andersson J, Orn A, Sunnemark D. Chronic murine Chagas’ disease: the impact of host and parasite genotypes. Immunol Lett. 2003;86:207-12. <br />24. Cummings KL, Tarleton RL. Rapid quantitation of Trypanosoma cruzi in host tissue by real-time PCR. Mol Biochem Parasitol. 2003;129:53-9. <br />25. Melo RC, Brener Z. Tissue tropism of different Trypanosoma cruzi strains. J Parasitol. 1978;64:475-82. <br />26. Pinto PL, Takami R, Nunes EV, Guilherme CS, Oliveira OC Jr, Gama-Rodrigues J, et al. Life cycle of Trypanosoma cruzi (Y strain) in mice. Rev Hosp Clin Fac Med Sao Paulo. 1999;54:141-6. <br />27. Soares MB, Pontes-De-Carvalho L, Ribeiro-Dos- Santos R. The pathogenesis of Chagas’ disease: when autoimmune and parasite-specific immune responses meet. An Acad Bras Cienc. 2001;73:547-59. <br />28. Lane JE, Olivares-Villagomez D, Vnencak-Jones CL, Mccurley TL, Carter CE. Detection of Trypanosoma cruzi with the polymerase chain reaction and in situ hybridization in infected murine cardiac tissue. Am J Trop Med Hyg. 1997;56:588-95. <br />29. Añez N, Carrasco HA, Parada H, Crisante G, Rojas A, Fuenmayor C, et al. Myocardial parasite persistence in chronic chagasic patients. Am J Trop Med Hyg. 1999;60:726-32. <br />30. Lane JE, Ribeiro-Rodrigues R, Olivares-Villagomez D, Vnencak-Jones CL, McCurley TL, Carter CE. Detection of Trypanosoma cruzi DNA within murine cardiac tissue sections by in situ polymerase chain reaction. Mem Inst Oswaldo Cruz. 2003;98:373-6. <br />31. Elias FE, Vigliano CA, Laguens RP, Levin MJ, Berek C. Analysis of the presence of Trypanosoma cruzi in the heart tissue of three patients with chronic Chagas’ heart disease. Am J Trop Med Hyg. 2003;68:242-7. <br />32. Thomas MC, Olivares M, Escalante M, Marañón C, Montilla M, Nicholls S, et al. Plasticity of the histone H2A genes in a Brazilian and six Colombian strains of Trypanosoma cruzi. Acta Trop. 2000;75:203-10. <br />33. Saravia NG, Holguín AF, Cibulskis RE, D’ Alessandro A. Divergent isoenzyme profiles of sylvatic and domiciliary Trypanosoma cruzi in the eastern plains, piedmont, and highlands of Colombia. Am J Trop Med Hyg. 1987;36:59-69. <br />34. Triana O, Jaramillo N, Moreno J. Genetic variability of Colombian populations of Trypanosoma cruzi and Trypanosoma rangeli. Biol Res. 1999; 32:1-10. <br />35. Nitz N, Gomes C, de Cássia Rosa A, D’souza-Ault MR, Moreno F, Lauria-Pires L, et al. Heritable integration of kDNA minicircle sequences from Trypanosoma cruzi into the avian genome: insights into human Chagas disease. Cell. 2004;118:175-86. <br />36. Diez M, Favaloro L, Bertolotti A, Burgos JM, Vigliano C, Lastra MP, et al. Usefulness of PCR strategies for early diagnosis of Chagas’ disease reactivation and treatment follow-up in heart transplantation. Am J Transplant. 2007;7:1633-40. <br />37. Maldonado C, Albano S, Vettorazzi L, Salomone O, Zlocowski JC, Abiega C, et al. Using polymerase chain reaction in early diagnosis of re-activated Trypanosoma cruzi infection after heart transplantation. J Heart Lung Transplant. 2004;23:1345-8. <br />38. Benvenuti LA, Roggério A, Sambiase NV, Fiorelli A, Higuchi M. Polymerase chain reaction in endomyocardial biopsies for monitoring reactivation of Chagas’ disease in heart transplantation: a case report and review of the literature. Cardiovasc Pathol. 2005;14:265-8.<br />
oai:oai.revistabiomedica.org:article/69
2016-11-22T10:33:02Z
biomedica:EDIT
Perspectivas del Sistema Nacional de Ciencia, Tecnología e Innovación
Miranda, Juan Francisco
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/69
10.7705/biomedica.v28i3.69
Biomedica; Vol. 28 No. 3 (2008); 315-316
Biomédica; Vol. 28 Núm. 3 (2008); 315-316
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/69/69
oai:oai.revistabiomedica.org:article/70
2016-11-22T10:33:02Z
biomedica:IMAG
Penetrating atherosclerotic ulcer of the aortic arch
Úlcera aterosclerótica penetrada en cayado aórtico
Gómez, Rubén
Fleitas, Cristina
Teja, Carlos
Carrascosa, Miguel
Arrastio, Xavier
Celemín, Isabel
palabras clave
aterosclerosis
aorta
tomografía
úlcera
atherosclerosis
aorta
tomography
ulcer
Acute aortic syndrome is an acute lesion of the aortic wall involving the aortic tunica media, with a potencial risk of severe complications. The aortic dissection is the main cause (80%), but other entities, such as the intramural hematoma (15%) and the penetrating aortic ulcer (5%), are a less frequent cause. A 49-year-old man, hypertensive, dyslipemic, and without drug treatment, was admitted in the emergency service due to a sudden pain in the mid-chest approximately 3 hr previously. No pain radiation or hemodynamic affectation were apparent. The symptoms were resistant to nitroglycerin and morphine. The chest X rays, electrocardiograms and cardiac enzymes were normal. A computed tomographic angiography was taken because an acute aortic symdrome was suspected (figure 1A). It showed a sacular formation compatible with an aortic ulcer in the left contour of the aortic arch, and situated one-half cm beyond the left subclavian artery and above a zone of parietal calcification. The acute symtomatic penetrating aortic ulcer syndrome carries an equal or greater risk than the typical dissection; therefore invasive treatment was recommended. Because of the potential risk of severe complicationsand unpredictable prognosis, a self-expanding endoluminal prosthesis (stent graft), Relay 30 x 100 mm, was implanted for femoral artery access with satisfactory results (figure 1B and 1C).
El síndrome aórtico agudo constituye un proceso agudo de la pared aórtica que debilita la capa media, condicionando un riesgo potencial de complicaciones graves. En la mayoría de los casos se debe a una disección de aorta (80%), pero existen otras dos entidades que con menor frecuencia lo condicionan, como el hematoma intramural (15%) y la úlcera aterosclerótica penetrada (5%) (1,2). Se presenta el caso de un varón de 49 años, fumador, hipertenso y dislipémico no controlado farmacológicamente, que acude al servicio de urgencias refiriendo un dolor en el centro del tórax de inicio súbito, intenso y no irradiado, de tres horas de evolución. No presentaba compromiso hemodinámico y el dolor no se aliviaba con nitroglicerina ni morfina. Los electrocardiogramas seriados, la radiografía de tórax, así como las enzimas cardiacas, no mostraron alteración alguna. Ante la sospecha clínica de un síndrome aórtico agudo. se realizó un angio-TC (figura 1A) que evidenció en el contorno izquierdo del cayado aórtico, medio centímetro después de la salida de la arteria subclavia izquierda, una formación sacular abollonada, sobre una zona de calcificaciones parietales, compatible con una úlcera aórtica aterosclerótica. La úlcera aterosclerótica penetrada aguda y sintomática tiene un riesgo igual o superior a la disección clásica, sobre todo las localizadas en aorta ascendente (3), por lo que se aconseja un tratamiento invasivo, ya sea quirúrgico o basado en el implante por cateterismo de prótesis endoluminales (4). Integrando el cuadro clínico con el hallazgo de la tomografía, ante el riesgo potencial de complicaciones graves y lo impredecible de la evolución, se implantó por vía femoral una endoprótesis autoexpandible Relay de 30 mm x 100 mm con buen resultado (figuras 1B y 1C).
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/70
10.7705/biomedica.v28i3.70
Biomedica; Vol. 28 No. 3 (2008); 317-318
Biomédica; Vol. 28 Núm. 3 (2008); 317-318
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/70/70
/*ref*/Vilacosta I, San Roman JA. Acute aortic syndrome. Heart. 2001;85:365-8.<br />2. Evangelista A. Avances en el síndrome aórtico agudo. Rev Esp Cardiol. 2007;60:428-39.<br />3. Coady MA, Rizzo JA, Elefteriades JA. Pathologic variants of thoracic aortic dicsections. Penetrating atherosclerotic ulcers and intramural hematomas. Cardiol Clin 1999;17:637-57.<br />4. Ince H, Nienaber CA. Tratamiento de los síndromes aórticos agudos. Rev Esp Cardiol. 2007;60:526-41.<br />
oai:oai.revistabiomedica.org:article/71
2016-11-22T10:33:02Z
biomedica:ARTI
Surveillance of Mycobacterium tuberculosis resistance to antituberculosis drugs
Vigilancia de la resistencia del Mycobacterium tuberculosis a los fármacos antituberculosos, Colombia 2004-2005
Garzón, María Consuelo
Angée, Dailyn Yorledy
Llerena, Claudia
Orjuela, Dora Leticia
Victoria, Jorge Ernesto
tuberculosis
tuberculosis resistente a múltiples medicamentos
Mycobacterium tuberculosis
susceptibilidad
resistencia a los medicamentos
Tuberculosis
multidrug-resistant tuberculosis
Mycobacterium tuberculosis
drug resistance
susceptibility
Introduction. Tuberculosis is an important cause of disease and death worldwide. An estimated 8.8 million new cases occurred in 2005 with 1.6 million deaths, including 195,000 among HIV infected people. According to World Health Organization, the incidence rate was stable or in decline worldwide; however, the total number of new cases rose due to regional increases. Anti-TB drug resistance is a significant public health problem and an obstacle for its control worldwide. Therefore, measures must be taken for the adequate management of patients and the adoption of strategies to prevent TB dissemination. Objective. The prevalence of resistance of Mycobacterium tuberculosis was determined in untreated cases and in previously treated cases of pulmonary tuberculosis in Colombia. Materials and methods. A cross-sectional study determined the prevalence of resistance of Mycobacterium tuberculosis to antituberculosis drugs in 1,189 untreated cases or previously treated cases of pulmonary tuberculosis between the years 2004 and 2005. Cultures were collected throughout the country for this one-year period. Drug susceptibility of the isolates was tested by the simplified variant of the Cannetti, Risk and Grooset multiple proportions technique. Results. The global resistance rate of 925 untreated patients was 11.8% (95% CI: 9-14%) and the rate of multidrug-resistant tuberculosis was 2.4% (95% CI: 1.6-3.6%). Among 264 previously treated patients, the rate of global resistance was 44.3% (95% CI: 38-50%) and that of multidrug resistance was 31.4% (95%CI: 26-37%). Conclusions. When compared to previous studies, these data show that there has not been a significant increase in drug resistance. The findings indicate that the current treatment scheme provided by the National Tuberculosis Program is adequate.
Introducción. La tuberculosis es una importante causa de enfermedad y muerte en el mundo. Se calcula que en el 2005 se presentaron 8,8 millones de casos nuevos y murieron 1,6 millones de personas, entre ellas 195.000 infectadas con VIH. Según la Organización Mundial de la Salud, la tasa de incidencia permaneció estable o disminuyó en todo el mundo; sin embargo, el número de casos nuevos se incrementó debido al aumento en algunas regiones. La resistencia a los medicamentos es un problema de salud pública y un obstáculo al control de la tuberculosis en el mundo. Por esta razón, es necesario generar medidas para el adecuado manejo de los pacientes y adoptar estrategias para prevenir su diseminación. Objetivo. Determinar la prevalencia de la resistencia de Mycobacterium tuberculosis tanto en casos no tratados como en casos previamente tratados de tuberculosis pulmonar en Colombia. Materiales y métodos. Estudio de corte transversal para determinar la prevalencia de la resistencia de M. tuberculosis a fármacos antituberculosos en 1.189 pacientes durante los años 2004 y 2005. La recolección de cultivos fue a nivel nacional durante 1 año; los aislamientos se procesaron para pruebas de susceptibilidad por la técnica de proporciones múltiples de Cannetti, Risk y Grooset en su variante simplificada. Resultados. Novecientos veinticinco pacientes no tratados presentaron una prevalencia de resistencia global de 11,78% (IC 95%: 9,86-14,02) y una tuberculosis multirresistente (multidrugresistant tuberculosis, MDR-TB) de 2,38% (IC 95%: 1,58-3,57). Los 264 pacientes previamente tratados presentaron una resistencia global de 44,32% (IC 95%: 38,45-50,35) y una tuberculosis multirresistente (MDR-TB) de 31,44% (IC 95%: 26,14-37,27).Conclusiones. Los resultados obtenidos, comparados con estudios previos, demuestran que no ha habido un aumento significativo en la resistencia a los medicamentos ni en la tuberculosis multirresistente. Los hallazgos indican que el esquema proporcionado por el Programa Nacional de Tuberculosis es adecuado para manejar los casos.
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/71
10.7705/biomedica.v28i3.71
Biomedica; Vol. 28 No. 3 (2008); 319-326
Biomédica; Vol. 28 Núm. 3 (2008); 319-326
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/71/71
/*ref*/ 1. World Health Organization. Global tuberculosis control - surveillance, planning, financing. Geneve: World Health Organization; 2007. p. 376. <br />2. World Health Organization. Directrices para el tratamiento programático de la tuberculosis drogorresistente. Geneve: World Health Organization; 2006. p. 361.<br />3. Ministerio de la Protección Social, Organización Panamericana de la Salud. Situación de Salud en Colombia. Indicadores básicos. Bogotá: Ministerio de la Protección Social; 2006.<br />4. Orozco LC, Aparicio G, Quintero O, Giraldo E, Ulloa I, León CI. Resistencia de M. tuberculosis a los fármacos. Biomédica. 1981;1:130-4. <br />5. León CI, Sierra C, Naranjo N, Garzón MC, Guerrero MI. Segundo estudio nacional de resistencia primaria del M. tuberculosis a las drogas antituberculosas en Colombia. Infectio. 2002;6:83.<br />6. World Health Organization/International Union Against Tuberculosis and Lung Disease. Global project on antituberculosis drug resistance surveillance.Guidelines for surveillance of drug resistance in tuberculosis. Geneve: World Health Organization; 2002.<br />7. Canetti G, Rist N, Grosset J. Medida de la sensibilidad del bacilo tuberculoso a las drogas antibacilares por el método de las proporciones. Buenos Aires: Dirección Lucha Antituberculosa; 1965.<br />8. Canetti G, Wallace F, Khomenko A, Mahler HT, Menon NK, Rist N, et al. Advances in techniques of testing mycobacterial drug sensitivity and the use of sensitivity tests in tuberculosis control programs. Bull WHO. 1969;41:21-43. <br />9. Garzón M, Naranjo N, Sierra C, Llerena C, Orjuela D. Bacteriología del M. tuberculosis y micobacterias no tuberculosas. Manual de procedimientos. Bogotá:Instituto Nacional de Salud; 2002. <br />10. Orozco LC, León CI, Giraldo de BE, Quintero de RO, Ulloa de MI. El cultivo de esputo para el diagnóstico de la tuberculosis pulmonar. Biomédica 1985;5:24-6. <br />11. Kudoh S, Kudoh A. A simple technique for culturing tubercle bacilli. Bull WHO. 1974;51:71-84. <br />12. Laszlo A, Rahman M, Raviglione M, Bustreo F. Quality assurance programme for drug susceptibility testing of Mycobacterium tuberculosis in the WHO/IUATLD Supranational Laboratory Network: first round of proficiency testing. Int Tuberc Lung Dis. 1997;1:231-8.<br />13. World Health Organization. Global tuberculosis programme. Surveillance of drug resistance in tuberculosis. A user’s guide to the software: SDRTB 4.0. Geneve: World Health Organization; 1996. p. 2.<br />14. World Health Organization. Anti-tuberculosis drug resistance in the world. Report No. 3. Geneve: World Health Organization; 2004. <br />15. Dirección General de Salud. Ministerio de Salud, Colombia. Normas técnicas y guías de atención. Resolución 00412 febrero 25 de 2000. Guías de Atención de la Tuberculosis pulmonar y extrapulmonar. Bogotá: Ministerio de Salud; 2000. p. 1-44.<br />16. Organización Mundial de la Salud. Plan mundial para detener la tuberculosis 2006-2015. Ginebra: Organización Mundial de la Salud; 2006. <br />17. Organización Panamericana de la Salud, Programas Nacionales de Control de la Tuberculosis, Ministerios de Salud Pública. Plan Regional de Tuberculosis 2006-2015. Washington D.C.: PAHO; 2006.<br />
oai:oai.revistabiomedica.org:article/72
2016-11-22T10:33:02Z
biomedica:ARTI
Evaluation of knowledge and practice on tegumentary leishmaniasis in an endemic area of Venezuela
Evaluación de conocimientos y prácticas sobre la leishmaniasis tegumentaria en un área endémica de Venezuela
Nieves, Elsa
Villarreal, Néstor
Rondón, Maritza
Sánchez, Mireya
Carrero, José
conocimientos
actitudes y práctica en salud
leishmaniasis/epidemiología
Psychodidae
vectores de enfermedades
Venezuela
health knowledge
attitudes
practice
leishmaniasis/epidemiology
Psychodidae
disease vectors
Venezuela
Introduction. Leishmaniases constitutes a serious public health problem in many parts of the Americas. However, the populations exposed to leishmaniasis lack information about this disease. For this reason, educational assessments and interventions were deemed necessary to contribute to a greater impact of control measures. Objective. The level of knowledge and practices was evaluated for tegumentary leishmaniasis and the phlebotomine sand fly vector species. Materials and Methods. Between September 2006 and July 2007, a survey was conducted on epidemiological aspects, prevention, and control of leishmaniasis in two endemic communities—Bolero Alto and Bajo, in the municipality of Pinto Salina, Mérida state, Venezuela. It was administered to persons 7 years of age, in randomly selected houses. Collections of sand fly vectors were made indoors and around the houses. Results. Approximately 68% of the population showed a level of knowledge on leishmaniasis considered as insufficient. The lowest level of knowledge found was on matters related to leishmaniasis transmission and prevention. Seven epidemiologically important Lutzomyia species were identified: L. youngi, L. ovallesi, L. gomezi, L. walkeri, L. panamensis, L. punctigeniculata and L. venezuelensis. The predominant species in both communities were L. youngi and L. ovallesi, constituting 55% and 24%, respectively, of the totals. Conclusions. The residents of the endemic communities studied had a low level of knowledge about leishmaniasis. This must be considered in the development of educational alternatives that complement control programs. A particular focus on the prevention of insect bites is recommended.
Introducción. La leishmaniasis es un grave problema de salud pública en muchas partes de América. Las poblaciones expuestas a la leishmaniasis carecen de información de la enfermedad, razón por la cual es necesario realizar intervenciones y evaluaciones educativas que contribuyan a que el control tenga un mayor impacto. Objetivo. Determinar el nivel de conocimientos y prácticas sobre la leishmaniasis tegumentaria y la fauna de flebótomos en las comunidades endémicas de Bolero Alto y Bajo del municipio Pinto Salina del Estado Mérida, Venezuela, entre septiembre de 2006 y julio de 2007. Materiales y métodos. Se elaboró una encuesta en la cual se incluyeron aspectos epidemiológicos, de prevención y de control de la leishmaniasis. Se aplicaron a personas mayores de siete años en viviendas seleccionadas aleatoriamente. También se realizaron capturas intradomiciliarias y peridomiciliarias de flebotominos vectores. Resultados. Más del 68% de los individuos de las comunidades poseía un nivel de conocimientos considerado como insuficiente; los aspectos de mayor desconocimiento fueron en relación con la transmisión y la prevención. Se detectaron siete especies de Lutzomyia de importancia epidemiológica: L youngi, L. ovallesi, L. gomezi, L. walkeri, L. panamensis, L. punctigeniculata y L. venezuelensis. Las especies predominantes para ambas comunidades fueron L. youngi con más del 55% y L. ovallesi con más del 24% del total de especímenes capturados. Conclusión. Se determinó un bajo nivel de conocimientos sobre la leishmaniasis en los pobladores de las comunidades endémicas estudiadas, lo cual se debe tener en cuenta en el desarrollo de alternativas educativas de impacto en el control complementario de la enfermedad. Las mismas deben dirigirse a cubrir las deficiencias de conocimientos más acentuadas en la población, enfocadas a evitar las picaduras del insecto vector.
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/72
10.7705/biomedica.v28i3.72
Biomedica; Vol. 28 No. 3 (2008); 347-356
Biomédica; Vol. 28 Núm. 3 (2008); 347-356
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/72/73
/*ref*/ 1. Grimaldi G Jr, Tesh RB. Leishmaniasis of the New World: current concepts and implications for future research. Clin Microbiol Rev. 1993;6:230-50. <br />2. Sánchez L, Sáens E, Pancorbo J, Zegarra R, Garcés N, Regis A. Leishmaniasis. Dermatología Peruana. 2004;14:82-98. <br />3. Alvar J, Yactayo S, Bern C. Leishmaniasis and poverty. Trends Parasitol. 2006;22:552-7. <br />4. Alexander B, Maroli M. Control of phlebotomine sandflies. Med Vet Entomol. 2003;17:1-18. <br />5. Maroli M, Khoury C. Prevention and control of leishmaniasis vector: current approaches. Parassitologia. 2004;46:211-5. <br />6. Lainson R, Shaw JJ. Epidemiology and ecology of leishmaniasis in Latin-America. Nature. 1978;273:595-600. <br />7. OMS. Serie de Informes Técnicos No. 793. Ginebra: Organización Mundial de la Salud; 2006. p. 1-7. <br />8. Gama ME, Barbosa JS, Pires B, Cunha AK, Freitas AR, Ribeiro IR, et al. Avaliaçao do nivel de conhecimento de pupolações residentes em áreas endêmicas têm sobre leishmaniose visceral; Estado do Maranhâo, Brazil. Cad Saude Publica. 1998;14:381-90. <br />9. Uchoa CM, Serra CM, Magalhaes C de M, Silva RM, Figlioulo LP, Leal CA, et al . Health education: teaching about American tegumentary leishmaniasis. Cad Saude Publica. 2004;20:935-41. <br />10. Saravia NG, Nicholls RS. Leishmaniasis: un reto para la salud pública que exige concertación de voluntades y esfuerzos. Biomédica. 2006;26(Supl.1):1-3. <br />11. dos Reis DC, Gazzinelli A, Silva CA, Gazzinelli MF. Educação em saúde e representações sociais: uma experiencia no controle da leishmaniose tegumentar em area endêmica de Minas Gerais, Brasil. Cad Saude Publica. 2006;22:2301-10. <br />12. Santos JB, Lauand L, Souza GS, Macedo VO. Fatores sócio-económicos e atitudes em relaçao à prevenção domiciliar da leishmaniose tegumentar americana, em uma área endêmica do sul da Bahia, Brazil. Cad Saude Publica. 2000;16:701-8. <br />13. Moreira R da C, Rebelo JM, Gama ME, Costa JM. Nivel de conhecimentos sobre leishmaniose tegumentar americana (LTA) e uso de terapias alternativas por populações de uma área endêmica da Amazônia do Maranhão, Brasil. Cad Saude Publica. 2002;18:187-95. <br />14. Vásquez ML, Kroeger A, Lipowsky R, Alzate A. Conceptos populares sobre la leishmaniasis cutánea en Colombia y su aplicabilidad en programas de control. Bol Of Sanit Panam. 1991;110:402-12. <br />15. Pardo R, Carvajal A, Ferro C, Davies C. Effect of knowledge and economic status on sandfly control activities by householders at risk of cutaneous leishmaniasis in the subandean region of Huila department, Colombia. Biomédica. 2006;26(Supl.1): 167-79. <br />16. López-Vélez R, Molina-Moreno R. Cambio climático en España y riesgo de enfermedades infecciosas y parasitarias transmitidas por artrópodos y roedores. Rev Esp Salud Pública. 2005;79:177-90. <br />17. Dujardin JC. Risk factors in the spread of leishmaniasis: towards integrated monitoring? Trends Parasitol. 2006;22:4-6. <br />18. Herwaldt BL. Leishmaniasis. Lancet. 1999;354:1191-9. <br />19. Scorza JV, Valera M, Moreno E, Jaimes R. Epidemiologic survey of cutaneous leishmaniasis: an experience in Mérida, Venezuela. Bull Pan Am Health Organ. 1983;17:361-74. <br />20. Scorza JV. Información ecológica sobre Phlebotominae de Venezuela. Bol Dir Malariol San Amb. 1989;29:1-9. <br />21. García B. Aporte de la etnografía en el conocimiento de los códigos socioculturales de la leishmaniasis cutánea localizada en un programa de educación para la salud, en Venezuela. Cad Saude Publica. 2007;(Supl.1):S75-83. <br />22. Arias J, Beltrán F, Desjeux P, Walton B. Epidemiología y control de la leishmaniasis en las Américas, por país o territorio. Cuaderno técnico No. 44. Washington, D.C.: Organización Panamericana de la Salud; 1996. <br />23. Suárez YE, Fabré Y, Soca M, Fuentes M, Cabrera C, Álvarez J. Metodología para el análisis de algunos indicadores de riesgo asociados al manejo territorial de las zoonosis. Rev Electro Vet. 2006;7:1-8. <br />24. Young DG, Duncan MA. Guide to the identification and geographic distribution of Lutzomyia sand flies in Mexico, West Indies, Central and South America (Diptera: Psychodidea). Mem Ann Ent Inst. 1994;54:50- 881. <br />25. Dobles-Ulloa A, Perriard C. Representations, attitudes, and practices related to cutaneous leishmaniasis in people from Acosta country, San José province, Costa Rica. An exploratory anthropological study. Cad Saude Publica. 1994;10:181-9. <br />26. Weigel MM, Armijos RX, Racines RJ, Zurita C, Izurieta R, Herrera E, et al. Cutaneous leishmaniasis in subtropical Ecuador: popular perceptions, knowledge, and treatment. Bull Pan Am Health Organ. 1994;28: 142-55. <br />27. Isaza DM, Restrepo BN, Arboleda M, Casas E, Hinestroza H, Yurgaqui T. La leishmaniasis: conocimientos y prácticas en poblaciones de la costa del Pacífico de Colombia. Rev Panam Salud Pública. 1999;6:177-84. <br />28. Yadon Z, Rodrigues L, Davies C, Quigley M. Indoor and peridomestic transmission of American cutaneous leishmaniasis in northwestern Argentina: A retrospective case-control study. Am J Trop. Med Hyg. 2003;68:519-26. <br />29. Desjeux P. The increase in risk factors for leishmaniasis worldwide. Trans R Soc Trop Med Hyg. 2001;95:239-43. <br />30. Ampuero J, Urdaneta M, Macedo V de O. Risk factors for cutaneous leishmaniasis transmission in children aged 0 to 5 years in an endemic area of Leishmania (Viannia) braziliensis. Cad Saude Publica. 2005;21:161- 70. <br />31. Campbell-Lendrum D, Dujardin JP, Martinez E, Feliciangeli MD, Perez JE, Silans LN, et al. Domestic and peridomestic transmission of American cutaneous leishmaniasis: changing epidemiological patterns present new control opportunities. Mem Inst Oswaldo Cruz. 2001;96:159-62. <br />32. Salomón OD, Sosa S, Canini L, Córdoba E. Tegumentary leihsmaniasis in an area with epidemic levels of transmission, Salta, Argentina, 1988. Medicina. 2001;61:284-93. <br />33. Walsh JF, Molyneux DH, Birley MH. Deforestation: effects on vector-borne disease. Parasitology. 1993;106(Suppl):S55-75. <br />34. Gramiccia M, Gradoni L. The current status of zoonotic leishmaniases and approaches to disease control. Int J Parasitol. 2005;35:1169-80. <br />35. Kroeger A, Avila EV, Morrison L. Insecticide impregnated curtains to control domestic transmission of cutaneous leishmaniasis in Venezuela: cluster randomised trial. BMJ. 2002;325:810-3. <br />36. Travi BL, Jaramillo C, Montoya J, Segura I, Zea A, Goncalves A, et al. Didelphis marsupialis, an important reservoir of Trypanosoma (Schizotrypanum) cruzi and Leishmania (Leishmania) chagasi in Colombia. Am J Trop Med Hyg. 1994;50:557-65. <br />37. Alexander B, Barbosa EB, Haigh E, Almeida LL. Transmission of Leishmania in coffee plantations of Minas Gerais, Brazil. Mem Inst Oswaldo Cruz. 2002;97:627-30. <br />38. Nieves E. Problemas de colonización de especies flebotominas bajo condiciones de laboratorio, con especial referencia a Lutzomyia youngi, Lutzomyia ovallesi y Lutzomyia migonei. Mérida: Facultad de Ciencias, Universidad de los Andes; 1995. p. 113. <br />39. Nieves E, Ribeiro A, Brazil R. Physical factors influencing the oviposition of Lutzomyia migonei (Diptera: Psychodidae) in laboratory conditions. Mem Inst Oswaldo Cruz. 1997;92:733-7. <br />40. Scorza JV, Castillo L, Rezzano S, Marquez M, Marquez JC. El papel del cafeto en la endemicidad de la leishmaniasis cutánea en Venezuela. Bol Malariol San Amb. 1985;25:82-8. <br />41. Traviezo LE. Phlebotomine sandflies in the southeast of Lara state, Venezuela. Biomédica. 2006;26(Suppl.1): 73-81. <br />42. Añez N, Cazorla D, Nieves E. Registro de especies flebotominas en focos endémicos para leishmaniasis en el estado Mérida, Venezuela. Bol Dir Malariol San Amb. 1989;29:12-34. <br />43. Salomon OD, Wilson ML, Munstermann LE, Travi BL. Spatial and temporal patterns of phlebotomine sand flies (Dipthera: Psychodidae) in cutaneous leishmaniasis focus in northern Argentina. J Med Entomol. 2004;41:33-9. <br />44. Azevedo AC, Rangel EF, Quieroz RG. Lutzomyia migonei (França, 1920) naturally infected with peripylarian flagellates in Baturité, a focus of leishmaniasis in Ceará State, Brazil. Mem Inst Oswaldo Cruz. 1990;85:479. <br />45. Nieves E, Pimienta PF. Development of Leishmania (Viannia) braziliensis and Leishmania (Leishmania) amazonensis in the sand fly Lutzomyia migonei (Diptera: Psychodidae). J Med Entomol. 2000;37:134-40. <br />46. Costa JM, Vale KC, França F, Costa MA, da Silva JO, Lago EL, et al. A leishmaniose tegumentar americana em uma região endêmica como fator de mobilização comunitária. Rev Soc Bras Med Trop. 1994;27:255-7.<br />
oai:oai.revistabiomedica.org:article/73
2016-11-22T10:33:02Z
biomedica:ARTI
Reproducibilidad y validez convergente de la Escala Abreviada del Desarrollo y una traducción al español del instrumento Neurosensory Motor Development Assessment
Hormiga, Claudia Milena
Camargo, Diana Marina
Orozco, Luis Carlos
desarrollo infantil
destreza motora
preescolar
diagnóstico precoz
validez de las pruebas
reproducibilidad de resultados
Introducción. El desarrollo motor es la adquisición y evolución de habilidades motoras; su valoración permite detectar alteraciones y promueve una atención oportuna y adecuada. Se han diseñado varios instrumentos para valorar el desarrollo motor en la niñez temprana, entre los que se encuentra el test Neurosensory Motor Development Assessment. En Colombia no hay estudios publicados sobre las propiedades psicométricas de cualquiera de estas pruebas y la vigilancia del desarrollo motor se realiza con la Escala Abreviada del Desarrollo, de la cual no existen reportes de validez o reproducibilidad. Objetivo. Evaluar la reproducibilidad del componente motor de la Escala Abreviada del Desarrollo y de una traducción al español del instrumento Neurosensory Motor Development Assessment, así como la validez convergente entre las dos pruebas. Materiales y métodos. Se realizó un estudio de evaluación de tecnologías diagnósticas. La población estuvo conformada por 260 niños de 4 y 5 años de edad. Para el análisis se aplicaron coeficientes de correlación intraclase y los límites de acuerdo de Bland y Altman, así como el coeficiente de correlación de Spearman (r). Resultados. El coeficiente de correlación intraclase y el promedio de las diferencias para el Neurosensory Motor Development Assessment, fueron 0,91 y 1,23, y para la Escala Abreviada del Desarrollo, 0,96 y 0,02, respectivamente. La validez convergente mostró un r de 0,51. Conclusiones. Los dos instrumentos tienen buena reproducibilidad entre evaluadores. La convergencia entre las pruebas es moderada y posiblemente se explica por las diferencias en el enfoque de medición de cada instrumento.
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/73
10.7705/biomedica.v28i3.73
Biomedica; Vol. 28 No. 3 (2008); 327-346
Biomédica; Vol. 28 Núm. 3 (2008); 327-346
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/73/72
/*ref*/American Physical Therapy Association. What types of tests and measures do physical therapist use? (A guide to physical therapist practice). Phys Ther. 2001; 81:51-103. <br />2. American Academy of Pediatrics. Developmental surveillance and screening of infants and young children. Committee on children with disabilities. Pediatrics. 2001;108:192-5. <br />3. Goyen TA, Liu K. Longitudinal motor development of «apparently normal» high-risk infants at 18 months, 3 and 5 years. Early Hum Dev. 2002;70:103-15. <br />4. Kroes M. Early motor, psychosocial and behavioural characteristics of attention-deficit/hyperactivity disorder (thesis). Maastricht: Maastricht University; 2000. <br />5. Sullivan MC, McGraft MM. Perinatal morbidity, mild motor delay and later school outcomes. Dev Med Child Neurol. 2003;45:104-12. <br />6. Merrell KW, Holland ML. Social-emotional behavior of preschool-age children with and without developmental delays. Res Dev Disabil. 1997;18:393-405. <br />7. Kroes M, Kessels AG, Kalff AC, Feron FJ, Vissers YL, Jolles J, et al. Quality of movement as predictor of ADHD: results from a prospective population study in 5-and 6-year- old children. Dev Med Child Neurol. 2002;44:753-60. <br />8. Largo RH, Fischer JE, Rousson V. Neuromotor development from kindergarten age to adolescence: developmental course and variability. Swiss Med Wkly. 2003;133:193-9. <br />9. Piper MC, Darrah J. Motor assessment of the developing infant. Philadelphia: W.B. Saunders Company; 1994. <br />10. Brenneman SK. Assessment and testing of infant and child development. En: Tecklin JS, editor. Pediatric physical therapy. 3ª edition. Philadelphia: Lippincott Williams & Wilkins; 1999. p. 28-70. <br />11. Boulton JE, Kirsch SE, Chipman M, Etele E, White AN, Pape KE. Reliability of the Peabody Developmental Gross Motor Scale in children with cerebral palsy. Phys Occup Ther Pediatr. 1995;15:35-51. <br />12. Schmidth LS, Westcott Sl, Crowe TK. Interrater reliability of the gross motor scale of the Peabody Developmental Motor Scales with 4- and 5- year-old children. Pediatr Phys Ther. 1993;5:169-75. <br />13. Wiart L, Darrah J. Review of four tests of gross motor development. Dev Med Child Neurol. 2001;43:279-85. <br />14. Flegel J, Kolobe T. Predictive validity of the test of infant motor performance as measured by the Bruininsks-Oseretsky test of motor proficiency at school age. Phys Ther. 2002;82:762-71. <br />15. Crawford SG, Wilson BN, Dewey D. Identifying developmental coordination disorder: Consistency between tests. Phys Occup Ther Pediatr. 2001;20:29- 50. <br />16. Frankenburg WK. Developmental surveillance and screening of infants and young children. Pediatrics. 2002;109;144-5. <br />17. Stengel TJ. Assessing motor development in children. En: Campbell SK, editor. Pediatric neurologic physical therapy. Second edition. Illinois: Churchill Livingstone; 1993. p. 33-65. <br />18. Rodger S, Ziviani J, Watter P, Ozanne A, Woodyatt G, Sprinfield E. Motor and functional skills of children with developmental coordination disorder: A pilot investigation of measurement issues. Hum Mov Sci. 2003;22:461-78. <br />19. Kroes M, Vissers YL, Sleijpen FA, Feron FJ, Kessels AG, Bakker E, et al. Reliability and validity of a qualitative and quantitative motor test for 5 to 6 year old children. Eur J Paediatr Neurol. 2004;8:135-43. <br />20. Provost B, Crowe T, McClain C. Concurrent validity of the Bayley Scales of Infant Development II Motor Scale and the Peabody Developmental Motor Scales in two-year-old children. Phys Occup Ther Pediatr. 2000; 20:5-18. <br />21. Burns YR. Physiotherapy assessment for infants and young children. Brisbane: Publishing Company Pty Ltd; 1991. <br />22. Burns YR, Ensbey RM, Norrie MA. The Neurosensory Motor Development Assessment. Part 1: Development and administration of the test. Aust J Physiother. 1989; 35:141-9. <br />23. Burns YR, Ensbey RM, Norrie MA. The Neurosensory Motor Development Assessment. Part 2: Predictive and concurrent validity. Aust J Physiother. 1989;35:151-7. <br />24. Burns YR, O’Callaghan M, Tudehope DI. Early identification of cerebral palsy in high risk infants. Aust Paediatr J. 1989;25:215-9. <br />25. Burns YR, Mohay H, Croker A. The predictive value of developmental testing of children under the age of 2 years. Physiother Theory Pract. 1987;3:2-10. <br />26. MacDonald JA, Burns YR, Mohay HA. Characteristics of neuro-sensory-motor performance of very low birth weight and high-risk infants at six years of age. NZ Journal of Physiotherapy. 1991; 19:17-20 <br />27. Burns YR, Ensbey R, O’Callaghan. Motor abilities at eight to ten years of children born weighing less than 1,000 gr. Physiotherapy. 1999;85:360-9. <br />28. Gray PH, O’Callaghan J, Mohay HA, Burns YR, King JF. Maternal hypertension and neurodevelopmental outcome in very preterm infants. Arch Dis Child Fetal Neonatal Ed. 1998;79:F88-93. <br />29. Burns Y, O’Callaghan M, McDowell B, Rogers Y. Movement and motor development in ELBW infants at 1 year is related to cognitive and motor abilities at 4 years. Early Hum Dev. 2004;80:19-29. <br />30. Ministerio de Salud. Resolución 412 de 2000. Santa Fe de Bogotá: Ministerio de Salud; 2000. <br />31. Grupo Interinstitucional de Programas de Salud del Niño en Antioquia. Salud Integral para la Infancia (SIPI). Crecimiento y desarrollo por grupos de edad. Tomo II. Medellín: Servicio Seccional de Salud de Antioquia; 1996. <br />32. Staquet M, Hays R, Fayer P. Assessing reliability and validity of measurement in clinical trials. En: Quality of life assessment in clinical trials. Methods and practice. New York: Oxford University Press; 1998. p. 171-5. <br />33. Kraemer HC. Evaluating medical test. California: Sage Publications; 1992. <br />34. Kraemer HC, Thieman S, Denenberg VH. Correlation coefficients. En: How many subjects? Statistical power analysis in research. London: Sage Publications; 1987. <br />35. Norman GR, Streiner DL. Bioestadística. Madrid: Mosby/Doyma Libros; 1996. p. 14-22. <br />36. Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet. 1986;1:307-10. <br />37. Lin L I-K. A concordance correlation coefficient to evaluate reproducibility. Biometrics. 1989;45:255-68. <br />38. Kraemer HC, Bloch D. Kappa coefficients in epidemiology an appraisal of a reappraisal. J Clin Epidemiol. 1998;41:959-68. <br />39. Kraemer HC, Periyakoil V, Noda A. Kappa coefficients in medical research. Stat Med. 2002;21: 2109-29. <br />40. Domholdt E. Rehabilitation research. Principles and applications. 3rd edition. St. Louis, Mo: Elsevier Saunders; 2005. p. 245-64. <br />41. Dean AG, Dean JA, Coulumbier D, Brendel KA, Smith DC, Burton AH, et al. Epi Info, Versión 6.01: a word processing, database, and statistics program for epidemiology on microcomputers. Atlanta: Centers for Disease Control and Prevention; 1995. <br />42. StataCorp. Stata Statistical Software. Release 9.0. College Station, TX: StataCorp LP; 2005. <br />43. Coughlin SS, Beauchamp TL. Ethics and epidemiology. New York: Oxford University Press; 1996. <br />44. Bland M, Altman D. Measuring agreement in method comparison studies. Stat Methods Med Res. 1999;8: 135-60. <br />45. Latour J, Abraira V, Cabello JB, López J. Métodos de investigación en cardiología clínica. Rev Esp Cardiol. 1997;50:117-28. <br />46. Bruns DE. The STARD initiative and the reporting of studies of diagnostic accuracy. Clin Chem. 2003;49:18-20. <br />47. Campbell SK. Measurement in developmental therapy: past, present and future. En: Miller LJ, editor. Developing norm-referenced standardized tests. New York: Haworth Press; 1989. <br />48. Shumway-Cook A, Woollacott MH. Motor control. Theory and practical applications. 2nd. edition. Baltimore: Lippincott Williams & Wilkins; 2001. p. 1-25. <br />49. Koseck K. Review and evaluation of psychometric properties of Revised Bayley Scales of Infant Development. Pediatr Phys Ther. 1999;11:198-204. <br />50. Keating J, Matyas T. Unreliable inferences from reliable measurements. Aust J Physiother. 1998;44:5-10. <br />51. Guyatt G, Walter S, Norman G. Measurement change over time: Assessing the usefulness of evaluates instruments. J Chronic Dis. 1987;40:171-8. <br />52. Patton N, Aslam T, Murray G. Strategies to assess reliability in ophthalmology. Eye. 2006;20:749-54. <br />53. Hays RD, Anderson RT, Revicki D. Assessing reliability and validity of measurement in clinical trials. En: Staquet M, Hays R, Fayer P, editores. Quality of life assessment in clinical trials. Methods and practice. New York: Oxford University Press; 1998. p. 171-5. <br />54. Provost B, Heimerl S, McClain C, Kim N-H, López BR, Kodituwakku P. Concurrent validity of the Bayley Scales of Infant Development II Motor Scale and the Peabody Developmental Motor Scales-2 in Children with Developmental Delays. Pediatr Phys Ther. 2004;1 6:149-56. <br />55. Jain M, Turner D, Worrel T. The Vulpe Assessment Battery and the Peabody Developmental Motor Scales: a preliminary study of concurrent validity between gross motor sections. Phys Occup Ther Pediatr. 1994;14: 23-32 <br />56. Hadders-Algra M. The Neuronal Group Selection Theory: a framework to explain variation in normal development. Dev Med Child Neurol. 2000;42:566-72. <br />57. Hadders-Algra M. Variability in the infant motor behavior: A hallmark of the healthy nervous system. Infant Behav Dev. 2002;25:433-51.<br />
oai:oai.revistabiomedica.org:article/74
2016-11-22T10:33:02Z
biomedica:ARTI
Correlation analysis of surnames and Y-chromosome genetic heritage in 3 provinces of southwestern Colombia
De genotipos e isonimias: análisis de correlación entre el apellido y el patrimonio genético heredado en el cromosoma Y en la población de tres departamentos del suroccidente colombiano
Gómez, Alberto
Ávila, Sandra J.
Briceño, Ignacio
genotipo
nombres
cromosoma Y
indios sudamericanos
Colombia
Genotype
names
Y chromosome
Indians
South American
Colombia
Introduction. In Colombia, surnames are characters usually passed to the children by the father, and they have been compared to neutral alleles associated with the Y-chromosome. Objective. Population frequencies were determined for 17 short tandem repeats (STR) DNA markers on the Y-chromosome to compare the two identity codes and define the correlation between haplotypes and surnames in each individual. Materials and methods. DNA was extracted from blood samples from 308 male individuals in provinces of Valle del Cauca, Cauca and Nariño, all in southwestern Colombia. Sample DNA was analyzed with the commercial kit AmpFLSTR® YfilerTM (Applied Biosystems) and examined for the following 17 Y-chromosome STR markers: DYS19, DYS389I, DYS389II, DYS390, DYS391, DYS392, DYS393, DYS385a/b, DYS437, DYS438, DYS439, DYS448, DYS456, DYS458, DYS635 and Y-GATA-H4. The frequencies of molecular haplotypes were associated with the surname reported by each individual, and a correlation table was constructed. Amerindian and European surnames were associated with the presence of allele DYS19/13, a characteristic of Amerindian populations. Results. Allele frequencies were reported for each of the 17 STR markers in the southwestern region of Colombia-high genetic and haplotypic diversities were obtained. Approximately 40% of lineage inconsistencies were found when the molecular genotype was compared with the European or Amerindian surnames. Conclusions. Surnames must be used as population markers with reservation. The genetic evidence indicates that traditional genealogies based on surnames with or without documental support, may be inconsistant with their biological provenance.
Introducción. Es bien sabido que, entre los caracteres transmitidos por la línea paterna, el apellido se ha configurado en diferentes culturas como un carácter semejante a un alelo genético neutral asociado al cromosoma Y.Objetivo. En este estudio se determinaron las frecuencias en la población de 17 STR del cromosoma Y en 308 individuos provenientes de las poblaciones de los departamentos del Valle del Cauca, Cauca y Nariño. Además, se propuso definir la correlación de los haplotipos obtenidos en cada individuo con su apellido paterno, para comparar estos dos códigos de identidad.Materiales y métodos. Se extrajo el ADN de cada individuo a partir de sangre periférica y se utilizó el estuche comercial AmpFLSTR® Yfiler™ (Applied Biosystems) para tipificarlo. Los resultados de los haplotipos moleculares se compararon con los apellidos reportados por cada individuo y se asociaron apellidos amerindios y europeos con haplotipos que incluyeran o no el marcador DYS19/13, característico de la población amerindia.Resultados. Se reportan las frecuencias alélicas de cada uno de los 17 marcadores del cromosoma Y analizados en esta región de Colombia, así como la diversidad génica y haplotípica hallada en los tres departamentos. Al comparar los resultados obtenidos a nivel molecular con los apellidos de origen europeo o amerindio reportados por cada uno de los individuos, se encontró cerca de 40% de inconsistencia de linaje.Conclusiones. La utilización del apellido como marcador de población debe hacerse con cautela, por cuanto las genealogías fundamentadas en éstos pueden no corresponder al origen biológico de sus portadores.
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/74
10.7705/biomedica.v28i3.74
Biomedica; Vol. 28 No. 3 (2008); 357-370
Biomédica; Vol. 28 Núm. 3 (2008); 357-370
2590-7379
0120-4157
spa
eng
https://revistabiomedica.org/index.php/biomedica/article/view/74/74
https://revistabiomedica.org/index.php/biomedica/article/view/74/4245
/*ref*/<p>1. Roewer L, Kayser M, Dieltjes P, Nagy M, Bakker E, Krawezak M, et al. Analysis of molecular variance (AMOVA) of Y-chromosome-specific microsatellites in two closely related human populations. Hum Mol Genet. 1996;5:1029-33. <br />2. Jobling MA, Pandya A, Tyler-Smith C. The Y chromosome in forensic analysis and paternity testing. Int J Legal Med. 1997;110:118-24. <br />3. Prinz M, Boll K, Baum H, Shaler B. Multiplexing of Y chromosome specific STR and performance for mixed samples. Forensic Sci Int.1997;85:209-18. <br />4. Kayser M, Cagliá A, Corach D, Fretwell N, Gehrig C, Graziosi G, et al. Evaluation of Y-chromosomal STR: a multicenter study. Int J Legal Med. 1997;110: 125-33. <br />5. De Knijff P, Kayser M, Cagliá A, Corach D, Fretwell N, Gehrig C, et al. Chromosome Y microsatellites: population genetic and evolutionary aspects. Int J Legal Med. 1997;110:134-49. <br />6. Paredes M, Galindo A, Bernal M, Avila S, Andrade D, Vergara C, et al. Analysis of the CODIS autosomal STR loci in four main Colombian regions. Forensic Science Int. 2003;137:67-73. <br />7. Bravo ML, Moreno MA, Builes JJ, Salas A, Lareu MV, Carracedo A. Autosomal STR genetic variation in negroid Chocó and Bogotá populations. Int J Legal Med. 2001;115:102-4. <br />8. Cifuentes L, Bonilla V, Rondón F, Cárdenas H, Barreto G. Evaluación de la diversidad genética mediante el análisis de STR en poblaciones aisladas del centro y suroccidente colombiano. Revista de la División de Ciencias de la Salud Universidad del Norte. 2004;18:96. <br />9. Yunis JJ, Acevedo LE, Campo DS, Yunis EJ. Population data of Y-STR minimal haplotypes in a sample of Caucasian-Mestizo and African descent individuals of Colombia. Forensic Sci Int. 2005;151:307-13. <br />10. Gaviria AA, Ibarra AA, Palacio OD, Posada YC, Triana O, Ochoa LM, et al. Y-chromosome haplotype analysis in Antioquia (Colombia). Forensic Sci Int. 2005;151:85-91. <br />11. Builes JJ, Bravo ML Martínez-Pancorbo M, Moreno MA, Gómez CP. Discrimination index of Y-chromosomal haplotypes in an Antioquia (Colombia) population sample. Int Congr Ser. 2004;1261:275-7. <br />12. Yunis JJ, García O, Cuervo AG, Guío E, Pineda CR, Yunis EJ. Population data for PowerPlex 16 in thirteen departments and the capital city of Colombia. J Forensic Sci 2005; 50:685-702. <br />13. Torres MM. La variabilidad genética una herramienta útil en el estudio de poblaciones humanas. (Tesis doctoral). Bogotá D.C.: Universidad de los Andes; 2005. <br />14. Builes JJ, Castañeda SP, Espinal C, Aguirre D, Gómez MV, Villamarin D, et al. Analysis of 16 Y-chromosomal STR in a Valle (Colombia) population sample. Int Congr Ser. 2006;1288:219-21. <br />15. Romero RH. Determinación de haplotipos del cromosoma-Y en población de la Costa Caribe colombiana y su utilidad en el campo forense. (Tesis de Maestría). Bogotá D.C.: Pontificia Universidad Javeriana; 2006. <br />16. Builes JJ, Bravo ML, Montoya A, Caraballo L, Martinez B, Moreno MA. Population genetics of eight new Y-chromosomal STR haplotypes in three Colombian populations: Antioquia, Chocó and Cartagena. Int Congr Ser. 2004;1261:310-2. <br />17. Carvajal-Carmona LG, Soto ID, Pineda N, Ortiz-Barrientos D, Duque C, Ospina-Duque J, et al. Strong Amerind/white sex bias and a possible sephardic contribution among the founders of a population in north-west Colombia. Am J Hum Genet. 2000;67:1287-95. <br />18. Guarino FD, Federle RA, van Oorschot RAH, Briceño I, Bernal JE, Papiha SS, et al. Genetic diversity among five native american tribes of Colombia. En: Papiha SS, Deka R, Chakraborty R, editors. Genetic diversity: Applications in human population genetics. New York: Kluwer Academic/Plenum Publishers; 1999.p.33-51. <br />19. Lopera JA, Soto ID, Mondragón MC, Caraballo L, Bedoya BG, Ruiz-Linares A. Estructura genética de la población actual del Palenque de San Basilio (Bolívar, Colombia). Revista de la División de Ciencias de la Salud Universidad del Norte. 2004;18:97. <br />20. Sykes B, Irven C. Surnames and the Y chromosome. Am. J Hum Genet. 2000;66:1417-9. <br />21. Jobling MA. In the name of the father: surnames and genetics. Trends Genet. 2001;17:353-7. <br />22. Vernay M. Répartition géographique des patronymes et structure génétique: le département de l´Ardèche au début du XXe siècle. C R Acad Sci III. 2001;324:589-99. <br />23. Morelli L, Paoli G, Francalacci P. Surname analysis of the Corsican population reveals an agreement with geographical and linguistic structure. J Biosoc Sci. 2002;34:289-310. <br />24. Bedoya G, García J, Montoya P, Rojas W, Amézquita ME, Soto I, et al. Análisis de isonimia entre poblaciones del noroeste de Colombia. Biomédica. 2006;26:538-45. <br />25. Zei G, Lisa A, Fiorani O, Magri C, Quintana-Murci L, Semino O, et al. From surnames to the history of Y chromosome: the Sardinian population as a paradigm. Eur J Hum Genet. 2003;11:802-7. <br />26. Mikerezi I, Pizzetti P, Lucchetti E, Ekonomi M. Isonymy and the genetic structure of Albanian populations. Coll Anthropol. 2003;27:507-14. <br />27. Bedoya G, Montoya P, García J, Soto I, Bourgeois S, Carvajal L, et al. Admixture dynamics in Hispanics: A shift in the nuclear genetic ancestry of a South American population isolate. Proc Nat Acad Sci USA. 2006;103:7234-9. <br />28. Walsh PS, Metzger DA, Higuchi R. Chelex 100 as a medium for simple extraction of DNA for PCR-based typing from forensic material. Biotechniques. 1991;4:506-13. <br />29. Mulero J, Chang C, Calandro L, Green R, Li Y,Johnson C, et al. Development and validation of the AmpFLSTR® Yfiler™ PCR amplification kit: A male specific, single amplification 17 Y-STR multiplex system. J Forensic Sci. 2006;51:64-75.<br />30. Romero RH, Lizarazo R. Validation of the AmpFLSTR Yfiler kit. Int Congr Ser. 2006;1288:280-2. <br />31. Sensabaugh GF, Biochemical markers of individuality. En: Saferstein R, editor. Forensic Science Handbook. Englewood Cliffs NJ: Prentice Hall, Inc: 1982. p. 379-414. <br />32. Butler JM. State of the Y chromosome: New advances and state of the science for Y chromosome DNA testing. [Consultado: 09/05/2008]. Disponible en: http:// www.cstl.nist.gov/biotech/strbase/pub_pres/ TorontoJune2005_Y.pdf <br />33. Jones DA. Blood samples probability of discriminations. J Forensic Sci Soc. 1972;12:355-9. <br />34. Nei M. Molecular evolutionary genetics. New York: Columbia University Press; 1987. p. 176-9. <br />35. Cagliá A, Dobosz M, Boschi I, d´Aloja E, Pascali VL. Increased forensic efficiency of a STR-based Y-specific haplotype by addition of the highly polymorphic DYS385 locus. Int J Legal Med. 1998;111:142-6. <br />36. Kayser M, Krawczak M, Excoffier L, Dieltjes P, Corach D, Pascali V, et al. An extensive analysis on Y-chromosomal microsatellite haplotypes in globally dispersed human populations. Am J Hum Genet. 2001;68:990-1018. <br />37. Cifuentes L, Morales R, Sepúlveda D, Jorquera H, Acuña M. DYS19 and DYS199 loci in a Chilean population of mixed ancestry. Am J Phys Anthropol. 2004;125:85-9. <br />38. Departamento Administrativo Nacional de Estadística. Censo 2005. [Consultado: 09/05/2008]. Disponible en: http://www.dane.gov.co/censo/ <br />39. Willuweit S, Roewer L. Y chromosome haplotype reference database (YHRD): Update. Forensic Sci Int Genet. 2007;1:83-7. <br />40. Bosch E, Calafell F, Perez-Lezaun A, Comas D, Izaabel H, Akhayat O, et al. Y-chromosome STR haplotypes in four populations from northwest Africa. Int J Legal Med. 2000;114:36-40. <br />41. Dipierri JE, Alfaro E, Martínez-Marignac VL, Bailliet G, Bravi CM, Cejas S, et al. Paternal directional mating in two Amerindian subpopulations located at different altitudes in northwestern Argentina. Hum Biol. 1998;70:1001-10. <br />42. Bailliet G, Castilla EE, Adams JP, Orioli IM, Martínez- Marignac VL, Richard SM, et al. Correlation between molecular and conventional genealogies in Aicuña: a rural population from northwestern Argentina. Hum Hered. 2001;51:150-9. <br />43. Pettener D, Pastor S, Tarazona-Santos E. Surnames and genetic structure of a high-altitude Quechua community from the Ichu River Valley, Peruvian Central Andes, 1825-1914. Hum Biol. 1998; 70:865-87. <br />44. King TE, Ballereau SJ, Shürer KE, Jobling MA. Genetic signatures of coancestry within surnames. Curr Biol. 2006;16:384-8.</p><p> </p>
oai:oai.revistabiomedica.org:article/75
2016-11-22T10:33:02Z
biomedica:ARTI
Differentiation by geometric morphometrics among 11 Anopheles (Nyssorhynchus) in Colombia
Discriminación por morfometría geométrica de once especies de Anopheles (Nyssorhynchus) presentes en Colombia
Jaramillo, Nicolás
Calle, David Alonso
Quiñones, Martha Lucía
Erazo, Holmes Francisco
Anopheles [anatomía e histología]
clasificación
vectores de enfermedades
malaria
Colombia
Systematics
Nyssorhynchus
Section Argyritarsis
Section Albimanus
geometric morphometrics
malaria vectors
Introduction. The correct identification of the Anopheles species of the subgenus Nyssorhynchus is important because this subgenus includes the main malaria vectors in Colombia. This information is necessary for focusing a malaria control program. Objective. Geometric morphometrics were used to evaluate morphometric variation of 11 species of subgenus Nyssorhynchus present in Colombia and to distinguish females of each species. Materials and methods. The specimens were obtained from series and family broods from females collected with protected human hosts as attractants. The field collected specimens and their progeny were identified at each of the associated stages by conventional keys. For some species, wild females were used. Landmarks were selected on wings from digital pictures from 336 individuals, and digitized with coordinates. The coordinate matrix was processed by generalized Procrustes analysis which generated size and shape variables, free of non-biological variation. Size and shape variables were analyzed by univariate and multivariate statistics. Results. The subdivision of subgenus Nyssorhynchus in sections is not correlated with wing shape. Discriminant analyses correctly classified 97% of females in the section Albimanus and 86% in the section Argyritarsis. In addition, these methodologies allowed the correct identification of 3 sympatric species from Putumayo which have been difficult to identify in the adult female stage. Conclusion. The geometric morphometrics were demonstrated to be a very useful tool as an adjunct to taxonomy of females the use of this method is recommended in studies of the subgenus Nyssorhynchus in Colombia
Introducción. Es importante determinar las especies de Anopheles pertenecientes al subgénero Nyssorhynchus, dado que allí se encuentran los vectores principales de malaria en Colombia. Objetivo. Utilizar la morfometría geométrica para evaluar la variación morfométrica de once especies del subgénero Nyssorhynchus, presentes en Colombia y la capacidad de diferenciar las hembras. Materiales y métodos. Los especímenes fueron obtenidos de mosquitos silvestres, series e isofamilias de hembras recolectadas en cebos humanos protegidos y fueron identificados en todos sus estadios asociados usando las claves convencionales. A partir de fotografías digitales del ala derecha de 336 ejemplares de las 11 especies se seleccionaron 12 puntos anatómicos. Los puntos se convirtieron en coordenadas, las cuales se procesaron mediante el análisis generalizado de Procrustes. Se obtuvieron variables de tamaño y conformación, las cuales fueron analizadas mediante estadísticas univariadas y multivariadas. Resultados. Las técnicas de morfometría geométrica demuestran que la división en secciones del subgénero Nyssorrhynchus no se correlaciona con la conformación de las alas y demostraron que sólo con 12 puntos anatómicos se logra diferenciar en sus respectivas especies el 97% de los especímenes de la sección Argyritarsis y el 86% de la sección Albimanus del subgénero Nyssorhynchus, de forma cuantitativa y sin ambigüedades. Además, se separaron los individuos de tres especies que habitan en simpatría en el Putumayo, difíciles de discriminar en el estadio de adulto hembra. Conclusión. La mayoría de especies de Anopheles (Nyssorhynchus) presentes en Colombia se pueden diferenciar al utilizar la morfometría geométrica como herramienta de apoyo a las claves convencionales
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/75
10.7705/biomedica.v28i3.75
Biomedica; Vol. 28 No. 3 (2008); 371-385
Biomédica; Vol. 28 Núm. 3 (2008); 371-385
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/75/75
/*ref*/<p>1. World Health Organization. Malaria. Fact Sheet Nº 94. Geneve: WHO; 2007. Consultado: marzo de 2008. Disponible en: <a href="http://www.who.int/mediacentre/factsheets/fs094/en/index.html">http://www.who.int/mediacentre/factsheets/fs094/en/index.html</a>. <br />2. Olano VA, Brochero LH, Saenz R, Quiñones ML, Molina JA. Mapas preliminares de la distribución de especies de Anopheles vectores de malaria en Colombia. Biomédica. 2001;21:402-8. <br />3. Quiñones ML, Ruiz F, Calle DA, Harbach RE, Erazo HF, Linton YM. Incrimination of Anopheles (Nyssorhynchus) rangeli and An. (Nys.) oswaldoi as natural vectors of Plasmodium vivax in Southern Colombia. Mem Inst Oswaldo Cruz. 2006;101:617-23. <br />4. Faran ME. Mosquito studies (Diptera: Culicidae). XXXIV. A revisions of the Albimanus Section of the subgenus Nyssorhynchus of Anopheles. Contrib Am Entomol Inst. 1980;15:1-215. <br />5. Faran ME, Linthicum KJ. A Handbook of the species of Anopheles (Nyssorhynchus) (Diptera: Culicidae). Mosq Syst. 1981;13:1-81. <br />6. Linthicum KJ. A revision of the Argyritarsis Section of the subgenus Nyssorhynchus of Anopheles (Diptera: Culicidae). Mosq Syst. 1988;20:99-271. <br />7. Suárez MF, Quiñones M, Fleming GA, Robayo M. Guía introductoria a la morfología de Anopheles y clave para determinación de las principales especies de Colombia. Bogotá, D.C.: Ministerio de Salud; 1988. <br />8. Quiñones ML, Harbach RE, Calle DA, Ruiz F, Erazo HF. Variante morfológica de Anopheles benarrochi (Diptera: Culicidae) en Putumayo, Colombia. Biomédica. 2001;21:351-9. <br />9. Frizzi G. Salivary gland chromosomes of Anopheles. Nature. 1947;160:226-8. <br />10. Frizzi G. Etude cytogenetique d´ Anopheles maculipennis en Italie. Bull World Health Organ. 1953;9:335-44. <br />11. Miles SJ. A biochemical key to adult members of the Anopheles gambiae group of species (Diptera: Culicidae). J Med Entomol. 1979;15:297-9. <br />12. Foley DH, Bryan JH. Electrophoretic keys to identify members of the Anopheles punctulatus complex of vector mosquitoes in Papua New Guinea. Med Vet Entomol. 1993;7:49-53. <br />13. Wilkerson RC, Parsons TJ, Klein TA, Gaffigan TV, Bergo E, Consolim J. Diagnosis by random amplified polymorphic DNA polymerase chain reaction of four cryptic species related to Anopheles albitarsis from Paraguay, Argentina and Brazil. J Med Entomol. 1995; 32:697-704. <br />14. Marelli MT, Malafronte RS, Florez-Mendoza C, Lourenco- de- Oliveira R, Kloetzel JK, Marinotti O. Sequence analysis of the second internal transcribed spacer of ribosomal DNA in Anopheles oswaldoi (Diptera: Culicidae). J Med Entomol. 1999;36:679-84. <br />15. Rohlf FJ, Marcus LF. A revolution in morphometrics. Trends Ecol Evol. 1993;8:129-32. <br />16. Matias A, De la Riva JX, Torrez M, Dujardin JP. Rhodnius robustus in Bolivia identified by its wings. Mem Inst Oswaldo Cruz. 2001;96:947-50. <br />17. Villegas J, Feliciangeli MD, Dujardin JP. Wing shape divergence between Rhodnius prolixus from Cojedes (Venezuela) and Rhodnius robustus from Mérida (Venezuela). Infect Genet Evol. 2002;2:121-8. <br />18. Gumiel L, Catala S, Noireau F, Rojas de Arias A, Garcia A, Dujardin JP. Wing geometry in Triatoma infestans (Klug) and T. melanosoma Martinez, Olmedo & Carcavallo (Hemiptera:Reduvidae). Syst Entomol 2003;28:173-9. <br />19. Dujardin JP. MOGwin (Software for Generalized Procrustes Analysis). Institut de Recherches pour le Développement. 2004. Consultado: marzo de 2008. Disponible en: <a href="http://www.mpl.ird.fr/morphometrics/mog/index.html">http://www.mpl.ird.fr/morphometrics/mog/index.html</a> <br />20. Dujardin JP. PADwin (Software for Discriminant Analysis). Institut de Recherches pour le Développement. 2004. Consultado: marzo de 2008. Disponible en: <a href="http://www.mpl.ird.fr/morphometrics/pad/">http://www.mpl.ird.fr/morphometrics/pad/</a> <br />21. Calle DA, Quiñones ML, Erazo H, Jaramillo O. Morphometric discrimination of females of five species of Anopheles of the subgenus Nyssorhynchus from Southern and Northwest Colombia. Mem Inst Oswaldo Cruz. 2002;97:1191-5. <br />22. Delgado N, Rubio-Palis Y. Identification of Anopheles (Nyssorhynchus) (Diptera: Culicidae) occurring in Western Venezuela. Mosq Syst. 1993;25:222-30. <br />23. Rubio-Palis Y. Caracterización morfométrica de poblaciones de Anopheles (Nyssorhynchus) darlingi del sur de Venezuela. Bol Entomol Venez. 1998;13: 141-72. <br />24. Rubio-Palis Y. Anopheles (Nyssorhynchus) de Venezuela: taxonomía, bionomía, ecología e importancia médica. Maracay: Escuela de Malariología y Saneamiento Ambiental; 2000. p. 120. <br />25. Jirakanjanakit N, Dujardin JP. Discrimination of Aedes aegypti (Diptera: Culicidae) laboratory lines based on wing geometry. Southeast Asian J Trop Med Public Health. 2005;36:858-61. <br />26. Jirakanjanakit N, Leemingsawat S, Thongrungkiat S, Apiwathnasor C, Singhaniyom S, Bellec C, et al. Influence of larval density or food variation on the geometry of the wing of Aedes (Stegomyia) aegypti. Trop Med Int Health. 2007;12:1354-60. <br />27. Ruiz F, Quiñones ML, Erazo H, Calle DA, Alzate FA, Linton YM. Molecular differentiation of Anopheles (Nyssorhynchus) benarrochi and A. (N.) oswaldoi from Southern Colombia. Mem Inst Oswaldo Cruz. 2005;100:155-60. <br />28. Rohlf J. tpsDig, version 1.04. Stony Brook, NY: Department of Ecology and Evolution, State University of New York at Stony Brook; 2004. Consultado: marzo de 2008. Disponible en: <a href="http://life.bio.sunysb.edu/morph">http://life.bio.sunysb.edu/morph</a>. <br />29. Rohlf FJ, Slice DE. Extensions of the Procrustes method for the optimal superimposition of landmarks. Syst Zool. 1990;39:40-59. <br />30. Bookstein FL. Morphometrics tools for landmark data: Geometry and biology. Cambridge: Cambridge University Press; 1991.p.435. <br />31. Rohlf J. tpsRelw, version 1.39. Stony Brook, NY: Department of Ecology and Evolution, State University of New York at Stony Brook; 2004. Consultado: marzo de 2008. Disponible en: <a href="http://life.bio.sunysb.edu/morph">http://life.bio.sunysb.edu/morph</a>. <br />32. SAS Institute Inc. JMP® Statistisc and Graphics Guide, version 3.1. Cary, NC: SAS Institute Inc; 1999.p.592. <br />33. Landis JR, Koch GG. The measurement of observer agreement for categorical data. Biometrics. 1977;33:159-74. <br />34. Rohlf, J. tpsRegr, version 1.28. Stony Brook, NY: Department of Ecology and Evolution, State University of New York at Stony Brook; 2003. Consultado: marzo de 2008. Disponible en: <a href="http://life.bio.sunysb.edu/morph">http://life.bio.sunysb.edu/morph</a>. <br />35. Sallum M, Schultz T, Foster P, Arostein K, Wirtz R, Wilkerson C. Phylogeny of Anophelinae (Diptera: Culicidae) based of nuclear, ribosomal and mitochondrial DNA secuences. Syst Entomol. 2002; 27:361-82. <br />36. dos Santos JM, Maia J de F, Tadei WP, Rodríguez GA. Isoenzymatic Variability among five Anopheles species belonging to the Nyssorhynchus and Anopheles subgenera of the Amazon region, Brazil. Mem Inst Oswaldo Cruz. 2003;98:247-53. <br />37. Sallum MA, Bergo ES, Flores DC, Forattini OP. Systematic Studies on Anopheles galvaoi Causey, Deane & Deane from the Subgenus Nysssorhynchus Blanchard (Diptera: Culicidae). Mem Inst Oswaldo Cruz. 2000;97:1177-89. <br />38. Gonzales R, Carrejo N. Introducción al estudio taxonómico de Anopheles de Colombia Claves y notas de distribución. Cali: Editorial Litocencoa; 2007. p. 237. </p>
oai:oai.revistabiomedica.org:article/76
2016-11-22T10:33:02Z
biomedica:ARTI
Self-reported physical activity in comparison with anthropometric body fat indicators in school children
Actividad física autorreportada, comparación con indicadores antropométricos de grasa corporal en un grupo de escolares de Bogotá y de cinco departamentos del centro-oriente, Colombia 2000-2002
Poveda, Elpidia
Giraldo, Diana
Forero, Yibby
Mendivil, Carlos
actividad motora
antropometría
composición corporal
hábitos alimenticios
obesidad
niño
Colombia
motor activity
anthropometry
body composition
food habits
obesity
child
Colombia
Introduction. Obesity is a public health problem associated with physical inactivity. Objective. Autoreported physical activity was related with anthropometric indicators of body fat in a group of school children. Materials and methods. The descriptive, cross-sectional study that included 1,593 children aged 10 to 14 years from Bogotá and five provinces of central and eastern Colombia. Body weight, height, arm circumference and triceps skinfold were measured. Data on leisure time physical activity and type of activity were obtained by interview of each participant. Results. The proportion of children reporting no leisure time physical activity was high (19% in Bogotá, 28% in the central-eastern areas). Low physical activity was characteristically higher in girls and associated with public schools (in contrast with private schools). Physical activity was not associated with anthropometric indicators. Conclusions. The lack of association between physical activity and body adiposity may be due to the method of inquiry where the physical activity being reported was insufficient to induce changes in body composition. Additional studies are necessary that evaluate in greater detail the frequency, intensity and duration of physical activity to provide more definitive conclusions. However, the higher prevalence of inactivity in girls and the differences by type school constitute causes for concern.
Introducción. La obesidad es un problema de salud pública que se asocia a inactividad física. Objetivo. Evaluar la práctica de actividad física autorreportada y relacionarla con indicadores antropométricos de grasa corporal en un grupo de escolares de Bogotá y de cinco departamentos del centro-oriente colombiano. Materiales y métodos. Estudio transversal descriptivo que incluyó 1.593 escolares de 10 a 14 años de edad, en quienes se midió peso, talla, circunferencia braquial y pliegue tricipital, y se estableció la proporción de niños que realizaban actividad física y el tipo de actividad efectuada. Resultados. La proporción de escolares de la muestra estudiada que no realizan actividad física fue alta (19% de la muestra estudiada en Bogotá y 28% de los escolares de la muestra de centro-oriente), y fue sistemáticamente mayor en niñas que en niños, con diferencias según el tipo de colegio. La práctica de actividad física en el tiempo libre no se asoció independientemente con ningún indicador antropométrico. Conclusiones. La falta de asociación entre la actividad física y la adiposidad corporal puede deberse a que la intensidad de las actividades realizadas no logra cambiar la composición corporal, o a limitaciones en el instrumento de evaluación de la actividad física. Estudios posteriores en donde se utilice una muestra representativa de estas dos zonas del país y se evalué con detalle la intensidad, la duración, la frecuencia y el tipo de actividad física brindarán conclusiones más definitivas. Sin embargo, la mayor prevalencia de inactividad en niñas y las diferencias por tipo de colegio en la muestra de estudio son un llamado a la acción.
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/76
10.7705/biomedica.v28i3.76
Biomedica; Vol. 28 No. 3 (2008); 386-395
Biomédica; Vol. 28 Núm. 3 (2008); 386-395
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/76/76
/*ref*/Organización Panamericana de la Salud, Organización Mundial de la Salud. 37a sesión del Subcomité de Planificación y Programación del Comité Ejecutivo. Washington, D.C: OPS-OMS; 26 al 28 de marzo de 2003. [Consultado: noviembre de 2005]. Disponible en: http: //www.paho.org/spanish/gov/ce/ spp/spp37-08-s.pdf. <br />2. Koch B, Dordel S, Schindler-Marlow S, Icks A, Schuller A, et al. Physical activity, leisure habits and obesity in first-grade children. Eur J Cardiovasc Prev Rehabil. 2004;4:284-90. <br />3. Goran MI, Treuth MS. Energy expenditure, physical activity, and obesity in children. Pediatr Clin North Am. 2001;4:931-53. <br />4. World Health Organization. Obesity: Preventing and managing the global epidemic. Report of a WHO Consultation on Obesity. Geneva: WHO; 1997. <br />5. Sidhu S, Marwah G, Prabhjot. Prevalence of overweight and obesity among the affluent adolescent school children of Amritsar, Punjab. Coll Antropol. 2005;29:53-5. <br />6. Fredriks AM, Van Buuren S, Sing RA, Wit JM, Verloove-Vanhorick SP. Alarming prevalences of overweight and obesity for children of Turkish, Moroccan and Dutch origin in The Netherlands according to international standards. Acta Paediatr. 2005;94:496-8. <br />7. Magnusson MB, Hulthen L, Kjellgren KI. Obesity, dietary pattern and physical activity among children in a suburb with a high proportion of immigrants. J Hum Nutr Diet. 2005;18:187-94. <br />8. Vargas LA. Obesidad, consenso. Mexico D.F: Editorial McGraw-Hill Interamericana; 2002. <br />9. Cole TJ, Bellizzi MC, Flegal KM, Dietz WH. Establishing a standard definition for child overweight and obesity worldwide: international survey. BMJ. 2000;320:1240-3. <br />10. Duperly J. Obesidad, enfoque integral. Bogotá: Facultad de Medicina, Universidad del Rosario; 2000. p. 17-21, 69,133. <br />11. Peña M, Bacallao J. La obesidad en la pobreza. Un nuevo reto para la salud pública. Publicación científica Nº 576. Washington D.C.: OPS; 2000. p. 3-11. <br />12. Ribeiro J, Guerra S, Pinto A, Oliveira J, Duarte J, Mota J. Overweight and obesity in children and adolescents: relationship with blood pressure, and physical activity. Ann Hum Biol. 2003;30:203-13. <br />13. Magnusson MB, Hulthen L, Kjellgren KI. Obesity, dietary pattern and physical activity among children in a suburb with a high proportion of immigrants. J Hum Nutr Diet. 2005;18:187-94. <br />14. Stamatakis E, Primatesta P, Chinn S, Rona R, Falascheti E. Overweight and obesity trends from 1974 to 2003 in English children: what is the role of socioeconomic factors? Arch Dis Child. 2005;90:999-1004. <br />15. Rennie KL, Livingstone MB, Wells JC, McGloin A, Coward WA, Prentice AM, et al. Association of physical activity with body-composition indexes in children aged 6-8 y at varied risk of obesity. Am J Clin Nutr. 2005;82:13-20. <br />16. Giugliano R, Carneiro EC. Factors associated with obesity in school children. J Pediatr (Rio J). 2004;80:17-22. <br />17. Hernández B, Gortmaker SL, Colditz GA, Peterson KE, Laird NM, Parra-Cabrera S. Association of obesity with physical activity, television programs and other forms of video viewing among children in Mexico city. Int J Obes Relat Metab Disord. 1999;23:845-54. <br />18. Summerbell CD, Waters E, Edmunds LD, Kelly S, Brown T, Campbell KJ. Interventions for preventing obesity in children. Cochrane Database Syst Rev. 2005;20:CD001871. <br />19. Carlisle LK, Gordon ST, Sothern MS. Can obesity prevention work for our children? J La State Med Soc. 2005;157:S34-41. <br />20. Going S, Thompson J, Cano S, Stewart D, Stone E, Harnack L, et al. The effects of the Pathways Obesity Prevention Program on physical activity in American Indian children. Prev Med. 2003;37:S62-9. <br />21. Batch JA, Baur LA. Management and prevention of obesity and its complications in children and adolescents. Med J Aust. 2005;182:130-5. <br />22. Sothern MS. Obesity prevention in children: physical activity and nutrition. Nutrition. 2004;20:704-8. <br />23. Goran MI, Reynolds KD, Lindquist CH. Role of physical- activity in the prevention of obesity in children. Int J Obes Relat Metab Disord. 1999;23(Supl.3):S18-33. <br />24. Molnar D, Livingstone B. Physical activity in relation to overweight and obesity in children and adolescents. Eur J Pediatr. 2000;159 (Supl.1):S45-55. <br />25. IPAQ Core Group. Cuestionario internacional de actividad física. IPAQ: formato corto autoadministrado de los últimos 7 días. [Consultado: marzo de 2001]. Disponible en: http://www.ipaq.ki.se/doc/ArgentIQshself. pdf. <br />26. Al-Hazzaa HM. Health-enhancing physical activity among Saudi adults using the International Physical Activity Questionnaire (IPAQ). Public Health Nutr. 2007; 10:59-64. <br />27. Hagströmer M, Oja P, Sjöström M. The International Physical Activity Questionnaire (IPAQ): a study of concurrent and construct validity. Public Health Nutr. 2006;9:755-62. <br />28. Gómez LF, Duperly J, Lucumí DI, Gámez R, Venegas AS. Physical activity levels in adults living in Bogotá (Colombia): prevalence and associated factors. Gac Sanit. 2005;19:206-13. <br />29. Rey de Serra T. Manual para estandarización en mediciones antropométricas. Bogotá: ICBF; 1998. <br />30. Rosner B, Prineas R, Loggie J, Daniels SR. Percentiles for body mass index in U.S. children 5 to 17 years of age. J Pediatr. 1998;132:211-22. <br />31. Hernández A. Obesidad y sobrepeso en población estudiantil costarricense entre los 8 y 17 años. Rev Costarric Cienc Med. 2003;24;3-4. <br />32. Frisancho AR. Triceps skin fold and upper arm muscle size norms for assessment of nutritional status. Am J Clin Nutr. 1974;27:1052-8. <br />33. Frisancho AR. New norms of upper limb fat and muscle areas for assessment of nutritional status. Am J Clin Nutr. 1981;34:2540-5. <br />34. Voorhoeve HW. A new reference for the mid-upper arm circunference? J Trop Pediatr.1990;36:256-62. <br />35. Dos Santos F, Salvador M. Anthropometric, body composition and physical activity of students. Rev Bras Cineantropom Desempenho Hum. 2005;1:21. <br />36. Samur A, Urteaga R, Rebolledo A, Delfín C, Ramos H. Patrones alimentarios y de actividad física en escolares de la región de Aysén. Rev Chil Pediatr. 1999;6:483-90. <br />37. Hedley AA, Ogden CL, Johnson CL, Carroll MD, Curtin LR, Flegal KM. Prevalence of overweight and obesity among US children, adolescents, and adults, 1999-2002. JAMA. 2004;291:2847-50. <br />38. Lobstein T, Baur L, Uauy R, IASO International Obesity TaskForce. Obesity in children and young people: a crisis in public health. Obes Rev. 2004;5 (Supl.1):4-104. <br />39. Møller NC, Kristensen PL, Wedderkopp N, Andersen LB, Froberg K. Objectively measured habitual physical activity in 1997/1998 vs 2003/2004 in Danish children: The European Youth Heart Study. Scand J Med Sci Sports. 2008 Feb 17; [Epub ahead of print]. <br />40. World Health Organization. The World Health Report 2002. Reducing risks, promoting health life. Geneve: OMS; 2002. [Consultado: noviembre de 2005]. Disponible en: http://www.who.int/entity/whr/2002/en/ whr02_en.pdf. <br />41. Pucciarelli H, Carnese F, Pinotti L, Guimarey M. Sexual dimorphism in schoolchildren of the Villa IAPI neighborhood (Quilmes, Buenos Aires, Argentina). Am J Phys Anthropol. 1993;92:165-72.<br /> 42. Ranieri J, Oyhenart E, Rodrigo M. Influencia de la nutrición sobre la diferenciación sexual. Rev Argent Antropol Biol. 1999;2:123-34. <br />43. López M, Espinosa I, Coromoto M, Contreras N. Maduración temprana: factor de riesgo de obesidad durante la pubertad. Arch Lat Nutr. 1999;49:12-9. <br />44. Bolzán A, Guimarey L. Composición corporal y prevalencia estandarizada de desnutrición en niños de 6 a 12 años de edad, La Costa, Argentina. Rev Bras Saude Matern Infant. 2003;3:253-63. <br />45. Guillaume M, Lapidus L, Bjorntorp P, Lambert A. Physical activity, obesity, and cardiovascular risk factors in children. The Belgian Luxembourg Child Study II. Obes Res. 1997;5:549-56. <br />46. Yoshioka M, Doucet E, St-Pierre S, Alméras N, Richard D, Labrie A, et al. Impact of high-intensity exercise on energy expenditure, lipid oxidation and body fatness. Int J Obes Relat Metab Disord. 2001;25:332-9.<br /> 47. Dionne I, Alméras N, Bouchard C, Tremblay A. The association between vigorous physical activities and fat deposition in male adolescents. Med Sci Sports Exerc. 2000;32:392-5.<br />
oai:oai.revistabiomedica.org:article/77
2016-11-22T10:33:02Z
biomedica:ARTI
Paragonimosis in the peri-urban zone of Medellín, Antioquia
Estudio de foco de paragonimosis en Fuente Clara, Robledo, área periurbana de Medellín, Antioquia
Velásquez, Luz Elena
Gómez, Catalina
Valencia, Erika
Salazar, Laura
Casas, Eudoro
Paragonimus
tremátodos
zoonosis
epidemiología
educación
salud
Paragonimus
trematoda
zoonoses
epidemiology
education
health
Introduction. Human paragonimosis in Colombia was assumed to be restricted to the sylvatic areas. However, in 2005, crabs infected with Paragonimus were found in Fuente Clara, an urban sector in Medellín. Objective. A study was designed to understand the ecoepidemiology of paragonimosis. Programs were initiated to educate the community in the suitable use of wetland ecosystems. Materials and methods. Infection rates of Paragonimus in human and wild hosts was documented in the Fuente Clara sector. The presence of larvae and digenic adult worms was detected in mollusks (1,312), crabs (27) and mammals (4). Sputum diagnosis was performed on samples from 18 volunteer individuals. The following determinants of water quality were measured in the stream “La Puerta”: total fecal/coliform, pH, conductivity and dissolved oxygen were measured. Recreational workshops were conducted with children and teenagers for educational purposes. Results. The percentage of infections found in hosts was as follows: snails, 0.07%; crabs, 55.5%; (wild) mammals, 25%; humans, 0%. During the workshops, children and teenagers identified the Paragonimus hosts and the risk factors for acquiring the disease. The water of the stream was found to be unsuitable for consumption and recreation (the most probable number of total coliforms/100 ml was in a scale of 104). Conclusions. Fuente Clara is the first urban locality in Colombia where a focus of Paragonimus was found. Exposure to and consumption of crabs may constitute a risk for human infection
Introducción. La información sobre paragonimosis humana en Colombia llevó a suponer que los focos de la enfermedad estaban localizados en sectores selváticos; sin embargo, durante 2005 se hallaron cangrejos infectados con Paragonimus sp. en Fuente Clara, zona urbana de Medellín. Esto motivó la investigación. Objetivo. Realizar un estudio ecoepidemiológico de la paragonimosis con la participación de la comunidad para promover un manejo adecuado de los ecosistemas acuáticos. Materiales y métodos. Se realizó búsqueda de huéspedes silvestres y humanos de Paragonimus sp. en Fuente Clara. La presencia de formas larvarias y gusanos adultos del digéneo se evaluó en moluscos, crustáceos y mamíferos. En las personas voluntarias se hizo diagnóstico en esputo. Al agua de la quebrada La Puerta se le midieron: coliformes totales/ fecales, pH, conductividad y oxígeno disuelto. Con niños y adolescentes se realizaron talleres educativos utilizando técnicas lúdicas. Resultados. Los porcentajes de infección encontrados fueron: caracoles, 0,07%; cangrejos, 55,5%; mamíferos, 25%, y personas, 0%. Durante los talleres educativos se manifestó la importancia de los recursos naturales del barrio. Los niños identificaron los huéspedes de Paragonimus sp. y detectaron los factores de riesgo para adquirir la enfermedad. Se determinó que el agua de la quebrada La Puerta no es apta para el consumo y la recreación de las personas. Conclusiones. Se señala a Fuente Clara como el primer foco de paragonimosis en zona urbana de Colombia, donde la manipulación y el consumo de cangrejos ponen en riesgo de adquirir la infección a sus habitantes; se sugiere realizar vigilancia de la enfermedad en el sector.
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/77
10.7705/biomedica.v28i3.77
Biomedica; Vol. 28 No. 3 (2008); 396-403
Biomédica; Vol. 28 Núm. 3 (2008); 396-403
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/77/77
/*ref*/Vélez ID, Velásquez LE. Paragonimosis: una investigación multidisciplinaria en salud, biología y cultura en Colombia. Medellín: Universidad de Antioquia; 2002. p. 7-8. <br />2. Churg CH. Human paragonimiasis. Pathology of protozoal and helminthic diseases with clinical correlation. Baltimore: Williams and Wilkins; 1971. p. 504. <br />3. Blair D, Xu ZB, Agatsuma T. Paragonimiasis and the genus Paragonimus. Adv Parasitol. 1999;42:113- 222. <br />4. Malek E, Little MD. Aroapyrgus colombiensis n. sp. (Gastropoda: Hydrobiidae), snail intermediate host of Paragonimus caliensis in Colombia. The Nautilus. 1971;85:20-6. <br />5. Vélez I, Velásquez LE, Vélez ID. Morphological description and life cycle of Paragonimus sp. (Trematoda: Troglotrematidae): causal agent of human paragonimiasis in Colombia. J. Parasitol. 2003;89:749- 55. <br />6. Lamothe-Argumedo R, Malek EA, Meave- Gallegos O. Aroapyrgus alleei Morrison, (Gastropoda: Hydrobiidae) first intermediate host of Paragonimus mexicanus in Colima, Mexico. J Parasitol. 1983;69:226-8. <br />7. Lamothe-Argumedo R, Caballero J, Lázaro E. Pseudothelphusa (P). dilatata Rathbun (Crustacea: Decapoda), segundo hospedador intermediario de Paragonimus mexicanus (Trematoda). An Inst Biol Unif Nal Auton México. 1976;48:295-8. <br />8. Lamothe-Argumedo R. La paragonimiasis en el continente americano. Salud Pública Mex. 1985; 27: 514-23. <br />9. Caballero YC, Montero-Gei F. Descripción de dos tremátodos de un marsupial de la República de Costa Rica y un catálogo de los tremátodos que parasitan a Marsupialia illger, 1811. Ann Esc Nac Cien Biol. (México). 1961;10:45-86. <br />10. Moné H, Théron A, Combes C. Interaction between the Biomphalaria glabrata-Schistosoma mansoni hostparasite system and the non-target mollusks: influence on cercarial production. J. Parasitol. 1986;72:410-6. <br />11. Campos MR, Rodriguez G. Two new species of freshwater crabs of the genus Hypolobocera from Colombia (Crustacea: Decapoda: Pseudothelpusidae). Proc Biol Soc Wash. 1995;108:649-55. <br />12. Campos MR. Freshwater crabs from Colombia a taxonomic and distributional study. Bogotá, D.C: Editora Guadalupe Ltda.; 2005. p. 224-94. <br />13. Vélez A. Guías de parasitología veterinaria. Medellín: Editorial Exitodinámica; 1983. p. 306. <br />14. Fuentes F, Masol-Deya A. Manual de Laboratorio Ecología de los microorganismos. Pt. 3. Puerto Rico: Universidad de Puerto Rico; 2002. p. 1-15. <br />15. The American Public Health Association, The American Water Works Association, Water Pollution Control Federation. Standard methods for the examination of water and wastewater. 15th ed. Washington, D.C. American Public Health Association; 1980. <br />16. Vélez I, Ortega J, Velásquez LE. Paragonimiasis: a view from Colombia. Clin Chest Med. 2002;23:421-31. <br />17. Little MD. Paragonimus caliensis sp. and paragonimiasis in Colombia. J Parasitol. 1968;54:738-46. <br />18. Velásquez LE, Bedoya JC, Areiza A, Vélez I. Primer registro de Centrocestus formosanus (Digenea: Heterophyidae) en Colombia. Revista Mexicana de Biodiversidad. 2006;77:119-21. <br />19. Velásquez LE, Restrepo S, Gómez MI, Vélez ID. Aspectos ecoepidemiológicos del caracol Aroapyrgus sp. Revista Asociación Colombiana de Ciencias Biológicas. 1999;11:7-15.<br />
oai:oai.revistabiomedica.org:article/78
2016-11-22T10:33:02Z
biomedica:ARTI
Validation by hydrodensitometry of skinfold thickness equations used for female body composition assessment
Validación por hidrodensitometría de ecuaciones de pliegues cutáneos utilizadas para estimar la composición corporal en mujeres
Aristizábal, Juan Carlos
Restrepo, María Teresa
López, Amalia
estudios de validación
densitometría
antropometría
grosor de pliegues cutáneos
composición corporal
índice de masa corporal
mujeres
Validation studies
densitometry
anthropometry
skinfold thickness
body composition
body mass index
female
Introduction. Skinfold thickness equations are widely used for body composition assessment. However the equations have not been validated in Colombia with a reference method. Objective. The skinfold thickness equations of Durning/Womersley, Jackson/Pollock and Ramírez/Torun were validated by hydrodensitometry in female from 18 to 40 years old. Materials and methods. The percentage of body fat was compared among 52 women, using underwater weighing (Chatillon scale) with simultaneous measured of residual lung volume (VMAX 22 Sensormedics spirometer) and skinfold thickness (Harpenden caliper) equations of Durning/Womersley, Jackson/Pollock and Ramírez/Torun. The statistic analysis included paired t test, Pearson and intraclass correlation coefficients, and the Bland-Altman method. Results. The mean percentage of body fat by hydrodensitometry (29.6±5.8%) was different (p Conclusion. The skinfold thickness equations showed poor validity for body fat assessment. The equations had significant differences and lower correlation coefficients with hydrodensitometry. In addition, the equations indicated agreement with hydrodensitometry over very wide limits. The outcomes suggested that the results obtained by hydrodensitometry were neither comparable nor interchangeable with those from Durning/Womersley, Jackson/Pollock y Ramírez/Torun skinfold thickness equations.
Introducción. Las ecuaciones de pliegues cutáneos son ampliamente utilizadas para estimar la composición corporal; sin embargo, en nuestra población no se han validado contra un método de referencia. Objetivo. Validar por hidrodensitometría las ecuaciones de Durning/Womersley, Jackson/Pollock y Ramírez/Torun en mujeres de 18 a 40 años. Materiales y métodos. Se comparó el porcentaje de grasa de 52 mujeres obtenido por hidrodensitometría, medición simultánea del peso bajo el agua (báscula Chatillon) y del volumen pulmonar residual (espirómetro VMAX 22 Sensormedics), con el estimado por las ecuaciones de pliegues cutáneos (calibrador Harpenden) de Durning/Womersley, Jackson/Pollock y Ramírez/Torun. Para el análisis estadístico se utilizaron la t de Student pareada, los coeficientes de correlación de Pearson e intraclase, y el método de Bland-Altman. Resultados. El porcentaje de grasa obtenido por hidrodensitometría (29,6±5,8) presentó diferencias (p Conclusión. Las ecuaciones de pliegues cutáneos presentaron pobre validez en la predicción del porcentaje de grasa, con diferencias significativas con la hidrodensitometría, una baja concordancia y unos amplios límites de ésta, lo cual, sugiere que sus resultados no son comparables ni intercambiables con este método.
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/78
10.7705/biomedica.v28i3.78
Biomedica; Vol. 28 No. 3 (2008); 404-413
Biomédica; Vol. 28 Núm. 3 (2008); 404-413
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/78/78
/*ref*/World Health Organization. Obesity: preventing and managing the global epidemic. In: Report of WHO Consultation. WHO Technical reports 894. Geneve: WHO; 2000. p. 1-61. <br />2. Instituto Colombiano de Bienestar Familiar. Valoración del estado nutricional por indicadores antropométricos. Encuesta Nacional de la Situación Nutricional en Colombia. Bogotá D.C: Panamericana Formas e Impresos S.A.; 2005. p. 69-122. <br />3. Oliveira FL, Taddei JA, Escrivão MA, Cobayashi F, Barros ME, Vítolo MR, et al. Accuracy of obesity diagnosis in Brazilian adolescents: comparison of Cole et al and Must et al criteria with DXA percentage of fat mass. Nutr Hosp. 2006;21:484-90. <br />4. Womersley J. A comparison of the skinfold method with extent of "overweight" and various weight-height relationships in assessment of obesity. Br J Nutr. 1977; 38:271-84. <br />5. Wang WW, Stuff JE, Butle NF, Smith EO, Ellis KJ. Estimating body fat in African American and white adolescent girls: a comparison of skinfold-thickness equations with a 4-compartment criterion model. Am J Clin Nutr. 2000;72:348-54. <br />6. Smalley KJ, Knerr AN, Kendrick ZV, Colliver JA, Owen OE. Reassessment of body mass indices. Am J Clin Nutr. 1990;52:405-8. <br />7. Brodie DA. Techniques of measurement of body composition. Part I. Sports Med. 1988;5:11-40. <br />8. Going SB. Densitometry. In: Roche AF, Heymsfield SB, Lohman TG, editors. Human body composition. Champaign IL: Human Kinetics Publishers; 1996. p. 3-22. <br />9. Durnin JV, Rahaman MM. The assessment of the amount of fat in the human body from measurements of skinfold thickness. Br J Nutr. 1967;21:681-9. <br />10. Lohman TG. Skinfolds and body density and their relation to body fatness: A review. Hum Biol. 1981;53: 181-225. <br />11. Jackson AS, Pollock ML. Generalized equations for predicting body density of men. Br J Nutr. 1978;40:497-504. <br />12. Jackson AS, Pollock ML. Practical assessment of body composition. Phys Sports Med. 1985;13:76-89. <br />13. Bellizari A, Roche AF. Antropometría y ecografía In: Heymsfield SB, Lohman TG, Wang ZM, Going SB. Composición corporal. 2ª Edición. México D.F.: McGraw-Hill; 2005. p. 109-28. <br />14. Deurenberg P, Deurenberg-Yap M. Validity of body composition methods across ethnic population groups. Acta Diabetol. 2003;40(Suppl.1):S246-9. <br />15. Durnin JV, Womersley J. Body fat assessed from total body density and its estimation from skin fold thickness: measurements on 481 men and women aged from 16 to 72 years. Br J Nutr. 1974;32:77-97. <br />16. Ramirez-Zea M, Torun B, Martorell R, Stein AD. Anthropometric predictors of body fat as measured by hydrostatic weighing in Guatemalan adults. Am J Clin Nutr. 2006; 83:795-802. <br />17. Harrison G, Buskirk ER, Carter JE, Johnston FE, Lohman TG, Pollock ML, et al. Skinfold thicknesses and measurement technique. In: Lohman TG, Roche AF, Martorell R, editors. Antropometric standardization reference manual. Champaign IL: Human Kinetics Publishers; 1988. p. 55-70. <br />18. Marfell-Jones M. Kinanthropometric assessement. Guidelines for athlete assessement in New Zealand sport kinanthropometric assessement. 2000. [Consultado: 3 de mayo de 2006]. Disponible en: http://www.ljmu.ac.uk/ECL/ECL_docs/2.08_ KinanthrEometric_Asses.pdf <br />19. Bellido D, Carreira J. Desarrollo de ecuaciones predictivas para el cálculo de composición corporal por impedanciometría. Rev Esp Obes. 2006;4:97-106. <br />20. Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet. 1986;1:307-10. <br />21. Mantha S, Roizen MF, Fleisher LA, Thisted R, Foss J. Comparing methods of clinical measurement: reporting standards for bland and altman analysis. Anesth Analg. 2000;90:593-602. <br />22. Landis JR, Koch GG. The measurement of observed agreement for categorical data. Biometrics. 1997;33: 159-74. <br />23. Barnhart HX. Lokhnygina,Y, Kosinski AS, Haber M. Comparison of concordance correlation coefficient and coefficient of individual agreement in assessing agreement. J Biopharm Stat. 2007;17:721-38. <br />24. Sociedad Española para el Estudio de la Obesidad (SEEDO). Consenso SEEDO 2000 para la evaluación del sobrepeso y la obesidad y el establecimiento de criterios de intervención terapéutica. Med Clin (Barc) 2000;115:589-97. <br />25. Lohman TG. Basic concepts in body composition assessment. In: Lohman TG, editor. Advances in body composition assessment. Champaign IL: Human Kinetics Publishers; 1992. p. 1-5. <br />26. Lohman TG. Prediction equations and skinfolds, bioelectric impedance, and body mass index. In: Lohman TG, editor. Advances in body composition assessment. Champaign IL: Human Kinetics Publishers; 1992. p. 37-56. <br />27. Zillikens MC, Conwa JM. Anthropometry in blacks: applicability of generalized skinfold equations and differences in fat patterning between blacks and whites. Am J Clin Nutr. 1990;52:45-51. <br />28. Norton K. Estimación antropométrica de la grasa o adiposidad. En: Norton K, Olds T, editors. Antropo-métrica. Rosario: Biosystem Servicio Educativo; 2000. p. 116-36. <br />29. Eston RG, Fu F, Fung L. Validity of conventional anthropometric techniques for predicting body composition in healthy Chinese adults. Br J Sports Med. 1995;29:52-6. <br />30. Peterson MJ, Czerwinski SA, Siervogel M. Development and validation of skinfold-thickness prediction equations with a 4-compartment model. Am J Clin Nutr. 2003;77:1186-91. <br />31. Moreno VM, Gómez JB, Antoranz MJ. Medición de la grasa corporal mediante impedancia bioeléctrica, pliegues cutáneos y ecuaciones a partir de medidas antropométricas. Análisis comparativo. Rev Esp Salud Pública. 2001;75:221-36. <br />32. Wang J, Thornton JC, Russell M, Burastero S, Heymsfield S, Pierson RN. Asians have lower body mass index (BMI) but higher percent body fat than do whites: comparisons of anthropometric measurements. Am J Clin Nutr. 1994;60:23-8. <br />33. Casas G, Schiller BC. DeSouza CA,Seals DR. Total and regional body composition across age in healthy Hispanic and white women of similar socioeconomic status. Am J Clin Nutr. 2001;73:13-8. <br />
oai:oai.revistabiomedica.org:article/79
2016-11-22T10:33:02Z
biomedica:ARTI
A comparison of the causes of adult mortality and its effects on life-expectancy across the regions of Colombia
Efectos de las causas de mortalidad adulta en la esperanza de vida, entre 1985 y 1999, según regiones colombianas
López, Elizabeth
Arce, Patricia
tasa de mortalidad
causa de muerte
causas externas
esperanza de vida
tablas de vida
Colombia
mortality rate
cause of death
external causes
life expectancy
life tables
Colombia
Introduction. When determining some populations state of health, an understanding of the causes of mortality is essential. Objectives. Changes in mortality due to causes was established to determine their contribution to the life-expectancy by gender and region of the Colombian population aged 15 to 74, between 1985 and 1999, by gender and region. Materials and methods. This was a descriptive, retrospective study; the sources of information were records of deaths from 1983 to 2001 and population projections according to Departamento Administrativo Nacional de Estadística. The age selected as a sample population was 15 to 74. Changes in mortality were measured by using Eduardo Arriagas methodology, which is based on calculating temporary life-expectancy, absolute and relative change indices, and how changes in mortality due to cause of death contribute to life-expectancy. Results. The main cause of reduced temporary life-expectancy in both genders was the increase in deaths by suicide, homicide and other violent causes (the reduction was greater for men than women in all regions studied). The greatest positive contribution to longevity was by the reduction in circulatory system diseases and accidents. Conclusions. A minimal gain in temporary life-expectancy was achieved as the positive affect of reduced mortality due to natural causes. This gain was annulled by the negative contributions of increased mortality due to suicide, homicide and other violent avoidable acts.
Introducción. El estudio de la mortalidad por causas es fundamental para conocer el estado de salud de una población. Objetivos. Establecer los cambios de la mortalidad por causas y su contribución a la esperanza de vida de la población de 15 a 74 años entre 1985 y 1999, según sexo y región. Materiales y métodos. Estudio descriptivo retrospectivo; las fuentes de información fueron las defunciones registradas de 1983 a 2001 y las proyecciones de población del Departamento Administrativo Nacional de Estadística. Los cambios en la mortalidad se midieron utilizando la metodología de Eduardo E. Arriaga, que se basa en el cálculo de la esperanza de vida temporal, los índices de cambio absoluto y relativo, y la contribución del cambio de la mortalidad por causa de muerte a la esperanza de vida. Resultados. La principal causa de la pérdida en la esperanza de vida temporal en ambos sexos fue el incremento de las defunciones por suicidios, homicidios y otras causas violentas, aunque la pérdida fue mayor para los hombres que para las mujeres en todas las regiones estudiadas. El mayor aporte positivo se logró por la disminución de las enfermedades del sistema circulatorio y los accidentes. Conclusión. La ganancia en la esperanza de vida temporal fue mínima puesto que los aportes positivos producidos por la disminución de la mortalidad por causas naturales se anulan con los aportes negativos producidos por el incremento de la mortalidad por suicidios, homicidios y otras violencias que son evitables
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/79
10.7705/biomedica.v28i3.79
Biomedica; Vol. 28 No. 3 (2008); 414-422
Biomédica; Vol. 28 Núm. 3 (2008); 414-422
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/79/79
/*ref*/Organización Panamericana de la Salud, Conselleria de Sanidade de la Xunta de Galicia. Demografía. En: Epidat v.3. Consultado: marzo de 2008. Disponible en: http://dxsp.sergas.es/ApliEdatos/Epidat/Ayuda/2-AyudaDemografEDa.pdf <br />2. Arriaga E. Adult mortality in the era of HIV/AIDS: Latin America and Caribbean. New York: Department of Economic and Social Affairs, Population Division, United Nations Secretariat; 2003. <br />3. Organización Panamericana de la Salud. La salud en las Américas. Volumen 1. Washington, D. C.: OPS; 2002. p. 13. <br />4. Balladelli PP. Elementos para establecer prioridades en investigación en salud pública. Bogotá, D.C., 25 de octubre de 2006 Consultado: junio de 2007 Disponible en: http://www.col.ops-oms.org/docs/ConferenciaCOLCIENCIAPrioridadesinvestigaciC3B3nSP251006.doc <br />5. Ordóñez M, Castaño L, Pinilla C, López E. La mortalidad en Colombia en el período 1982-1996. Bogotá, D.C.: Instituto Nacional de Salud, Ministerio de la Protección Social; 2003. Consultado: febrero 2006. Disponible en: http://www.ins.gov.co/pdf_investiga/2005_ss_mortalidad_general_1982_1996.pdf <br />6. Arriaga E. Measuring and explaining the change in life expectancies. Demography. 1984;21:83-96 <br />7. Organización Panamericana de la Salud/Organización Mundial de la Salud. Clasificación Inter-nacional de Enfermedades. Washington, D. C.: OPS; 1975. <br />8. Organización Panamericana de la Salud/Organización Mundial de la Salud. Clasificación Estadística internacional de enfermedades y problemas relacionados con la salud, CIE-10. 10a revisión. Washington, D. C.: OPS; 1995. <br />9. López E, Arce P. Impacto de las causas de muerte en la esperanza de vida. Colombia, Bogotá, Antioquia y Valle, 1985-1999. Boletín Epidemiológico Distrital. 2006;9:2-15. <br />10. Serna C, Grisales H, Caicedo B, Uribe D. Causas de mortalidad en jóvenes y su contribución al cambio en la esperanza de vida. Bogotá 1989-1999. Boletín Epidemiológico Distrital. 2004;8:2-10. <br />11. Grisales H, Caicedo B, Serna C, Uribe D. Causas de mortalidad en jóvenes y su contribución al cambio en la esperanza de vida. Cali, 1989-1999. Colomb Med. 2005;36:85-93.<br />12. Aristizábal E, Posada M, Estrada G, Grisales H. Cambio en la esperanza de vida de la población de Medellín por las seis principales causas de muerte entre 1989-91 y 1994-96. En: Fernández S, Grisales H, editores. Estudios sobre la mortalidad: diferentes enfoques. Medellín: DANE, Universidad de Antioquia; 2003. p. 13-25. <br />13. Grisales H, Estrada GS, Aristizábal M, Posada M. Cambio en la esperanza de vida según tres grandes grupos de causas de muerte en Medellín, Colombia, de 1989-1991 a 1994-19996. Rev Panam Salud Pública. 2002;12:305-12. <br />14. Boleda M, Arriaga EE. América Latina: mortalidad por accidentes y por violencia contra las personas. Notas de población No. 70. CEPAL 2000. p 87-119. Consultado: marzo de 2006. Disponible en: http://www.eclac.org/publicaciones/xml/6/6776/lcg21003.pdf. <br />15. Londoño J, Grisales R, Fernández S, Cadena E, Años de vida saludable perdidos por la población de Medellín. Un análisis especial por homicidio y accidentes de vehículo de motor. Rev Fac Nac Salud Pública. 1999;17:63-92. <br />
oai:oai.revistabiomedica.org:article/80
2016-11-22T10:33:02Z
biomedica:ARTI
Molecular and immunological analyses suggest the absence of hydrophilic surface proteins in Leishmania (Viannia) panamensis
El análisis molecular y el inmunogénico sugieren la ausencia de las proteínas hidrofílicas de superficie en Leishmania (Viannia) panamensis
Marín, Marcel
Aguilar, Yudy Alexandra
Ramírez, José Robinson
Triana, Omar
Muskus, Carlos Enrique
Leishmania
reacción en cadena de la polimerasa
clonación molecular
datos de secuencia molecular
prueba ELISA
Western blotting
Leishmania
polymerase chain reaction
cloning
molecular
molecular sequence data
enzyme-linked immunosorbent assay
blotting
Western
Introduction. The genus Leishmania is divided into two subgenera: Leishmania and Viannia. The two subgenera present several important differences such as the pathology they cause in susceptible hosts, their in vitro growth behavior, their genetic characteristics, and the expression pattern of several proteins, including those of the hydrophilic surface protein family. Objective. To characterize the hydrophilic surface protein family in Leishmania (Viannia) panamensis. Materials and methods. The hasp genes were amplified in L. (V.) panamensis, using specific primers previously designed to amplify this gene in Leishmania (Leishmania) major. The PCR products were cloned, sequenced, and the sequences analyzed using common bioinformatics tools. Secondly, a serological screening was undertaken with an enzyme-linked immunosorbent assay and Western blot to detect specific antibodies against the hydrophilic surface recombinant protein from L. (L.) major. Results. A copy of a pseudogene was amplified in L. (V.) panamensis which was 60% homologous with the L. (L.) major orthologous gene. Antibodies responded to the hydrophilic surface recombinant proteins only in sera from patients with visceral leishmaniasis [Leishmania (Leishmania) chagasi]. Conclusión. These results suggest the lack of a functional hasp gene in L. (V.) panamensis, suggesting probably the loss of the complete gene family in this species of the Viannia subgenus.
Introducción. Los dos subgéneros en los cuales se divide el género Leishmania: Viannia y Leishmania, presentan diferencias significativas en las manifestaciones clínicas que causan, en su comportamiento de crecimiento en cultivos in vitro, en sus características genéticas y en la expresión de varias proteínas, entre ellas las de la familia hidrofílica de superficie superficie. Objetivo. Caracterizar las proteínas hidrofílicas de superficie en Leishmania (Viannia) panamensis. Materiales y métodos. Se amplificaron los genes hasp en L. (V.) panamensis usando cebadores específicos para la especie Leishmania (Leishmania) major. Los productos de la amplificación fueron clonados, secuenciados y analizados con herramientas bioinformáticas. Posteriormente, se realizó un análisis serológico por medio de ensayo inmunoabsorbente ligado a enzimas y Western blot para detectar la presencia de anticuerpos específicos contra las proteínas hidrofílicas recombinantes de superficie de L. (L.) major en sueros de pacientes con leishmaniasis de zonas endémicas de Colombia. Resultados. Se encontró una copia de un pseudogen en L. (V.) panamensis, el cual presentó una identidad del 60% con el gen haspa de L. (L.) major. Sólo se encontraron anticuerpos contra las proteínas recombinantes de superficie hidrofílicas en sueros de pacientes con leishmaniasis visceral. Conclusión. Estos resultados sugieren que no existe ninguna copia de un gen funcional hasp en L. (V.) panamensis, lo que indica una pérdida de la familia de genes en esta especie de Leishmania perteneciente al subgénero Viannia.
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/80
10.7705/biomedica.v28i3.80
Biomedica; Vol. 28 No. 3 (2008); 423-432
Biomédica; Vol. 28 Núm. 3 (2008); 423-432
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/80/80
/*ref*/Killick-Kendrick R. Biology of leishmania in phlebotomine sand flies. In: Lumsden WH, Evans DA, editors. Biology of the kinetoplastida. London: Academic Press; 1979. p. 395-460. <br />2. Vélez ID, Hendrick E, Robledo SM, Agudelo SP. Leishmaniosis cutánea en Colombia y género. Cad Saúde Pública. 2001;17:171-80. <br />3. Ovalle CE, Porras L, Rey M, Ríos M, Camargo YC. Distribución geográfica de especies de Leishmania aisladas de pacientes consultantes al Instituto Nacional de Dermatología Federico Lleras Acosta, E.S.E., 1995-2005. Biomédica. 2006;26(Supl.1):145-51. <br />4. Lane RP. Sandflies (Phlebotominae). In: Lane RP, Crosskey RW, editors. Medical insects and arachnids. Cambridge: Chapman and Hall; 1993. p. 78-119. <br />5. Kedzierski L, Montgomery J, Bullen D, Curtis J, Gardiner E, Jimenez-Ruiz A, et al. A leucine-rich repeat motif of Leishmania parasite surface antigen 2 "binds to macrophages through the complement receptor 3. J Immunol. 2004;172:4902-6. <br />6. McMahon-Pratt D, Traub-Cseko Y, Lohman KL, Rogers DD, Beverley SM. Loss of the GP46/M-2 surface membrane glycoprotein gene family in the Leishmania braziliensis complex. Mol Biochem Parasitol. 1992;50:151-60. <br />7. McMahon-Pratt D, Alexander J. Does the Leishmania major paradigm of pathogenesis and protection hold for New World cutaneous leishmaniases or the visceral disease?. Immunol Rev. 2004;201:206-24. <br />8. Marín M, Muskus C, Ramírez JR, Arbeláez LF, Alzate JF, Berberich C. The gene encoding the metacyclogenesis-associated transcript Mat-1 is conserved in the genus Leishmania and shows a tendency to form dimers upon protein expression. Parasitol Res. 2000;86:431-5. <br />9. Peacock CS, Seeger K, Harris D, Murphy L, Ruiz JC, Quail MA, et al. Comparative genomic analysis of three Leishmania species that cause diverse human disease. Nat Genet. 2007;39:839-47. <br />10. Muskus, C, Segura I, Oddone R, Turco SJ, Leiby DA, Toro L, et al. Carbohydrate and LPG expression in Leishmania Viannia subgenus. J Parasitol. 1997;83: 671-8. <br />11. Hommel M, Jaffe CL, Travi B, Milon G. Experimental models for leishmaniasis and for testing anti-leishmanial vaccines. Ann Trop Med Parasitol. 1995;89(Suppl.1):55-73. <br />12. Henao HH, Osorio Y, Saravia NG, Gómez A, Travi B. Eficacia y toxicidad de los antimoniales pentavalentes (Glucantime® y Pentostam®) en un modelo animal de leishmaniasis cutánea americana: aplicación de la luminometría. Biomédica. 2004;24:393-402. <br />13. Britto C, Ravel C, Bastien P, Blaineau C, Pages M, Dedet JP, et al. Conserved linkage groups associated with large-scale chromosomal rearrangements between Old World and New World Leishmania genomes. Gene. 1998;222:107-17. <br />14. Robinson KA, Beverley SM. Improvements in transfection efficiency and tests of RNA interference (RNAi) approaches in the protozoan parasite Leishmania. Mol Biochem Parasitol. 2003;128:217-28. <br />15. Flinn HM, Rangarajan D, Smith DF. Expression of hydrophilic surface protein in infective stages of Leish-mania major. Mol Biochem Parasitol. 1994;65:259-70. <br />16. Pimenta PF, Pinto da Silva P, Rangarajan D, Smith DF, Sacks DL. Leishmania major: association of the differentially expressed gene B protein and the surface lipophosphoglycan as revealed by membrane capping. Exp Parasitol. 1994;79:468-79. <br />17. Rangarajan D, Gokool S, McCrossan MV, Smith DF. The gene B protein localise to the surface of Leishmania major parasites in the absence of metacyclic stage lipophosphoglycan. J Cell Sci. 1995; 108:3359-66. <br />18. Jensen AT, Gaafar A, Ismail A, Christensen CB, Kemp M, Hassan AM, et al. Serodiagnosis of cutaneous leishmaniasis: assessment of an enzyme-linked immunosorbent assay using a peptide sequence from gene B protein. Am J Trop Med Hyg. 1996;55:490-5. <br />19. Jensen AT, Gasim S, Moller T, Ismail A, Gaafar A, Kemp M, et al. Serodiagnosis of Leishmania donovani infections: assessment of enzyme-linked immunosorbent assays using recombinant L. donovani gene B protein (GBP) and a peptide sequence of L. donovani GBP. Trans R Soc Trop Med Hyg. 1999;93:157-60. <br />20. Stager S, Smith DF, Kaye PM. Immunization with a recombinant stage-regulated surface protein from Leishmania donovani induces protection against visceral leishmaniasis. J Immunol. 2000;165:7064-71. <br />21. Medina-Acosta E, Cross G. Rapid isolation of DNA from trypanonosomatid protozoa using a simple "mini-prep" procedure. Mol Biochem Parasitol. 1993;59:327-9. <br />22. Bhatia A, Daifalla NS, Jen S, Badaro R, Reed SG, Skeiky YA. Cloning, characterization and serological evaluation of K9 and K26: two related hydrophilic antigens of Leishmania chagasi. Mol Biochem Parasitol. 1999;102:249-61. <br />23. Alce TM, Gokool S, McGhie D, Stager S, Smith DF. Expression of hydrophilic surface proteins in infective stages of Leishmania donovani. Mol Biochem Parasitol. 1999;102:191-6. <br />24. Lainson R, Shaw JJ. Evolution, classification and geographical distribution. In: Peters W, Killick-Kendrick R, editors. The leishmaniases in biology and medicine. London: Academic Press; 1987. p. 1-120. <br />25. Folgueira C, Canavate C, Chicharro C, Requena JM. Genomic organization and expression of the HSP70 locus in New and Old World Leishmania species. Parasitology. 2007;134:369-77. <br />26. Smith DF, Peacock CS, Cruz AK. Comparative genomics: from genotype to disease phenotype in the leishmaniases. Int J Parasitol. 2007;37:1173-86. <br />27. Eschenlauer SC, Coombs GH, Mottram JC. PFPI-like genes are expressed in Leishmania major but are pseudogenes in other Leishmania species. FEMS Microbiol Lett. 2006;260:47-54. <br />28. Denny PW, Gokool S, Russell D, Field M, Smith D. Acylation-dependent protein export in Leishmania. J Biol Chem. 2000;275:11017-25. <br />29. McKean PG, Denny PW, Knuepfer E, Keen JK, Smith DF. Phenotypic changes associated with deletion and overexpression of a stage-regulated gene family in Leishmania. Cell Microbiol. 2001;3:511-23. <br />30. McKean PG, Trenholme KR, Rangarajan D, Keen J, Smith DF. Diversity in repeat-containing surface proteins of Leishmania major. Mol Biochem Parasitol. 1997;86:225-35.
oai:oai.revistabiomedica.org:article/81
2016-11-22T10:33:02Z
biomedica:BREV
Species of Lutzomyia involved in an urban focus of visceral and cutaneous leishmaniasis
Especies de Lutzomyia en un foco urbano de leishmaniasis visceral y cutánea en El Carmen de Bolívar, Bolívar, Colombia
Cortés, Luis Alberto
Fernández, Jhon James
Leishmania
leishmaniasis [epidemiología]
leishmaniasis visceral
leishmaniasis cutánea
Psychodidae
hábitat
Leishmania
leishmaniasis [epidemiology]
leishmaniasis
visceral
cutaneous
Psychodidae
habitat
Introduction. A focus of leishmanias transmission was reported in the municipality of El Carmen de Bolívar in the province of Bolívar, Colombia, where both cutaneous and visceral leishmaniasis cases have occured. Vector identification, ecology and behavior of potential vector species have not been characterized in this region, however. Objectives. Sand fly species of the genus Lutzomyia were identified, patterns of behavior were established, and their possible roles in leishmaniasis transmission were evaluated. Materials and methods. CDC light traps were used in several different habitats; in addition, monthly collections were made with human bait as attraction inside houses as well as outdoor Shannon trap collections. The collection data were compared with independent variables including precipitation, temperature, relative humidity and wind velocity by means of a Pearson correlation matrix to estimate levels of association and to determine the influence of the climatic conditions on the density of adults of Lutzomyia evansi and L. gomezi in each of the habitats. Results. Five species of Lutzomyia were captured: L. evansi, L. cayennensis cayennensis, L. gomezi, L. dubitansi, and L. walkeri. Lutzomyia evansi and L. gomezi presented a significant relationship in the abundance of adults indoors with respect to outdoor wind velocity. The Lutzomyia species captured showed an anthropophagic behavior with a constant activity between the 18:00 and 20:00 hrs. Conclusions. Lutzomyia evansi and L. gomezi are inversely proportional in relationship to wind velocity-when the wind diminishes, the activity of these species increases.
Introducción. Se describen algunos aspectos de la ecología y de la importancia de las especies de Lutzomyia presentes en un foco de leishmaniasis en El Carmen de Bolívar, departamento de Bolívar. Objetivos. Establecer algunos de los patrones del comportamiento de las especies de Lutzomyia y asociar su posible papel en la transmisión de leishmaniasis en un foco de leishmaniasis visceral y cutánea. Materiales y métodos. Se utilizaron trampas CDC en diferentes hábitat, se hicieron capturas mensuales en cebo humano protegido en el intradomicilio y capturas en trampas Shannon en el extradomiclio. Estos datos se compararon con variables independientes, como precipitación, temperatura, humedad relativa y velocidad del viento mediante una correlación de Pearson para estimar el grado de asociación y determinar la influencia de las condiciones climáticas sobre la densidad de adultos de L. evansi y L. gomezi en diferentes hábitat. Resultados. Se capturaron cinco especies de Lutzomyia: L. evansi, L. cayennensis cayennensis, L. gomezi, L. dubitansi y L. walkeri. L. evansi y L. gomezi presentaron una relación significativa en la abundancia de adultos contra la velocidad del viento en el intradomicilio, las especies de Lutzomyia capturadas mostraron un comportamiento antropofílico con una actividad constante entre las 18:00 y las 20:00 horas. Conclusión. L. evansi y L. gomezi están en relación inversamente proporcional a la velocidad del viento, al disminuir, aumentan la actividad de las poblaciones de estas especies.
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/81
10.7705/biomedica.v28i3.81
Biomedica; Vol. 28 No. 3 (2008); 433-440
Biomédica; Vol. 28 Núm. 3 (2008); 433-440
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/81/81
/*ref*/Desjeux. P. Human leismaniases: Epidemiology and public health aspects. Word Health Stat Q. 1992; 45:267-75. <br />2. Barreto M, Burbano E, Barreto P. Registros de Lutzomyia (Díptera: Psychodidae) en nuevas localida-des de Colombia. Colombia Médica. 2006;37:39-45. <br />3. Barata RA, Franca-Silva JC, Mayrink W, Costa da Silva J, Prata A, Loroso E, et al. Aspectos da ecologia e do comportamento de flebotomíneos em área endêmica de leishmaniose visceral, Minas Gerais. Revista da Sociedade Brasileira de Medicina Tropical. 2005;38:421-5. <br />4. Young DG, Duncan MA. Guide to the identification and geographic distribution of Lutzomyia sandflies in Mexico, the West Indies, Central and South America (Diptera Psychodidae). Mem Amer Ent Inst. 1994:54; 1-881. <br />5. Gonzáles C, Cabrera O, MustermanL E, Ferro M. Distribución de los vectores de Leishmania infantum (Kinetoplastida: Trypanosomatidea) en Colombia. Biomédica. 2006;26(Suppl.1):64-72. 6. Scorza JV, Macias P, Rojas J. Encuestas epidemiológicas sobre leishmaniasis cutánea urbana en la ciudad de Trujillo, Venezuela. Bol Dir Malariol Saneam Amb. 1985;22:389-404. <br />7. Vélez ID, Travi BL, Gallego J, Palma GL, Agudelo SP, Montoya J. Evaluación ecoepidemiológica de la leishmaniosis visceral en la comunidad indígena Zenu de San Andrés de Sotavento, Córdoba: primer paso para su control. Revista Colombiana de Entomología. 1995; 21: 111-2. <br />8. Sanchis MC, Martín J, Amate P, Acedo C, Miras N, Mostpha L, et al. Estudio epidemiológico de la leishmaniosis en Almería, España. Pharmaceutica. 1997;38:53-61. <br />9. Silva ES, Gantijo CM, Santos SG, Amorin VD, Lemos FL, Primes C, et al. Visceral leishmaniasis in Riberao das Neves, Municipality of Metropolitan region of Belo Horizonte, MG, Brasil. Mem Inst Oswaldo Cruz. 1998;93:138-9. <br />10. Sandoval MC, Gutiérrez R, Cárdenas R, Ferro C. Especies de género Lutzomyia (Psycodidea, Phlebotominae) en áreas de transmisión de leishmaniasis tegumentaria y visceral en el departamento de Santander, en la cordillera oriental de los Andes colombianos. Biomédica. 2006;26(Suppl.1): 218-27. <br />11. Perruolo G. Aspectos ecológicos de Lutzomyia spp. (Diptera: Psychodidea) en un foco endémico de leishmaniasis cutánea en el Estado Tachira, Venezuela. Bol Dir Malariol Saneam Amb. 2004;44:35-44. <br />12. Bejarano EE. Lista actualizada de los psicódidos (Diptera: Psychodidae) de Colombia. Folia Entomológica Mexicana. 2006;45:47-56. <br />13. Santamaría E, Ponce N, Zipa,Y Ferro C. Presencia en el peridomicilio de vectores infectados con Leishmania (Viannia) panamensis en dos focos endémicos en el occidente de Boyacá, piedemonte del valle del Magdalena medio, Colombia. Biomédica. 2006;26(Suppl.1):82-94. <br />14. Cortés LA. Foco de leishmaniasis en El Hobo, municipio de El Carmen de Bolívar, Bolívar, Colombia. Biomédica. 2006;26(Suppl.1):236-41.<br />15. Flórez M, Martínez J, Gutiérrez R, Luna K, Serrano VH, Ferro C, et al. Lutzomyia longipalpis (Diptera: Psychodidea) en un foco suburbano de leishmaniosis visceral en el Cañón del Chicamocha en Santander Colombia. Biomédica. 2006;26(Suppl.1):19-20. <br />16. Sandoval CM, Angulo VM, Gutiérrez R. Muñoz G, Ferro C. Especies de Lutzomyia (Diptera: Psychodidae) posibles vectores de leishmaniasis en la ciudad de Bucaramanga, Santander, Colombia. Biomédica. 1998;18:161-8. <br />17. Montoya J, Ferro C. Flebótomos (Diptera:Psychodidae) de Colombia. En: Amat G, Andrade MG, Fernández F, editores. Insectos de Colombia. Volumen II. Colección Jorge Álvarez Lleras No. 13. Academia Colombiana de Ciencias Exactas, Físicas y Naturales. Santa Fe de Bogota: Centro Editorial Javeriano; 1999. p. 211-45. <br />18. Traviezo LE. Flebotomofauna al sureste del estado Lara, Venezuela. Biomédica. 2006;26(Suppl.1):73-81. <br />19. Zeledón R, Murillo J, Gutiérrez H. Flebótomos antropofílicos y leishmaniasis cutánea en Costa Rica. Bol Of Sanit Panam. 1985;99:163-72. <br />20. Bejarano EE, Uribe S, Rojas W, Vélez ID. Phlebotomine sand flies (Diptera: Psychodidae) associated with the appearance of urban leishmaniasis in the city of Sincelejo, Colombia. Mem Inst Oswaldo Cruz. 2002;97: 645-7. <br />21. Adier GH, Becerra MT, Travi BL. Feeding success of Lutzomyia evansi (Diptera: Psychodidae) experimentally exposed to small mammal hosts in an endemic focus of Lehismania chagasi in northern Colombia. Biomédica. 2003;23:396-400. <br />22. Travi BL, Montoya J, Gallego J, Jaramillo C, Llano R, Vélez ID. Bionomics of Lutzomyia evansi (Diptera: Psychodidae), vector of visceral leishmaniasis in northern Colombia. J Med Entomol. 1996;33:278-85. <br />23. Gallego JL, Vélez ID. Presencia en Isla Fuerte, Bolívar, de Lutzomyia evansi, vector de leishmaniasis visceral. Iatreia. 1994;7:33-5. <br />24. Lozano RE, Ortega EM. Datos preliminares sobre el ciclo nictimeral de Phlebotomus perniciosus Newstead, 1991 y Phlebotomus sergenti Parrot,1917 (Díptera, Ppsychodidae). Anales de Biología. 2001;23:9-17. <br />25. Wolf M, Sierra D, Murcia LM, Vélez IB. Phlebotominae fauna (Diptera: Psychodidae) in the Department of Amazonas, Colombia. Neotrop Entomol. 2003;32:523-6 <br />26. Salomón OD, Rossi GC, Cousiño B, Spinelli GR, Rojas A, López DG, Ortiz A. Phlebotominae sand flies in Paraguay. Abundance distribution in the Southeastern región. Mem Inst Oswaldo Cruz. 2003;98:185-90. <br />27. Martínez E, Romero E, Gallego E. Estudio comparado de la antropofilia y el fototropismo de los flebótomos en un foco de leishmaniasis del sureste de la Península Ibérica. Parassitologia. 1991;33(Suppl.1):413-9. <br />28. Petersona AT, Shaw J. Lutzomyia vectors for cutaneous leishmaniasis in Southern Brazil: ecological niche models, predicted geographic distributions, and climate change effects. Int J Parasitol. 2003;33:19-31. <br />29. Salomón OD, Rossi GC, Cousiño B, Spinelli GR. Ecological aspects of Phebotomine (Diptera, Psychodidae) in an endemic area of tegumentary leishmaniasis in the Northeastern Argentina, 1993-1998. Mem Inst Oswaldo Cruz. 2002;97:163-8. <br />
oai:oai.revistabiomedica.org:article/83
2016-11-22T10:33:02Z
biomedica:NOTA
Isolate of Encephalitozoon intestinalis from stools of a Colombian patient with AIDS
Primer aislamiento de Encephalitozoon intestinalis a partir de muestra de materia fecal de un paciente colombiano con sida
Galván, Ana Luz
Bedoya, Katherine
Montoya, Martha Nelly
Botero, Jorge
Encephalitozoon
microsporidiosis
síndrome de inmunodeficiencia adquirida
aislamiento de pacientes
células cultivadas
heces
Acquired immunodeficiency sindrome
microsporidiosis
patient isolate
diarrhea
cell cultures
feces
Introduction. Microsporidia are obligate intracellular parasites that are recognized as important opportunistic pathogens of immunocompromised and transplanted patients. Enterocytozoon bieneusi and, less frequently, Encephalitozoon intestinalis are the most prevalent species in humans; both of them are associated with enteric infections. Cell cultures have been useful in the study of microsporidia biology. In Colombia, however, no isolates of microsporidia from patients with AIDS have been obtained. Objective. A cell culture of intestinal microsporidia was established from stools of positive patients in order to isolate a native strain. Materials and methods. Stool from a single AIDS patient was concentrated with the water-ether technique, and the sediment was treated with a mixture of antibiotics and antifungal agents for 18 hours at 37o C. Vero cells were cultivated in 24-well plates with Gibco® RPMI medium supplemented with 10% bovine fetal serum and antibiotics. The culture was subsequently inoculated with previously concentrated spores. The medium was changed every second day and the presence of spores was evaluated with the Quick Hot Gram chromotrope stain. Results. Two weeks post-infection, microsporidial spores were identified with characteristic morphology and staining properties. PCR results showed that Encephalitozoon intestinalis was the isolated species. Conclusions. A cell culture of microsporidia was established from a stool sample. This protocol is important to isolate and maintain additional native Colombian strains and it will contribute to biochemical, immunological and epidemiological studies of the currently established strain.
Introducción. Los microsporidios son agentes de infecciones oportunistas en pacientes con sida y con trasplantes, principalmente. Enterocytozoon bieneusi y Encephalitozoon intestinalis son los más frecuentes, asociados con infecciones entéricas. Los cultivos celulares han contribuido al conocimiento de los microsporidios. En Colombia no se han obtenido aislamientos provenientes de pacientes con microsporidiosis y, por consiguiente, no existen cepas autóctonas de los mismos. Objetivo. Establecer el cultivo celular de microsporidios intestinales a partir de materia fecal de pacientes parasitados. Materiales y métodos. Se realizó concentración agua-éter de la materia fecal positiva para microsporidios y el sedimento resultante se trató con una mezcla de antibióticos y antimicóticos durante 18 horas a 37 oC. Se inocularon células Vero previamente cultivadas en placas de 24 pozos y en medio RPMI con suplemento de suero bovino fetal al 10% y antibióticos, con las esporas concentradas. Los cultivos se mantuvieron a 37 oC al 5% de CO2. Se cambió de medio cada dos días y se evaluó la presencia de esporas en los sobrenadantes mediante Gram-cromótropo rápido en caliente. Resultados. En la segunda semana después de la infección, se encontraron esporas de microsporidios con morfología y coloración características. Mediante PCR se determinó que el microsporidio encontrado correspondía a la especie E. intestinalis. Conclusión. Se estableció el cultivo in vitro de microsporidios de materia fecal. Este protocolo es importante para la obtención y el mantenimiento de cepas autóctonas en Colombia, y contribuirá a las investigaciones de aspectos bioquímicos, inmunológicos y epidemiológicos de dichas cepas.
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/83
10.7705/biomedica.v28i3.83
Biomedica; Vol. 28 No. 3 (2008); 441-447
Biomédica; Vol. 28 Núm. 3 (2008); 441-447
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/83/82
/*ref*/Sprague VV, Becnel JJ. Note on the name-author-date combination for the taxon Microsporidies Balbiani, 1882, when ranked as Phylum. J Invertebr Pathol. 1998;71:91-4. <br />2. Franzen C, Müller A. Microsporidiosis: human diseases and diagnosis. Microbes Infect. 2001;3:389-400. <br />3. Mathis A, Weber R, Deplazes P. Zoonotic potential of the microsporidia. Clin Microbiol Rev. 2005;18:423-45. <br />4. Franzen C, Müller A. Molecular techniques for detection, species differentiation, and phylogenetic analysis of microsporidia. Clin Microbiol Rev. 1999;12:243-85. <br />5. Wasson K, Peper RL. Mammalian microsporidiosis. Vet Pathol. 2000;37:113-28. <br />6. Didier S. Microsporidiosis: An emerging and opportunistic infection in humans and animals. Acta Trop. 2005;94:61-76. <br />7. Kotler DP, Orenstein JM. Prevalence of intestinal microsporidiosis in HIV-infected individuals referred for gastroenterological evaluation. Am J Gastroenterol. 1994;8:1998-2002. <br />8. Gamboa Domínguez A, Bencosme Vinas C, Kato Maeda M. Microsporidiasis in AIDS patients with chronic diarrhea. Experiences at the National Institute of Nutrition "Salvador Zubriran". Rev Gastroenterol Mex. 1999;64: 70-4. <br />9. Brasil P, de Lima DB, de Paiva DD, Lobo MS, Sodre FC, Silva SP, et al. Clinical and diagnostic aspects of intestinal microsporidiosis in HIV-infected patients with chronic diarrhea in Rio de Janeiro, Brazil. Rev Inst Med Trop Sao Paulo. 2000;42:299-304. <br />10. Flórez AC, García DA, Moncada LI, Beltrán M. Prevalencia de microsporidios y otros parásitos intestinales en pacientes con infección por VIH, Bogotá, 2001. Biomédica. 2003;23:274-82. <br />11. Botero J, Montoya MN, Agudelo S, Vanegas AL, Diaz A, Bornay FJ, et al. Frecuencia de microsporidiosis intestinal en pacientes VIH positivos determinada mediante las técnicas de quick-hot gram chromotropo y PCR. Biomédica. 2004;24:375-84. <br />12. Visvesvara GS. Microsporidia: in vitro cultivation of microsporidia of clinical importance. Clin Microbiol Rev. 2002;15:401-13. <br />13. Del Aguila C, Croppo GP, Moura H, da silva AJ, Leitch GJ, Moss DM, et al. Ultrastructure, immunofluorescence, western blot, and PCR analysis of eight isolates of Encephalitozoon (septata) intestinalis established in culture from sputum and urine samples and duodenal aspirates of five patients with AIDS. J Clin Microbiol. 1998;36:1201-8. <br />14. van Gool T, Canning EU, Gilis H, van den Bergh Weerman MA, Eeftinck Schattenkerk JK, Dankert J. Septata intestinalis frequently isolated from stool of AIDS patients with a new cultivation method. Parasitology. 1994;109:281-9. <br />15. Visvesvara GS, da Silva AJ, Croppo GP, Pieniazek NJ, Leitch GJ, Ferguson D, et al. In vitro culture and serologic and molecular identification of Septata intestinalis isolated from urine of a patient with AIDS. J Clin Microbiol. 1995;33:930-6. <br />16. da Silva AJ, Schwartz DA, Visvesvara GS, de Moura H, Slemenda SB, Pieniazek NJ. Sensitive PCR diagnosis of infections by Enterocytozoon bieneusi (microsporidia) using primers based on the region coding for small-subunit rRNA. J Clin Microbiol. 1996;34:986-7.
oai:oai.revistabiomedica.org:article/85
2016-11-22T10:33:02Z
biomedica:NOTA
Construction of an adenoassociated, viral derived, expression vector to correct the genetic defect in Morquio A disease
Construcción de un vector de expresión derivado de virus adenoasociados para corregir in vitro el defecto genético de la enfermedad de Morquio A
Barrera, Luis Alejandro
Gutiérrez, Mónica A.
García Vallejo, Felipe
Tomatsu, Shunji
Cerón, Flavio
Alméciga Díaz, Carlos J.
Domínguez, Martha C.
mucopolisacaridosis IV A [genética]
dependovirus
terapia de gen
técnicas de transferencia de gen
cultivo de virus
técnicas de cultivo
Mucopolysaccharidosis IV [genetics]
dependovirus
gene therapy
gene transfer techniques
virus cultivation
culture techniques
Introduction. Mucopolysaccharidosis IVA (Morquio A) is caused by a deficiency of N-acetylgalactosamine-6-sulphate-sulphatase, a lysosomal enzyme required for the stepwise degradation of keratan-sulfate and chondroitin-6-sulfate. A deficiency in this enzyme results in an accumulation of glycosaminoglycans in several tissues. Currently, no effective therapies exist and only supportive measures are used to treat some manifestations of the disease. An ideal therapy is one that can be administrated early in life, has low mortality, and leads to long-term expression of the enzyme. Gene therapy emerges as a potential alternative to correct the genetic defect in MPS IVA. Objective. Adenoassociated virus-derived expression vectors (AAV) were constructed to correct in vitro the enzyme deficiency in mucopolysaccharidosis IVA. Materials and methods. Adenoasociated virus-derived vectors containing the human GALNS gene and driven by the citomegalivirus immedited-early promoter were constructed using a free-adenoviral protocol. HEK293 cells and human skin Morquio A fibroblasts were transfected with the recombinat vectors. Enzyme activity was measured in cells 24 and 48 hours post-transfection. Results. Free-adenovirus recombinant AAV vectors were obtained with titres up to 2.08x1010 capsids/mL. HEK293 cells and Morquio A fibroblasts transfected with vectors showed GALNS activity up to 3.05 nmoles/mg/h 48 hours post-transfection. Conclusion. The AAV mediated the in vitro expression of GALNS enzyme in the transfected cells. These results are the first step towards a gene therapy alternative to Morquio A disease using adenoassociated virus-derived vectors.
Introducción. La mucopolisacaridosis IV A (Morquio A) es una enfermedad de depósito lisosómico causada por la deficiencia en la actividad de la enzima N-acetil-galactosamina- 6-sulfato-sulfatasa que produce la acumulación intralisosómica de queratán y condroitín-6-sulfato. Hasta el momento, su manejo es paliativo, por lo que las investigaciones se han enfocado en establecer una terapia que pueda aplicarse tempranamente y garantice la expresión estable de la enzima. En este sentido, la terapia génica se presenta como una de las potenciales alternativas terapéuticas para corregir el defecto genético en la mucopolisacaridosis IV A. Objetivo. Construir vectores de expresión derivados de virus adenoasociados para corregir in vitro la deficiencia enzimática en la mucopolisacaridosis IV A. Materiales y métodos. Se produjeron vectores derivados de virus adenoasociados que portaban el gen humano de la enzima N-acetil-galactosamina-6-sulfato-sulfatasa dirigido por el promotor temprano del citomegalovirus humano, empleando un sistema libre de adenovirus. Se transfectaron células HEK293 y fibroblastos humanos Morquio A con los virus recombinantes, y se determinó la actividad enzimática en el lisado celular a las 24 y 48 horas después de la transfección. Resultados. Se obtuvieron virus adenoasociados recombinantes, libres de adenovirus, con títulos hasta de 2,08 x 1010 cápsides/ml. Tanto en células HEK293 como en fibroblastos Morquio A transfectados, se obtuvieron actividades enzimáticas hasta de 3,05 nmoles/mg por hora, 48 horas después de la transfección. Conclusión. Los virus recombinantes producidos expresaron in vitro la enzima GALNS en las células transfectadas. Estos resultados constituyen el paso inicial para el desarrollo de una terapia génica para la enfermedad de Morquio A empleando vectores derivados de virus adenoasociados.
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/85
10.7705/biomedica.v28i3.85
Biomedica; Vol. 28 No. 3 (2008); 448-459
Biomédica; Vol. 28 Núm. 3 (2008); 448-459
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/85/83
/*ref*/Neufeld E, Muenzer J. The mucopolysaccharidosis. En: Scriver C, Beaudet A, Sly W, Valle D, editores. The metabolic and molecular bases of inherited diseases. New York: McGraw-Hill; 2001. p. 3421-52. <br />2. Montaño AM, Tomatsu S, Gottesman G, Smith M, Orii T. International Morquio A registry: Clinical manifestation and natural course of Morquio A disease. J Inherit Metab Dis. 2007;30:165-74. <br />3. Tomatsu S, Montaño A, Nishioka T, Gutiérrez M, Peña O, Trandafirescu G, et al. Mutation and polymorphism spectrum of the GALNS gene in mucopolysaccharidosis IVA (Morquio A). Hum Mutat. 2005;26:500-12. <br />4. Northover H, Cowie RA, Wraith JE. Mucopoly-saccharidosis type IVA (Morquio syndrome): a clinical review. J Inherit Metab Dis. 1996;19:357-65. <br />5. Cheng SH, Smith AE. Gene therapy progress and prospects: gene therapy of lysosomal storage disorders. Gene Ther. 2003;10:1275-81. <br />6. Tomatsu S, Fukuda M, Masue K, Sukegawa T, Fukao A, Yamagishi T, et al. Morquio disease: isolation, characterization and expression of full-length cDNA for human N-acetylgalactosamine-6-sulfate sulfatase. Biochem Biophys Res Commun. 1991;181:677-83. <br />7. Cooper D, Ball E, Stenson P, Phillips A, Howells K, Mort M. The Human Gene Mutation Data Base at the Institute of Medical Genetics in Cardiff. Consultado: los autores deben colocar la fecha de consulta. Disponible en: http://www.hgmd.cf.ac.uk. <br />8. Kato Z, Fukuda S, Tomatsu S, Vega H, Yasunaga T, Yamahishi A, et al. A Novel Common Missense Mutation G301C in the N-Acetylgalactosamine-6-sulfate Sulfatase Gene in Mucopolysaccharidosis IVA. Hum Genet. 1997;101:97-101. <br />9. Bernal J, Briceño I. Genetic and other diseases in the pottery of Tumaco-La Tolita culture in Colombia-Ecuador. Clin Genet. 2006;70:188-91. <br />10. Herzog RW, Hagstrom JN, Kung SH, Tai SJ, Wilson JM, Fisher KJ, et al. Stable gene transfer and expression of human blood coagulation factor IX after intramuscular injection of recombinant adeno-associated virus. Proc Natl Acad Sci U S A. 1997;94:5804-9. <br />11. Snyder RO, Miao CH, Patijn GA, Spratt SK, Danos O, Nagy D, et al. Persistent and therapeutic concentrations of human factor IX in mice after hepatic gene transfer of recombinant AAV vectors. Nat Genet. 1997;16:270-6. <br />12. Rutledge EA, Russell DW. Adeno-associated virus vector integration junctions. J Virol. 1997;71:8429-36. <br />13. Xiao W, Berta SC, Lu MM, Moscioni AD, Tazelaar J, Wilson JM. Adeno-associated virus as a vector for liver-directed gene therapy. J Virol. 1998;72:10222-6. <br />14. Xiao X, Li J, Samulski R. Production of high-titer recombinant adeno-associated virus vectors in the absence of helper adenovirus. J Virol. 1998;72:2224-32. <br />15. Fisher KJ, Kelley WM, Burda JF, Wilson JM. A novel adenovirus-adeno-associated virus hybrid vector that displays efficient rescue and delivery of the AAV genome. Hum Gene Ther. 1996;7:2079-87. <br />16. Vincent KA, Piraino ST, Wadsworth SC. Analysis of recombinant adeno-associated virus packaging and requirements for rep and cap gene products. J Virol. 1997;71:1897-905. <br />17. Samulski RJ, Chang LS, Shenk T. Helper-free stocks of recombinant adeno-associated viruses: normal integration does not require viral gene expression. J Virol. 1989;63:3822-8. <br />18. Sands M, Davidson B. Gene therapy for lysosomal storage diseases. Mol Ther. 2006;13:839-49. <br />19. Daly TM, Vogler C, Levy B, Haskins ME, Sands MS. Neonatal gene transfer leads to widespread correction of pathology in a murine model of lysosomal storage disease. Proc Natl Acad Sci USA. 1999;96:2296-300. <br />20. McEachern K, Nietupski J, Chuang W, Armentano D, Johnson J, Hutto E, et al. AAV8-mediated expression of glucocerebrosidase ameliorates the storage pathology in the visceral organs of a mouse model of Gaucher disease. J Gene Med. 2006;8:719-29. <br />21. Daly TM, Ohlemiller KK, Roberts MS, Vogler CA, Sands MS. Prevention of systemic clinical disease in MPS VII mice following AAV-mediated neonatal gene transfer. Gene Ther. 2001;8:1291-8. <br />22. Fraites TJ Jr, Schleissing MR, Shanely RA, Walter GA, Cloutier DA, Zolotukhin I, et al. Correction of the enzymatic and functional deficits in a model of Pompe disease using adeno-associated virus vectors. Mol Ther. 2002;5:571-8. <br />23. Park J, Murray GJ, Limaye A, Quirk JM, Gelderman MP, Brady RO, et al. Long-term correction of globotriaosylceramide storage in Fabry mice by recombinant adeno-associated virus-mediated gene transfer. Proc Natl Acad Sci USA. 2003;100:3450-4. <br />24. Hennig AK, Ogilvie JM, Ohlemiller KK, Timmers AM, Hauswirth WW, Sands MS. AAV-mediated intravitreal gene therapy reduces lysosomal storage in the retinal pigmented epithelium and improves retinal function in adult MPS VII mice. Mol Ther. 2004;10:106-116. <br />25. Daly TM, Okuyama T, Vogler C, Haskins ME, Muzyczka N, Sands MS. Neonatal intramuscular injection with recombinant adeno-associated virus results in prolonged beta-glucuronidase expression in situ and correction of liver pathology inmucopolysa-ccharidosis type VII mice. Hum Gene Ther. 1999;10: 85-94. <br />26. Ponder K, Haskins M. Gene therapy for muco- polysaccharidosis. Expert Opin Biol Ther. 2007;7: 1333-45. <br />27. Miwa K, Matsui K, Terabe M, Ito K, Ishida M, Takagi H, et al. Construction of novel shuttle vectors and a cosmid vector for the glutamic acid-producing bacteria Brevibacterium lactofermentum and Corynebacterium glutamicum. Gene. 1985;39:281-6. <br />28. Grimm D, Kern A, Pawlita M, Ferrari F, Samulski R, Kleinschmidtl J. Titration of AAV-2 particles via a novel capsid ELISA: packaging of genomes can limit production of recombinant AAV-2. Gene Ther. 1999; 6: 1322-30. <br />29. Russell DW, Alexander IE, Miller AD. DNA synthesis and topoisomerase inhibitors increase transduction by adeno-associated virus vectors. Proc Natl Acad Sci USA. 1995;92:5719-23. <br />30. vanDiggelen O, Zhao H, Kleijer W, Janse H, Poorthuis B, Pelt JV, et al. A fluorometric enzyme assay for the diagnosis of Morquio type A. Clin Chem Acta. 1990;187:131-40. <br />31. Barrera L, Gutierrez M, Ceron F, Garcia L. Evaluation of an episomal expression construct containing the cDNA of iduronate sulfatase in (IDS) in fibroblasts from a patient with hunter syndrome. J Inherit Metab Dis. 2002;25(Suppl.1):160. <br />32. Zolotukhin S. Production of recombinant adeno-associated virus vectors. Hum Gene Ther. 2005; 16: 551-7. <br />33. Zolotukhin S, Byrne B, Mason E, Zolotukhin I, Potter M, Chesnut K, et al. Recombinant adeno-associated virus purification using novel methods improves infectious titer and yield. Gene Ther. 1999;6:973-85. <br />34. Aucoin MG, Perrier M, Kamen AA. Critical assessment of current adeno-associated viral vector production and quantification methods. Biotechnol Adv. 2008;26:73-88. <br />35. Okoyama H, Chen C. Calcium phosphate mediated gene transfer into established cell lines. En: Murray EJ, editor. Methods in molecular biology: Gene transfer and expression protocols. Clifton: The Humana Press; 1991. p. 15-20. <br />36. Lu Y. Recombinant adeno-associated virus as delivery vector for gene therapy-a review. Stem Cells Dev. 2004;13:133-45. <br />37. Ward P, Clément N, Linden M. cis effects in adeno-associated virus type 2 replication. J Virol. 2007;81: 9976-89. <br />38. Summerford C, Samulski RJ. Membrane-associated heparan sulfate proteoglycan is a receptor for adeno-associated virus type 2 virions. J Virol. 1998;72:1438-45. <br />39. Wu Z, Asokan A, Samulski R. Adeno-associated virus srotypes: vector toolkit for human gene therapy. Mol Ther. 2006;14:316-27. <br />40. Toietta G, Severini G, Traversari C, Tomatsu S, Sukegawa K, Fukuda S, et al. Various cells retrovirally transduced with N-acetylgalactosoamine-6-sulfate sulfatase correct Morquio skin fibroblasts in vitro. Hum Gene Ther. 2001;12:2007-16. <br />41. Hacein-Bey-Abina S, von Kalle C, Schmidt M, Le Deist F, Wulffraat N, McIntyre E, et al. A serious adverse event after successful gene therapy for X-linked severe combined immunodeficiency. N Engl J Med. 2003;348:255-6. <br />42. Lewinski MK, Bushman FD. Retroviral DNA integration-mechanism and consequences. Adv Genet. 2005;55:147-81. <br />43. Landgrebe J, Dierks T, Schamidt B, Figura Kv. The human SUMF1 gene, required for posttranslational sulfatase modification, defines a new gene family which is conserved from pro- to eukaryotes. Gene. 2003;316:47-56. <br />44. Cosma M, Pepe P, Annunziata I, Newbold R, Grompe M, Parenti G, et al. The multiple sulfatase deficiency gene encodes an essential and limiting factor for the activity of sulfatases. Cell. 2003;113:445-56.
oai:oai.revistabiomedica.org:article/86
2016-11-22T10:33:02Z
biomedica:INME
Jaime Eduardo Ortiz Varón
biomedica, biomedica
Instituto Nacional de Salud
2008-09-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/86
10.7705/biomedica.v28i3.86
Biomedica; Vol. 28 No. 3 (2008); 461
Biomédica; Vol. 28 Núm. 3 (2008); 461
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/86/84
oai:oai.revistabiomedica.org:article/87
2010-01-16T13:29:25Z
biomedica:EDIT
El Plan Nacional de Salud Pública: tesis, antítesis, síntesis
Segura, Omar
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/87
10.7705/biomedica.v28i2.87
Biomedica; Vol. 28 No. 2 (2008); 177-180
Biomédica; Vol. 28 Núm. 2 (2008); 177-180
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/87/85
oai:oai.revistabiomedica.org:article/88
2010-01-16T13:29:25Z
biomedica:EDUC
Haga usted el diagnóstico Primera parte
Knudson, Ángelica
Motta, Adriana
Sopó, Leticia
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
250
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/88
10.7705/biomedica.v28i2.88
Biomedica; Vol. 28 No. 2 (2008); 181-182
Biomédica; Vol. 28 Núm. 2 (2008); 181-182
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/88/86
oai:oai.revistabiomedica.org:article/89
2010-01-26T00:47:42Z
biomedica:CASO
Biopercular syndrome: report of two cases and literature review
Síndrome biopercular: presentación de dos casos y revisión de la literatura
Uribe, Carlos Santiago
Millán, Paula Andrea
Montes, María Isabel
Cabrera, Dagoberto
Arboleda, Alejandra
infarto cerebral
parálisis seudobulbar
retraso mental
trastornos de la deglución
trastornos del lenguaje
cerebral infarction
pseudobulbar palsy
mental retardation
deglutition disorders
language disorders
The anterior opercular or biopercular syndrome is a cortical pseudobulbar palsy due to bilateral lesions of the anterior brain operculum. It is characterized by preservation of reflex function and automatic activity, without mental impairment. Two cases are reported herein and the relevant literature reviewed.The first case was a 73-year-old female with a history of a stroke occurring seven years previously, without sequelae in the interim. She presented with sudden loss of consciousness. The neurological examination showed a right facial central palsy and anarthria, with reflex acts such as smiling, blinking and yawning, not elicited by commands; she also had a right hemiparesis and walking impairment. A brain CT scan showed an old ischemic infarction in the region of the right medial cerebral artery. Because the right motor involvement did not correlate with the findings of the initial CT scan, another CT scan two days later showed an acute brain infarction in the vicinity of the left medial cerebral artery.The second case was an 8-year-old girl with mental retardation and impairment of verbal development, caused by of biopercular pachygyria. Facio-pharyngo-glosso-masticatory diplegia and volitional selective palsy of the oro-facial muscles was seen in both patients. The neuropsychological assessment showed cognitive, emotional and social interaction impairment in both cases -as part of the frontal convexity syndrome in the first case and of mental retardation in the second. The two patients had difficulty in mastication and swallowing. The prognosis for recovery of verbal capacity is poor, although generally most patients recover the ability to swallow.
El síndrome biopercular es una parálisis pseudobulbar cortical causada por lesiones bilaterales que comprometen el opérculo cerebral anterior. Se caracteriza por preservación de la función refleja y de la actividad automática, sin deterioro mental. Se presentan dos casos clínicos y se hace una revisión de la literatura.Caso 1. Se trata de una mujer de 73 años de edad con antecedentes de enfermedad cerebrovascular hace siete años sin secuelas. Presentó pérdida súbita del conocimiento y en el examen neurológico se le encontró paresia facial central derecha y anartria, con actos reflejos como sonreír, parpadear y bostezar –los cuales no se producían al mandato–, hemiparesia derecha e imposibilidad para la marcha.En la tomografía cerebral se encontraron signos de lesión isquémica antigua en el territorio de la arteria cerebral media derecha. Por el compromiso motor derecho, que no se correlacionaba con los hallazgos de la imagen inicial, se solicitó nueva tomografía, en la que se evidenció infarto agudo en territorio de la arteria cerebral media izquierda.Caso 2. Se trata de una niña de ocho años con retardo mental y trastorno en el desarrollo del lenguaje verbal por paquigiria biopercular.Las pacientes presentan diplejía facio-faringo-gloso-masticatoria y parálisis volitiva selectiva de músculos oro-faciales. La evaluación neuropsicológica evidenció compromiso cognitivo, emocional y de la interacción social como parte de un síndrome de la convexidad frontal en el primer caso y, de retardo mental, en el segundo caso. La fonoaudiología demostró que las dos pacientes tenían dificultades en el proceso de masticación y deglución, y dificultades graves en el lenguaje verbal. El pronóstico de recuperación del lenguaje verbal es pobre, pero muchos pacientes pueden recuperar la deglución.
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/89
10.7705/biomedica.v28i2.89
Biomedica; Vol. 28 No. 2 (2008); 183-190
Biomédica; Vol. 28 Núm. 2 (2008); 183-190
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/89/87
/*ref*/ Foix C, Chavany JA, Marie J. Diplégie facio-linguo-masticatrice dorigine cortico-sous-corticale sans paralysie des membres. Rev Neurol (Paris). 1926;33: 214-9. <br />2. De Smet Y. The anterior operculum syndrome. J Neurol. 1994;241:570-1. <br />3. Mao CC, Coull BM, Golper LA, Rau MT. Anterior operculum syndrome. Neurology. 1989;39:1169-72. <br />4. Bakar M, Kirshner HS, Niaz F. The opercular-subopercular syndrome: four cases with review of the literature. Behav Neurol. 1998;11:97-103. <br />5. Pineda DA, Mejía SE, Rosselli M, Ardila A, Romero MG, Pérez C. Variabilidad en la prueba de Boston para el diagnóstico de las afasias en adultos laboralmente activos. Rev Neurol. 1998;26:962-70. <br />6. Godefroy O. Frontal syndrome and disorders of executive functions. J Neurol. 2003;250:1-6<br />7. Trimble MR. Behavior and personality disturbances. En: Bradley WG, Bradley WG, Daroff RB, Fenichel GM, editors. Neurology in Clinical Practice. Boston: Butterworth-Heinemann; 1991. p. 81-100. <br />8. Bruyn GW, Gathier JC. The operculum syndrome. Handbook of Clinical Neurology. En: Vinken PJ, Bruyn GW, editors. Localization in clinical neurology. Vol. 2. Amsterdam: North Holland Publishing; 1969. p. 776-87. <br />9. Christen HJ, Hanefald F, Kruse E, Imhauser S, Ernst JP, Finkenstaedt M. Foix-Chavany-Marie (anterior operculum) syndrome in childhood: a reappraisal of Worster-Drought syndrome. Dev Med Child Neurol. 2000;42:122-32. <br />10. Kuzniecky R, Andermann F, Guerrini R. Congenital bilateral perisylvian syndrome: study of 31 patients. The CBPS Multicenter Collaborative Study. Lancet. 1993;341:608-12. <br />11. Gropman AL, Barkovich AJ, Vezina LG, Conry JA, Dubovsky EC, Packer RJ. Pediatric congenital bilateral perisylvian syndrome: clinical and MRI feature in 12 patients. Neuropediatrics. 1997;28:198-203. <br />12. Puertas I, García-Soldevilla M, Jiménez FJ, Cabrera F, Jabbour T, García E. Mano distónica bilateral secundaria a síndrome biopercular o síndrome de Foix-Chavany-Marie. Rev Neurol. 2002;35:430-3. <br />13. Bara-Jiménez W, Shelton P, Sanger TD, Hallett M. Sensory discrimination capabilities in patients with focal hand dystonia. Ann Neurol. 2000;47:377-80. <br />14. Santos S, Casadevall T, Ríos C, López-García E, Tejero C, Garcés-Redondo M, et al. Síndrome opercular de etiología vascular. Rev Neurol. 2002;34:1129-32. <br />15. Wolf RW, Schultze D, Fretz C, Weissert M, Waibel P. Atypical herpes simplex encephalitis presenting as operculum syndrome. Pediatr Radiol. 1999;29:191-3. <br />16. Van der Poel JC, Haenggeli CA, Overweg-Plansoen. Operculum syndrome: unusual feature of herpes simplex encephalitis. Pediatr Neurol. 1995;12:246-9. <br />17. Moodley M, Bamber S. The Operculum syndrome: an unusual complication of tuberculosis meningitis. Dev Med Child Neurol. 1990;32:919-22. <br />18. Laurent-Vannier A, Fadda G, Laigle P, Dusser A, Leroy-Malherbe V. Syndrome de Foix-Chavany-Marie dorigine traumatique. Rev Neurol (Paris). 1999; 155:387-90. <br />19. Biller J, Asconape J, Challa VR, Toole JF, McLean WT. A case for cerebral thromboangiitis obliterans. Stroke. 1981;12:686-9. <br />20. Alajouanine TH, Boudin G, Pertuiset B, Pépin B. Le syndrome unilatéral de lopercule rolandique avec atteinte contralatérale du territoire des V, VII, IX, X, XI et XII nerfs craniens. Rev Neurol (Paris). 1959;101:168-71. <br />21. Pascual-Castroviejo I, Pascual-Pascual SI. Síndrome opercular tras cirugía cerebral bilateral: presentación de un caso. Rev Neurol. 2004;39:624-7. <br />22. Broussolle E, Bakchine S, Tommasi M, Laurent B, Bazin B, Cinotti L, et al. Slowly progressive anarthria with late anterior opercular syndrome: a variant form of frontal cortical atrophy syndromes. J Neurol Sci. 1996;144:44-58. <br />23. Shevell MI, Carmant L, Meagher-Villemure K. Developmental bilateral perisylvian dysplasia. Pediatr Neurol. 1992;8:299-302.<br />24. Márquez-Belandria G, Rondón-Hernández F, Pascual-Castroviejo I. Síndrome opercular bilateral congénito: presentación de tres casos. Rev Neurol. 2003;36:938-40. <br />25. Gropman AL, Barkovich AJ, Vezina LG, Conry JA, Dubovsky EC, Packer RJ. Pediatric congenital bilateral perisylvian syndrome: clinical and MRI feature in 12 patients. Neuropediatrics. 1997;28:198-203. <br />26. Yamamoto T, Koeda T, Maegaki Y, Tanaka C, Takeshita K. Bilateral opercular syndrome caused by perinatal difficulties. Europ J Paediatr Neurol. 1997;1: 73-7. <br />27. Prats JM, Garaizar C, García-Nieto ML, Madoz P. El síndrome opercular epiléptico: una forma peculiar de epilepsia parcial benigna de la infancia con paroxismos rolándicos. Rev Neurol. 1999;29:375-80. <br />28. Colamaria V, Sgro V, Caraballo R, Simeone M, Zullini E, Fontana E, et al. Status epilepticus in benign rolandic epilepsy manifesting as anterior operculum syndrome. Epilepsia. 1991;32:329-34. <br />29. Pascual-Castroviejo I, Pascual-Pascual SI, Peña W, Talavera M. Status epilepticus-induced brain damage and opercular syndrome in childhood. Dev Med Child Neurol. 1999;41:420-3. <br />30. Besson G, Bogousslavsky J, Maeder P. Acute pseudobulbar or suprabulbar palsy. Arch Neurol. 1991;48:501-7. <br />31. Pineda D, Ardila A. Lasting mutism associated with buccofacial apraxia. Aphasiol. 1992;6:285-92. <br />
oai:oai.revistabiomedica.org:article/90
2010-01-26T13:17:30Z
biomedica:ENSA
Right to die with dignity?
¿Derecho a morir con dignidad?
Ruiz, Álvaro
derecho a morir/ética
bioética
derechos del paciente
negativa del paciente al tratamiento
cuidado terminal
tanatología
right to die/ethics
bioethics
patient rights
treatment refusal
terminal care
thanatology
The right to die with dignity is an ill-defined concept, with multiple, often inappropriate, interpretations. The current proposition is that the physician take full responsibility for protecting the patients rights, for ensuring a rational use of resources and for overseeing the decision-making process such that the information is adequate and the steps proportioned. This responsibility extends not only to the health status of the patient situation, to the patients prognosis, and to his/her expectations and wishes, but also to the benefits foreseen and to the cost-benefit ratio. Emphasis is placed on two aspects of this relationship. First, dignity can be interpreted in many ways and sometimes, in the name of dignity, the patient is exposed (or exposes him/herself) to suffering, pain and complications that can be avoided. Second, when no reasonable probability of survival is present and a better "quality of life" is impossible, efforts are better redirected to offering a better quality of death.
El derecho a morir con dignidad es un concepto vago y que recibe múltiples interpretaciones, muchas de ellas inapropiadas. Se propone la necesidad de que sea el médico quien se haga responsable de proteger los derechos del paciente, de garantizar el uso racional de los recursos y de velar porque las decisiones sean apropiadas y proporcionadas a la situación del paciente, a su pronóstico, expectativas y deseos, pero también, a la utilidad esperada y a la relación costo-beneficio. Se enfatiza que la dignidad puede ser entendida de muchas maneras y que, a veces, en su nombre se somete al paciente, o lo hace él mismo, a sufrimientos, dolor y complicaciones que podrían haberse evitado, no necesariamente en busca de prolongar la vida. Se hace énfasis en que, cuando no hay probabilidades razonables de supervivencia o cuando no puede ya buscarse mejorar la calidad de vida, deben enfocarse los esfuerzos en procurar calidad de muerte.
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/90
10.7705/biomedica.v28i2.90
Biomedica; Vol. 28 No. 2 (2008); 191-194
Biomédica; Vol. 28 Núm. 2 (2008); 191-194
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/90/88
/*ref*/Swarte NB, van der Lee ML, van der Bom JG, van den Bout J, Heintz PM. Effects of euthanasia on the bereaved family and friends: a cross sectional study. BMJ. 2003;327:189. <br />2. Grayling AC. Right to die. BMJ. 2005;330:799. <br />3. Hardwig J. Is there a duty to die? Hastings Cent Rep. 1997;27:34-42. <br />4. Chochinov HM, Hack T, McClement S, Kristjanson L, Harlos M. Dignity in the terminally ill: a developing empirical model. Soc Sci Med. 2002;54:433-43. <br />5. Turner K, Chye R, Aggarwal G, Philip J, Skeels A, Lickiss JN. Dignity in dying: a preliminary study of patients in the last three days of life. J Palliat Care. 1996;12:7-13. <br />6. Mendoza-Vega J. El derecho a morir con dignidad. Biomédica. 2005;25:165-6. <br />7. Macklin R. Dignity is a useless concept. BMJ. 2003;327:1419-20. <br />8. Ashcroft RE. Making sense of dignity. J Med Ethics. 2005;31:679-82. <br />
oai:oai.revistabiomedica.org:article/91
2010-01-26T13:31:03Z
biomedica:ARTI
Gametocytemia in falciparum malaria treated with amodiaquine or artesunate
Gametocitemia en malaria por Plasmodium falciparum tratada con amodiaquina o artesunato
Carmona-Fonseca, Jaime
Arango, Eliana
Blair, Silvia
malaria/ terapia
malaria falciparum
Plasmodium falciparum
antipalúdicos
amodiaquina
sulfadoxina
pirimetamina
Artemisia annua
malaria/ therapy
malaria
falciparum
Plasmodium falciparum
antimalarials
amodiaquine
sulfadoxine
pyrimethamine
Artemisia annua
Introduction. Antimalarial treatment effects on Plasmodium falciparum gametocytemia has been the focus of few studies in the Americas.Objective. Relationships are described that occur between falciparum gametocytemia and the treatment with amodiaquine-sulfadoxine-pyrimethamine, artesunate-sulfadoxine-pyrimethamine or amodiaquine-artesunate.Materials and methods. The experimental design consisted of a randomized selection of patients not balanced or blinded. A total of 241 patients were evaluated, residents of Turbo, El Bagre and Zaragoza (Antioquia, Colombia).The follow up occurred 21-28 days after antimalarial treatment. The World Health Organization (1998) protocol was used.Results. The therapeutic efficacy of amodiaquine-sulfadoxine-pyrimethamine, artesunate-sulfadoxine-pyrimethamine and amodiaquine-artesunate were equal at day 21 of the follow up. Four cases (1.7%) were therapeutic failures. Amodiaquine-sulfadoxine-pyrimethamine was less effective than the artesunate treatments in reducing the gametocyte load. On day 7, none of the three traetments had eliminated completely the gametocytes. Most patients (56.0%) were observed not to have circulating gametocytes pre-treatment and did not develop them later.Conclusion. The three treatment schemes were similar in their therapeutic efficacy and in their incapacity to eliminate gametocytes at day seven.
Introducción. Las relaciones de la gametocitemia de Plasmodium falciparum con el tratamiento antipalúdico han sido poco estudiadas en América.Objetivo. Describir relaciones de la gametocitemia falciparum con el tratamiento con amodiaquina-sulfadoxina-pirimetamina, artesunato-sulfadoxina-pirimetamina o amodiaquina-artesunato.Materiales y métodos. Se usó un diseño experimental, aleatorio, no balanceado, no ciego. El seguimiento fue de 21 a 28 días. La eficacia terapéutica se clasificó según el protocolo de la Organización Mundial de la Salud, 1998.Resultados.Se evaluaron 241 pacientes en Turbo, El Bagre y Zaragoza (Antioquia, Colombia). El esquema de amodiaquina-sulfadoxina-pirimetamina tuvo igual eficacia que el de artesunato-sulfadoxina-pirimetamina y amodiaquina-artesunato para controlar las fallas terapéuticas el día 21. Hubo cuatro fallas (1,66%). El esquema de amodiaquina-sulfadoxina-pirimetamina fue menos eficaz que los tratamientos con artesunato para reducir la presencia de gametocitos. Al séptimo día, ninguno de los tres tratamientos había eliminado totalmente los gametocitos. La mayoría (56%) de nuestros pacientes no tenía gametocitos antes del tratamiento y nunca los desarrolló. El tiempo para eliminar los gametocitos que se tenían al iniciar el tratamiento no fue mayor cuando la gametocitemia inicial era mayor. Conclusión.Los tres tratamientos fueron iguales en cuanto a eficacia terapéutica e incapacidad de eliminar los gametocitos en siete días.
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/91
10.7705/biomedica.v28i2.91
Biomedica; Vol. 28 No. 2 (2008); 195-212
Biomédica; Vol. 28 Núm. 2 (2008); 195-212
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/91/89
/*ref*/Day KP, Hayward RE, Dyer M. The biology of Plasmodium falciparum transmission stages. Parasitology. 1998; 116 ( Suppl.): S95-109. <br />2. Eichner M, Diebner HH, Molineaux L, Collins WE, Jeffery GM, Dietz K. Genesis, sequestration and survival of Plasmodium falciparum gametocytes: parameter estimates from fitting a model to malariatherapy data. Trans R Soc Trop Med Hyg. 2001; 95: 497-501. <br />3. Robert V, Boudin C. Biologie de la transmission homme-moustique du Plasmodium. Bull Soc Pathol Exot. 2003; 96: 6-20. <br />4. Field JW, Shute PG. The microscopic diagnostic of human malaria. In: A morphological study of the erythrocytic parasites. Kuala Lumpur: Government Press; 1956. p. 142. <br />5. Talman AM, Domarle O, McKenzie FE, Ariey F, Robert V. Gametocytogenesis: the puberty of Plasmodium falciparum. Malar J. 2004; 3: 24. <br />6. Rogers NJ, Hall BS, Obiero J, Targett GA, Sutherland CJ. A model for sequestration of the transmission stages of Plasmodium falciparum: adhesion of gametocyte-infected erythrocytes to human bone marrow cells. Infect Immun. 2000; 68: 3455-62. 7. Lensen A, Bril A, van de Vegte M, van Gemert GJ, Eling W, Sauerwein R. Plasmodium falciparum: infectivity of cultured, synchronized gametocytes to mosquitoes. Exp Parasitol. 1999; 91: 101-3. <br />8. Sinden RE, Smalley ME. Gametocytogenesis of Plasmodium falciparum in vitro: the cell-cycle. Parasitology. 1979; 79: 277-96. <br />9. Smalley ME, Sinden RE. Plasmodium falciparum gametocytes their longevity and infectivity. Parasitology. 1977; 74: 1-8. <br />10. Drakeley C, Sutherland C, Bousema JT, Sauerwein RW, Targett GA. The epidemiology of Plasmodium falciparum gametocytes: weapons of mass dispersion. Trends Parasitol. 2006; 22: 424-30. <br />11. Carter R, Miller LH. Evidence for environmental modulation of gametocytogenesis in Plasmodium falciparum in continuous culture. Bull World Health Organ. 1979; 57 ( Suppl.1): 37-52. <br />12. Dyer M, Day KP. Commitment to gametocytogenesis in Plasmodium falciparum. Parasitol Today. 2000; 16: 102-7. <br />13. Targett G, Drakeley C, Jawara M, von Seidlein L, Coleman R, Deen J, et al. Artesunate reduces but does not prevent posttreatment transmission of Plasmodium falciparum to Anopheles gambiae. J Infect Dis. 2001; 83: 1254-9. <br />14. Sowunmi A, Fateye BA. Plasmodium falciparum gametocytaemia in Nigerian children: before, during and after treatment with antimalarial drugs. Trop Med Int Health. 2003; 8: 783-92. <br />15. von Seidlein L, Drakeley C, Greenwood B, Walraven G, Targett G. Risk factors for gametocyte carriage in Gambian children. Am J Trop Med Hyg. 2001; 65: 523-7. <br />16. von Seidlein L, Jawara M, Coleman R, Doherty T, Walraven G, Targett G. Parasitaemia and gametocytaemia after treatment with chloroquine, pyrimethamine/sulfadoxine, and pyrimethamine/sulfadoxine combined with artesunate in young Gambians with uncomplicated malaria. Trop Med Int Health. 2001; 6: 92-8. <br />17. Sutherland CJ, Ord R, Dunyo S, Jawara M, Drakeley CJ, Alexander N, et al. Reduction of malaria transmission to Anopheles mosquitoes with a six-dose regimen of co-artemether. PLoS Med. 2005; 2: e92. <br />18. Hallett RL, Dunyo S, Ord R, Jawara M, Pinder M, Randall A, et al. Chloroquine-sulphadoxine-pyrimethamine for uncomplicated malaria in Gambian children: enhanced transmission to mosquitoes of multi-drug-resistant Plasmodium falciparum. PloS Clin Trials. 2006; 1: e15. <br />19. Contreras-Ochoa C, Ramsey JM. Gametocitos de Plasmodium vivax y Plasmodium falciparum: estadios olvidados en el desarrollo de vacunas. Salud Pública Mex. 2004; 46: 64-70. <br />20. Carmona-Fonseca J. Profilaxis primaria con primaquina para el paludismo. Revisión. Anuario Enfermedades Infecciosas (Medellín). 2004; 2: 51-84. <br />21. Litter M. Compendio de farmacología. Cuarta edición. Buenos Aires: El Ateneo; 1988. p. 794-805. <br />22. Grewal RS. Pharmacology of 8-aminoquinolines. Bull World Health Organ. 1981; 59: 397-406. <br />23. Ponsa N, Sattabongkot J, Kittayapong P, Eikarat N, Coleman RE. Transmission-blocking activity of tafenoquine (WR-238605) and artelinic acid against naturally circulating strains of Plasmodium vivax in Thailand. Am J Trop Med Hyg. 2003; 69: 542-7. <br />24. López-Antuñano FJ. Is primaquine useful and safe as true exo-erythrocytic meronticidal, hyponociticial and gametocidal antimalarial drugs? Salud Pública Mex. 1999; 41: 410-9. <br />25. Portela MJ, Moreira R, Valente E, Constantino L, Iley J, Pinto J, et al. Dipeptide derivatives of primaquine as transmission-blocking antimalarials: effect of aliphatic side-chain acylation on the gametocytocidal activity and on the formation of carboxyprimaquine in rat liver homogenates. Pharm Res. 1999; 16: 949-55. <br />26. Coleman RE, Nath AK, Schneider I, Song GH, Klein TA, Milhous WK. Prevention of sporogony of Plasmodium falciparum and P. berghei in Anopheles stephensi mosquitoes by transmission-blocking antimalarials. Am J Trop Med Hyg. 1994; 50: 646-53. 27. Shao BR, Ye XY. Tissue schizontocidal effect of trifluoroacetyl primaquine in Plasmodium yoelii infected mice and Plasmodium cynomolgi infected monkeys. Southeast Asian J Trop Med Public Health. 1991; 22: 81-3. <br />28. Rastogi M, Pal NL, Sen AB. Gametocytocidal and sporontocidal activity of some standard antimalarials on P. berghei (NK 65) infection M. natalensis. Indian J Malariol. 1989; 26: 9-18. <br />29. Teklehaimanot A, Nguyen-Dinh P, Collins WE, Barber AM, Campbell CC. Evaluation of sporontocidal compounds using Plasmodium falciparum gametocytes produced in vitro. Am J Trop Med Hyg. 1985; 34: 429-34. <br />30. Gotay NJ, Kamtekar KD, Dalvi SS, Mehta SS, Chogle AR, Aigal U, et al. A randomized, parallel study of the safety and efficacy of 45 mg primaquine versus 75 mg bulaquine as gametocytocidal agents in adults with blood schizonticide-responsive uncomplicated falciparum malaria ISCRTN50134587. BMC Infect Dis. 2006; 6: 16. <br />31. Pukrittayakamee S, Chotivanich K, Chantra A, Clemens R, Looareesuwan S, White NJ. Activities of artesunate and primaquine against asexual- and sexual-stage parasites in falciparum malaria. Antimicrob Agents Chemother. 2004; 48: 1329-34. <br />32. Kamtekar KD, Gogtay NJ, Dalvi SS, Karnad DR, Chogle AR, Aigal U, et al. A prospective study evaluating the efficacy of a single, 45-mg dose of primaquine, as a gametocytocidal agent, in patients with Plasmodium falciparum malaria in Mumbai, India. Ann Trop Med Parasitol. 2004; 98: 453-8. <br />33. Gogtay NJ, Chogle AR, Sorabjee JS, Marathe SN, Kshirsagar NA. Poor gametocytocidal activity of 45 mg primaquine in chloroquine-treated patients with acute, uncomplicated, P. falciparum malaria in Mumbai (Bombay): an issue of public-health importance. Ann Trop Med Parasitol. 1999; 93: 813-6. <br />34. Kaneko A, Kamei K, Suzuki T, Ishii A, Siagian R, Panjaitan W. Gametocytocidal effect of primaquine in a chemotherapeutic malaria control trial in North Sumatra, Indonesia. Southeast Asian J Trop Med Public Health. 1989; 20: 351-9. <br />35. Chomcharn Y, Surathin K, Bunnag D, Sucharit S, Harinasuta T. Effect of a single dose of primaquine on a Thai strain of Plasmodium falciparum. Southeast Asian J Trop Med Public Health. 1980; 11: 408-12. <br />36. World Health Organization. Guidelines for the treatment of malaria. WHO/HTM/MAL/2006.1108. Geneva: WHO; 2006. <br />37. Kshirsagar NA. Malaria: anti malarial resistance and policy ramifications and challenges. J Postgrad Med. 2006; 52: 291-3. <br />38. Carmona-Fonseca J. La primaquina tiene alta eficacia en la quimioprofilaxis primaria simple antipalúdica. Metanálisis. Iatreia. 2006; 19: 244-60. <br />39. Hill DR, Baird JK, Parise ME, Lewis LS, Ryan ET, Magill AL. Primaquine: report from CDC expert meeting on malaria chemoprophylaxis. I Am J Trop Med Hyg 2006; 75: 402-15. <br />40. Marquiño W, Ylquimiche L, Hermenegildo Y, Palacios AM, Falconi E, Cabezas C, et al. Efficacy and tolerability of artesunate plus sulfadoxine-pyrimethamine and sulfadoxine-pyrimethamine alone for the treatment of uncomplicated Plasmodium falciparum malaria in Peru. Am J Trop Med Hyg. 2005; 72: 568-72. <br />41. Mockenhaupt FP, Ehrhardt S, Dzisi SY, Teun Bousema J, Wassilew N, Schreiber J, et al. A randomized, placebo-controlled, double-blind trial on sulfadoxine-pyrimethamine alone or combined with artesunate or amodiaquine in uncomplicated malaria. Trop Med Int Health. 2005; 10: 512-20. <br />42. Adjuik M, Babiker A, Garner P, Olliaro P, Taylor W, White N. International Artemisinin Study Group. Artesunate combinations for treatment of malaria: meta-analysis. Lancet. 2004; 363: 9-17. <br />43. Nacher M, Silachamroon U, Singhasivanon P, Wilairatana P, Phumratanaprapin W, Fontanet A, et al. Comparison of artesunate and chloroquine activities against Plasmodium vivax gametocytes. Antimicrob Agents Chemother. 2004; 48: 2751-2. <br />44. Abacassamo F, Enosse S, Aponte JJ, Gomez-Olive FX, Quinto L, Mabunda S, et al. Efficacy of chloroquine, amodiaquine, sulphadoxine-pyrimethamine and combination therapy with artesunate in Mozambican children with non-complicated malaria. Trop Med Int Health. 2004; 9: 200-8. <br />45. Chen PQ, Li GQ, Guo XB, He KR, Fu YX, Fu LC, et al. The infectivity of gametocytes of Plasmodium falciparum from patients treated with artemisinin. Chin Med J (Engl). 1994; 107: 709-11. <br />46. White NJ. Antimalarial drug resistance and combination chemotherapy. Philos Trans R Soc Lond B Biol Sci. 1999; 354: 739-49. <br />47. Schneider P, Bousema T, Omar S, Gouagna L, Sawa P, Schallig H, et al. (Sub)microscopic Plasmodium falciparum gametocytaemia in Kenyan children after treatment with sulphadoxine-pyrimethamine monotherapy or in combination with artesunate. Int J Parasitol. 2006; 36: 403-8. <br />48. Sowunmi A, Fateye BA, Adedeji AA, Fehintola FA, Bamgboye AE, Babalola CP, et al. Effects of antifolates-co-trimoxazole and pyrimethamine-sulfadoxine-on gametocytes in children with acute, symptomatic, uncomplicated, Plasmodium falciparum malaria. Mem Inst Oswaldo Cruz. 2005; 100: 451-5. <br />49. Sowunmi A, Fateye BA, Happi TC, Gbotosho GO, Oduola AM. Plasmodium falciparum gametocytaemia in Nigerian children: Peripheral immature gametocytaemia as an indicator of a poor response to chloroquine treatment, and its relationship to molecular determinants of chloroquine resistance. Ann Trop Med Parasitol. 2003; 97: 453-68. <br />50. Sowunmi A, Fateye BA. Gametocyte sex ratios in children with asymptomatic, recrudescent, pyrimethamine- sulfadoxine-resistant, Plasmodium falciparum malaria. Ann Trop Med Parasitol. 2003; 97: 671-82. <br />51. Sokhna CS, Trape JF, Robert V. Gametocytaemia in Senegalese children with uncomplicated falciparum malaria treated with chloroquine, amodiaquine or sulfadoxine + pyrimethamine. Parasite. 2003; 8: 243-50. <br />52. Puta C, Manyando C. Enhanced gametocyte production in Fansidar-treated Plasmodium falciparum malaria patients: implications for malaria transmission control programmes. Trop Med Int Health. 1997; 2: 227-9. <br />53. Tin F, Nyunt- Hlaing. Comparative drug trial of a sulfadoxine/pyrimethamine and a sulfalene/pyrimethamine combination against Plasmodium falciparum infections in semi-immune populations of Burma. Southeast Asian J Trop Med Public Health. 1984; 15: 238-48. <br />54. Robert V, Read AF, Essong J, Tchuinkam T, Mulder B, Verhave JP, et al. Effect of gametocyte sex ratio on infectivity of Plasmodium falciparum to Anopheles gambiae. Trans R Soc Trop Med Hyg. 1996; 90: 621-4. <br />55. Bukirwa H, Critchley J. Sulfadoxine-pyrimethamine plus artesunate versus sulfadoxine-pyrimethamine plus amodiaquine for treating uncomplicated malaria. Cochrane Database Sys Rev. 2006; 25: CD004966. <br />56. Ali E, Mackinnon MJ, Abdel-Muhsin AM, Ahmed S, Walliker D, Babiker HA. Increased density but not prevalence of gametocytes following drug treatment of Plasmodium falciparum. Trans R Soc Trop Med Hyg. 2006; 100: 176-83. <br />57. Robert V, Awono-Ambene HP, Le Hesran JY, Trape JF. Gametocytemia and infectivity to mosquitoes of patients with uncomplicated Plasmodium falciparum malaria attacks treated with chloroquine or sulfadoxine plus pyrimethamine. Am J Trop Med Hyg. 2000; 62: 210-6. <br />58. Handunnetti SM, Gunewardena DM, Pathirana PP, Ekanayake K, Weerasinghe S, Mendis KN. Features of recrudescent chloroquine-resistant Plasmodium falciparum infections confer a survival advantage on parasites and have implications for disease control. Trans R Soc Trop Med Hyg. 1996; 90: 563-7. <br />59. Hogh B, Gamage-Mendis A, Butcher GA, Thompson R, Begtrup K, Mendis C, et al. The differing impact of chloroquine and pyrimethamine/sulfadoxine upon the infectivity of malaria species to the mosquito vector. Am J Trop Med Hyg. 1998; 58: 176-82. <br />60. Schneider P, Schoone G, Schallig H, Verhage D, Telgt D, Eling W, et al. Quantification of Plasmodium falciparum gametocytes in differential stages of development by quantitative nucleic acid sequence-based amplification. Mol Biochem Parasitol. 2004; 137: 35-41. <br />61. Arango E, Álvarez T, Carmona J, Blair S. Gametocitemia de Plasmodium falciparum según la respuesta terapéutica a sulfadoxina-pirimetamina y cloroquina en dos municipios de Antioquia, Colombia. Biomédica. 2004; 24: 79-88. <br />62. Osorio L, González I, Olliaro P, Taylor WR. Artemisinin-based combination therapy for uncomplicated Plasmodium falciparum malaria in Colombia. Malar J. 2007; 286: 25. <br />63. Osorio L, Ferro BE, Castillo CM. Effects of chloroquine and sulfadoxine/pyrimethamine on gametocytes in patients with uncomplicated Plasmodium falciparum malaria in Colombia. Mem Inst Oswaldo Cruz. 2002; 97: 1221-3. <br />64. Méndez F, Muñoz A, Carrasquilla G, Jurado D, Arévalo-Herrera M, Cortese JF, et al. Determinants of treatment response to sulfadoxine-pyrimethamine and subsequent transmission potential in falciparum malaria. Am J Trop Med Hyg. 2002; 156: 230-8. <br />65. Carmona-Fonseca J, Álvarez G, Blair S. Malaria por Plasmodium vivax: curación del ataque agudo con tres dosis diferentes de primaquina y dosis fija de cloroquina; Antioquia (Colombia), 2003-2004. Biomédica. 2006; 26: 353-65. <br />66. Blair S, Tobón A, Echeverri M, Álvarez G, Carmona-Fonseca J. Adecuada respuesta clínica y parasitológica de Plasmodium vivax a la cloroquina en Colombia (Turbo, Antioquia), 2001. Infectio. 2002; 6: 21-6. <br />67. Lacharme L, Carmona-Fonseca J, Tobón A, Blair S. Respuesta de P. vivax al esquema terapéutico cloroquina-primaquina en Zaragoza y Turbo, Colombia, 1998. Infectio. 1998; 2: 90-4. <br />68. Blair S, Carmona-Fonseca J, Piñeros JG, Ríos A, Álvarez T, Álvarez G, et al. Therapeutic efficacy test in malaria falciparum in Antioquia, Colombia. Malar J. 2006; 5: 14. <br />69. Carmona-Fonseca J, Tobón A, Álvarez G, Blair S. El tratamiento amodiaquina-sulfadoxina-pirimetamina tiene eficacia del 98% para la malaria falciparum no complicada (Antioquia, Colombia; 2003). Iatreia. 2005; 18: 5-27. <br />70. Carmona-Fonseca J. La malaria en Colombia, Antioquia y las zonas de Urabá y Bajo Cauca: panorama para interpretar la falla terapéutica antimalárica Parte 1.. Iatreia. 2003; 16: 299-318. <br />71. Carmona-Fonseca J. La malaria en Colombia, Antioquia y las zonas de Urabá y Bajo Cauca: panorama para interpretar la falla terapéutica antimalárica. Parte 2. Iatreia. 2004; 17: 34-53. <br />72.Carmona-Fonseca J. Malaria, desnutrición y parasitosis intestinal en los niños colombianos: interrelaciones. Iatreia. 2004; 17: 354-69. <br />73. Organización Mundial de la Salud, Organización Panamericana de la Salud. Evaluación de la eficacia terapéutica de los medicamentos para el tratamiento del paludismo por Plasmodium falciparum sin complicaciones en las Américas. Documento OPS/HCP/HCT/113/98. Washington: OPS; 1998. <br />74. López-Antuñano FJ, Schmunis G. Diagnótico de malaria. Publicación científica No. 512. Washington DC: OPS; 1988. <br />75. Ministerio de Salud. Guía de atención clínica para el diagnóstico y tratamiento de la malaria. Bogotá: Instituto Nacional de Salud; 1999. <br />76. Baird JK, Fryauff DJ, Hoffmann SL. Primaquine for prevention of malaria in travelers. Clin Infect Dis. 2003; 37: 1659-67. <br />77. Villa-Restrepo AF. Mutaciones puntuales en los genes dhps y dhfr de Plasmodium falciparum asociadas con la respuesta terapéutica a sulfadoxina-pirimetamina en Antioquia-Colombia. (Tesis). Medellín: Grupo Malaria, Corporación de Ciencias Básicas Biomédicas, Universidad de Antioquia; 2005. <br />78. Suputtamongkol Y, Chindarat S, Silpasakorn S, Chaikachonpatd S, Lim K, Chanthapakajee K, et al. The efficacy of combined mefloquine-artesunate versus mefloquine-primaquine on subsequent development of Plasmodium falciparum gametocytemia. Am J Trop Med Hyg. 2003; 68: 620-3. <br />79. van den Broek IV, Maung UA, Peters A, Liem L, Kamal M, Rahman M, et al. Efficacy of chloroquine+sulfadoxine-pyrimethamine, mefloquine+artesunate and artemether+lumefantrine combination therapies to treat Plasmodium falciparum malaria in the Chittagong Hill Tracts, Bangladesh. Trans R Soc Trop Med Hyg. 2005; 99: 727-35. <br />80. Ávila JC, Villaroel R, Marquino W, Zegarra J, Mollinedo R, Ruebush TK. Efficacy of mefloquine and mefloquine-artesunate for the treatment of uncomplicated Plasmodium falciparum malaria in the Amazon region of Bolivia. Trop Med Int Health. 2004; 9: 217-22. <br />81. Marquiño W, Huilca M, Calampa C, Falconi E, Cabezas C, Naupay R, et al. Efficacy of mefloquine and a mefloquine-artesunate combination therapy for the treatment of uncomplicated Plasmodium falciparum malaria in the Amazon Basin of Peru. Am J Trop Med Hyg. 2003; 68: 608-12. <br />82. Omari AA, Gamble C, Garner P. Artemether-lumefantrine (six-dose regimen) for treating uncomplicated falciparum malaria. Cochrane Database Sys Rev. 2005; 19: CD005564. <br />83. Guthmann JP, Cohuet S, Rigutto C, Fortes F, Saraiva N, Kiguli J, et al. High efficacy of two artemisinin-based combinations (artesunate + amodiaquine and artemether + lumefantrine) in Caala, Central Angola. Am J Trop Med Hyg. 2006; 75: 143-5. <br />84. Peters W, Stewart LB, Robinson BL. The chemotherapy of rodent malaria. LXI. Drug combinations to impede the selection of drug resistance, part 4: the potential role of 8-aminoquinolines. Ann Trop Med Parasitol. 2003; 97: 221-36. <br />85. Lederman ER, Maguire JD, Sumawinata IW, Chand K, Elyazar I, Estiana L, et al. Combined chloroquine, sulfadoxine/pyrimethamine and primaquine against Plasmodium falciparum in Central Java, Indonesia. Malar J. 2006; 5: 108. <br />86. Bunnag D, Harinasuta T, Pinichpongse S, Suntharasami P. Effect of primaquine on gametocytes of Plasmodium falciparum in Thailand. Lancet. 1980; 2: 91. <br />87. Shekalaghe S, Drakeley C, Gosling R, Ndaro A, van Meegeren M, Enevold A, et al. Primaquine clears submicroscopic Plasmodium falciparum gametocytes that persist after treatment with sulphadoxine-pyrimethamine and artesunate. PLoS ONE. 2007; 2: e1023. <br />
oai:oai.revistabiomedica.org:article/92
2010-01-26T13:38:43Z
biomedica:ARTI
In vitro susceptibility of Colombian Plasmodium falciparum isolates to different antimalarial drugs
Susceptibilidad in vitro de aislamientos colombianos de Plasmodium falciparum a diferentes antipalúdicos
Blair, Silvia
Arango, Eliana
Carmona Fonseca, Jaime
malaria/terapia
Plasmodium falciparum
antipalúdicos
resistencia a las drogas
Colombia
malaria/therapy
Plasmodium falciparum
antimalarials
drug resistance
Colombia
Introduction. The in vitro assays for susceptibility of Plasmodium falciparum to antimalarial drugs are important tools for monitoring drug resistance, however few such studies have been undertaken in Colombia.Objective. P. falciparum isolates were obtained from several municipalities in western Colombia (Urabá, Bajo Cauca, Pacific Coast) and characterized for their in vivo susceptibility to chloroquine (CQ), amodiaquine (AQ), mefloquine (MQ), quinine (QN) and artesunate (AS).Material and methods. Patients with only P. falciparum infection (parasitemia=1,000 rings/µl) were included. Each antimalaria drug was tested with 7 dilutions, two-fold doses, with 2 replications and its effect evaluated using the histidine-rich protein (HRP-2) antigen detection method. Controls included FCB2 (chloroquine-resistant) and NF54 (chloroquine-sensitive) strains. IC50>100, 80, 64, 500 and 10.5 nM were used as the threshold criteria of resistance to CQ, AQ, MQ, QN and AS, respectively.Results. Twenty-five isolates were evaluated from Urabá (18), Bajo Cauca (2) and the Pacific Coast (5). The mean IC50 obtained with CQ, AQ, MQ, QN and AS were 422.9; 131.4; 56.3; 269.7 and 1.9 nM, respectively, and the number of resistant isolates for these drugs was 19 (76%), 4 (16%), 8 (32%), 6 (24%) and 1 (4%), respectively.Conclusions. The low sensitivity to CQ found here agrees with both in vitro and in vivo studies in Colombia. Ninety-six percent of the isolates were sensitive to AS. However, this study and previous reports have found isolates with low sensitivity to artemisinines (IC50>10.5 nM). This suggests that the indiscriminate use of these drugs put their efficacy at risk and eventually leave no options for falciparum malaria treatment.
Introducción. Los estudios de susceptibilidad in vitro de Plasmodium falciparum a los medicamentos antipalúdicos son herramientas importantes para vigilar la utilidad de esos medicamentos; tales estudios son escasos en Colombia.Objetivo. Evaluar la susceptibilidad in vitro de aislamientos colombianos de P. falciparum a cloroquina, amodiaquina, mefloquina, quinina y artesunato.Materiales y métodos. Se obtuvieron aislamientos clínicos de P. falciparum en varias regiones colombianas. De cada antipalúdico se probaron siete diluciones dobles seriadas, por duplicado, con la técnica HRP-2 y las cepas FCB2 (resistente a cloroquina) y NF54 (sensible a cloroquina) como controles. Se utilizaron las concentraciones inhibitorias 50 (CI50) mayor de 100, 80, 64, 500 y 10,5 nM como puntos de corte para clasificar la resistencia a cloroquina, amodiaquina, mefloquina, quinina y artesunato, respectivamente.Resultados. Se evaluaron 25 aislamientos: 72% de Urabá, 8% de Bajo Cauca y 20% de la Costa Pacífica. Las CI50 promedio de cloroquina, amodiaquina, mefloquina, quinina y artesunato fueron 422,9; 131,4; 56,3; 269,7 y 1,88 nM, respectivamente, y la proporción de aislamientos resistentes fue, en el mismo orden, 76%, 16%, 32%, 24% y 4%.Conclusiones. La baja sensibilidad a la cloroquina concuerda con otros estudios in vitro y con la baja eficacia terapéutica in vivo. Aunque 96% de los aislamientos fueron sensibles a artesunato, éste y otros estudios han observado aislamientos con disminución de la sensibilidad a las artemisininas (CI50>10,5 nM), lo que sugiere que el uso indiscriminado de estos medicamentos pone en riesgo su efectividad y podría dejarnos sin opciones para el tratamiento del paludismo por P. falciparum.
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/92
10.7705/biomedica.v28i2.92
Biomedica; Vol. 28 No. 2 (2008); 213-223
Biomédica; Vol. 28 Núm. 2 (2008); 213-223
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/92/90
/*ref*/ Bloland P. Drug resistance malaria. Malaria Epidemiology Branch. Centers for Disease Control and Prevention. WHO/CDS/CSR/DRS/2001. Chamblee, GA: World Health Organization; 2001. <br />2. Ringwald P. Susceptibility of Plasmodium falciparum to antimalarial drugs. Report on global monitoring 1996-2004. WHO/HTM/MAL/2005.1103. Geneve: World Health Organization; 2005. <br />3. Kaddouri H, Nakache S, Houzé S, Mentré F, Le Bras J. Assessment of the drug susceptibility of Plasmodium falciparum clinical isolates from Africa by using a Plasmodium lactate dehydrogenase immunodetection assay and an inhibitory maximum effect model for precise measurement of the 50-percent inhibitory concentration. Antimicrob Agents Chemother. 2006;50: 3343-9. <br />4. Zambrano P. Enfermedades transmitidas por vectores (ETV). Informe final de malaria, semanas 1 a 52 Colombia, 2005. Inf Quinc Epidemiol Nac. 2006;11:49-64. <br />5. OMS. Evaluación de la eficacia terapéutica de los medicamentos para el tratamiento del paludismo por Plasmodium falciparum sin complicaciones en las Américas. OPS/HCP/HCT/113/98. Washington: Organización Mundial de la Salud; 1998. <br />6. WHO. Assessment and monitoring of antimalarial drug efficacy for the treatment of uncomplicated falciparum malaria. WHO/HTM/RBM/2003.50. Geneva: World Health Organization; 2003. <br />7. Blair S, Carmona-Fonseca J, Pineros JG, Ríos A, Álvarez T, Álvarez G, et al. Therapeutic efficacy test in malaria falciparum in Antioquia, Colombia. Malar J. 2006;5:14 <br />8. Espinal C, Moreno E, Guerra P, De la Vega P. Aislamiento y caracterización de cepas colombianas de Plasmodium falciparum. Biomédica. 1982;2:118-28. <br />9. Arias A, Espinal C, Guerra P, Cortés G. In vitro and in vivo susceptibilities of P. falciparum to antimalarial drugs in some regions of Colombia. Acta Med Colomb. 1982;7:385. <br />10. Espinal CA, Cortés GT, Guerra P, Arias AE. Sensitivity of Plasmodium falciparum to antimalarial drugs in Colombia. Am J Trop Med Hyg. 1985;34:675-80. <br />11. Blair S, Lacharme LL, Fonseca JC, Tobón A. Resistance of Plasmodium falciparum to 3 antimalarials in Turbo (Antioquia, Colombia), 1998. Rev Panam Salud Pública. 2001;9:23-9. <br />12. Blair S, Lacharme LL, Carmona J, Tobón A. Resistance of P. falciparum to antimalarial drugs en Zaragoza (Antioquia, Colombia). Mem Inst Oswaldo Cruz. 2002;97:401-6. <br />13. González IJ, Varela RE, Murillo C, Ferro BE, Salas J, Giraldo LE, et al. Polymorphisms in cg2 and pfcrt genes and resistance to chloroquine and other antimalarials in vitro in Plasmodium falciparum isolates from Colombia. Trans R Soc Trop Med Hyg. 2003;97: 318-24. <br />14. Noedl H, Wongsrichanalai C, Wernsdorfer WH. Malaria drug-sensitivity testing: new assays, new perspectives. Trends Parasitol. 2003;19:175-81. <br />15. Noedl H, Wernsdorfer WH, Miller RS, Wongsrichanalai C. Histidine-rich protein II: a novel approach to malaria drug sensitivity testing. Antimicrob Agents Chemother. 2002;46:1658-64. <br />16. Noedl H, Wernsdorfer WH, Kollaritsch H, Looareesuwan S, Miller RS, Wongsrichanalai C. Malaria drug-susceptibility testing. HRP-2-based assays: current data, future perspectives. Wien Klin Wochenschr. 2003;115(Suppl.3):23-7. <br />17. Noedl H, Attlmayr B, Wernsdorfer WH, Kollaritsch H, Miller RS. A histidine-rich protein 2-based malaria drug sensitivity assay for field use. Am J Trop Med Hyg. 2004;71:711-4. <br />18. Noedl H. Malaria. Department of Immunology and Medicine, Armed Forces Research Institute of Medical Sciences (USAMC-AFRIMS, Bangkok, Thailand) Consultado: marzo de 2006. Disponible en: <a href="http://www.malaria.farch.net">www.malaria.farch.net</a> <br />19. Ljungström I, Perlmann H, Schlichtherle M, Scherf A, Wahlgren M. Methods in malaria research. Manassas, Virginia: Malaria Research and Reference Reagent Resource Center (MR4); 2004. <br />20. Ponnudurai T, Leeuwenberg AD, Meuwissen JH. Chloroquine sensitivity of isolates of Plasmodium falciparum adapted to in vitro culture. Trop Geog Med. 1981;33:50-4. <br />21. Moreno C. Actividad antiplasmodial in vitro de plantas del género Piper (tesis). Medellín: Universidad de Antioquia; 2005. <br />22. WHO. In vitro micro-test (Mark III) for the assessment of the response of Plasmodium falciparum to chloroquine, mefloquine, quinine, amodiaquine, sulfadoxine/pyrimethamine and artemisinin. Instructions for use of the in vitro micro-test kit (Mark III). CTC/MAL/97.20 Rev.2. Geneva: World Health Organization, Division of Control of Tropical Diseases; 2001. <br />23. Cerutti Junior C, Marques C, Alencar FE, Durlacher RR, Alween A, Segurado AA, et al. Antimalarial drug susceptibility testing of Plasmodium falciparum in Brazil using a radioisotope method. Mem Inst Oswaldo Cruz. 1999;94:803-9. <br />24. Pradines B, Tall A, Rogier C, Spiegel A, Mosnier J, Marrama L, et al. In vitro activities of ferro-chloroquine against 55 Senegalese isolates of Plasmodium falciparum in comparison with those of standard antimalarial drugs. Trop Med Int Health. 2002;7: 265-70. <br />25. Wongsrichanalai C, Lin K, Pang LW, Faiz MA, Noedl H, Wimonwattrawatee T, et al. In vitro susceptibility of Plasmodium falciparum isolates from Myanmar to antimalarial drugs. Am J Trop Med Hyg. 2001;65:450-5. <br />26. Rahman NN. Evaluation of the sensitivity in vitro of Plasmodium falciparum and in vivo of Plasmodium chabaudi Malaria to various drugs and their combinations. Med J Malaysia. 1997;52:390-8. <br />27. Kayser O, Kiderlen AF, Brun R. In vitro activity of aurones against Plasmodium falciparum strains K1 and NF54. Planta Med. 2001;67:718-21. <br />28. Garavito G, Rincon J, Arteaga L, Hata Y, Bourdy G, Gimenez A, et al. Antimalarial activity of some Colombian medicinal plants. J Ethnopharmacol. 2006; 107:460-2. <br />29. Aubouy A, Mayombo J, Keundjian A, Bakary M, Le Bras J, Deloron P. Short report: lack of prediction of amodiaquine efficacy in treating Plasmodium falciparum malaria by in vitro tests. Am J Trop Med Hyg. 2004;71:294-6. <br />30. Brasseur P, Agnamey P, Ekobo AS, Samba G, Favennec L, Kouamouo J. Sensitivity of Plasmodium falciparum to amodiaquine and chloroquine in central Africa: a comparative study in vivo and in vitro. Trans R Soc Trop Med Hyg. 1995;89:528-30. <br />31. Tinto H, Rwagacondo C, Karema C, Mupfasoni D, Vandoren W, Rusanganwa E, et al. In-vitro susceptibility of Plasmodium falciparum to monodese-thylamodiaquine, dihydroartemisinin and quinine in an area of high chloroquine resistance in Rwanda. Trans R Soc Trop Med Hyg. 2006;100:509-14. <br />32. Mount DL, Patchen LC, Nguyen-Dinh P, Barber AM, Schwartz IK, Churchill FC. Sensitive analysis of blood for amodiaquine and three metabolites by high-performance liquid chromatography with electro-chemical detection. J Chromatogr. 1986;383:375-86. <br />33. Brasseur P, Guiguemde R, Diallo S, Guiyedi V, Kombila M, Ringwald P, et al. Amodiaquine remains effective for treating uncomplicated malaria in west and central Africa. Trans R Soc Trop Med Hyg. 1999;93: 645-50. <br />34. Gorissen E, Ashruf G, Lamboo M, Bennebroek J, Gikunda S, Mbaruku G, et al. In vivo efficacy study of amodiaquine and sulfadoxine/ pyrimethamine in Kibwezi, Kenya and Kigoma, Tanzania. Trop Med Int Health. 2000; 5:459-63. <br />35. Gonzalez I, Padilla J, Giraldo L, Saravia N. Eficacia de amodiaquina y sulfadoxina/pirimetamina en el tratamiento de malaria no complicada por Plasmodium falciparum en Nariño, Colombia, 1999-2002. Biomédica. 2003;23:38-46. <br />36. Ong CE, Coulter S, Birkett DJ, Bhasker CR, Miners JO. The xenobiotic inhibitor profile of cytochrome P4502C8. Br J Clin Pharmacol. 2000;50:573-80. <br />37. Dai D, Tang J, Rose R, Hodgson E, Bienstock RJ, Mohrenweiser HW, et al. Identification of variants of CYP3A4 and characterization of their abilities to metabolize testosterone and chlorpyrifos. J Pharmacol Exp Ther. 2001;299:825-31. <br />38. Dai D, Zeldin DC, Blaisdell JA, Chanas B, Coulter SJ, Ghanayem BI, et al. Polymorphisms in human CYP2C8 decrease metabolism of the anticancer drug paclitaxel and arachidonic acid. Pharmacogenetics. 2001;11:597-607. <br />39. Guzmán V. Respuesta terapéutica a la mefloquina y la amodiaquina según el CYP450 y el estado nutricional de pacientes con malaria falciparum (tesis). Medellín: Universidad de Antioquia; 2005. <br />40. Ministerio de Salud. Resolución No. 00412 de 2000. Guía de atención clínica para el diagnóstico y tratamiento de la malaria. Bogotá: Ministerio de Salud: 2000. <br />41. Jambou R, Legrand E, Niang M, Khim N, Lim P, Volney B, et al. Resistance of Plasmodium falciparum field isolates to in-vitro artemether and point mutations of the SERCA-type PfATPase6. Lancet. 2005;366:1960-3. <br />
oai:oai.revistabiomedica.org:article/93
2010-01-26T13:51:29Z
biomedica:ARTI
Evaluation of the triflumuron and the mixture of Bacillus thuringiensis plus Bacillus sphaericus for control of the immature stages of Aedes aegypti and Culex quinquefasciatus (Diptera: Culicidae) in catch basins
Evaluación del triflumurón y la mezcla de Bacillus thuringiensis más Bacillus sphaericus para el control de las formas inmaduras de Aedes aegypti y Culex quinquefasciatus en sumideros en Cali, Colombia
Ocampo, Clara Beatriz
Giraldo Calderon, Gloria I.
Perez, Mauricio
Morales, Carlos A.
control biológico de plagas
eficacia
Bacillus
Aedes
Culex
pest control
biological
efficacy
Bacillus
Aedes
Culex
Introduction. In Cali, Colombia, catch basins (streetside storm drains) are one of the main larval habitats of Aedes aegypti and Culex quinquefasciatus. Since 1999, these mosquitoes have been controlled by the Secretaría de Salud Municipal (Secretary of Municipal Public Health) using the larvicide triflumuron. Because of high densities of these mosquitoes that remain in the city, treatment failure was suspected -possibly insecticide resistance of the target species.Objectives. The efficacy of triflumuron and VectoMax® (biorational mixture of Bacillus thuringiensis var. israelensis plus Bacillus sphaericus) were evaluated in the control of A. aegypti and C. quinquefasciatus in catch basins. The residual effect of a single application of the biorational formulation was determined in catch basins during periods of high and low rainfall.Materials and methods. The efficacy of the products was measured in 60 catch basins located in a residential neighborhood of Cali for a period of 90 days. The mean number of immature.Control de estadios inmaduros de mosquitos en sumideros instars ( A. aegypti and C. quinquefasciatus larvae and pupae of both species) was determined biweekly from 40 catch basins with insecticide intervention (20 treated with triflumuron, 20 with VectoMax®) and 20 untreated (control group). The residual effect of the biorational larvicide was evaluated biweekly in 10 catch basins during each of the 2 climatic periods.Results. The catch basins treated with VectoMax® presented a significantly lower mean number of immature instars of both species compared with the control ( p<0.01). In contrast, the triflumuron treatment significantly reduced only immature instars of A. aegypti compared with the control ( p<0.001). The residual effect of VectoMax® was higher during low rainfall compared to the control ( p<0.001).Conclusion. The biorational formulation was the more effective treatment for the control of both species during the period of evaluation (15 days).
Introducción. En Cali los sumideros son uno de los principales criaderos de Aedes aegypti y Culex quinquefasciatus que son controlados por la Secretaría de Salud Municipal utilizando el insecticida triflumurón desde 1999. Se sospecha falla al tratamiento.Objetivos. Evaluar la eficacia del Starycide® (triflumurón) y VectoMax® (mezcla bacteriana de Bacillus thuringiensis var. israelensis y Bacillus sphaericus) en el control de A. aegypti y C. quinquefasciatus en los sumideros y determinar el efecto residual de una única aplicación de VectoMax®, en épocas de alta y baja pluviosidad.Materiales y métodos. La eficacia de los productos fue medida en 60 sumideros de una zona residencial de Cali por un período de 90 días. La media de individuos inmaduros (larvas y pupas de A. aegypti y C. quinquefasciatus) fueron obtenidas quincenalmente de 40 sumideros intervenidos (20 con triflumurón y 20 con VectoMax®) y 20 sin tratamiento (grupo testigo). El efecto residual de la mezcla bacteriana se evaluó quincenalmente en 10 sumideros en cada temporada climática.Resultados. Los sumideros tratados con VectoMax® presentaron diferencias en el promedio de estadios inmaduros en ambas especies frente al testigo (p<0,01). En contraste, el tratamiento con triflumurón sólo presentó diferencias en los estadios inmaduros de A. aegypti con respecto al testigo (p<0,001). El efecto residual del VectoMax® fue mayor en la época de baja pluviosidad con respecto al testigo (p<0,001).Conclusión. La mezcla bacteriana fue el tratamiento más eficaz en el control de ambas especies durante el período evaluado (15 días).
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/93
10.7705/biomedica.v28i2.93
Biomedica; Vol. 28 No. 2 (2008); 224-233
Biomédica; Vol. 28 Núm. 2 (2008); 224-233
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/93/91
/*ref*/Nelson MJ. Aedes aegypti: Biology and ecology. Washigton, D.C.: PAHO; 1986. <br />2. World Health Organization. Integrated vector control. Seventh Expert Committee on Vector Biology and Control. Technical Report Series 688. Geneva: WHO; 1983. <br />3. Woodring J, Davidson EW. Biological control of mosquitoes. En: Beaty BJ, Marquardt WC, editors. The biology of disease vectors. Colorado: University Press of Colorado; 1996. p. 530-48. <br />4. Wirth MC, Georghiou GP, Federici BA. CytA enables CryIV endotoxins of Bacillus thuringiensis to overcome high levels of CryIV resistance in the mosquito, Culex quinquefasciatus. Proc Natl Acad Sci USA. 1997;94:10536-40. <br />5. Cupp EW, Travi BL, González R. Filariasis. En: Travi BL, Montoya-Lerma J, editores. Manual de entomología médica para investigadores de América Latina. Cali: Centro Internacional de Entrenamiento e Investigaciones Médicas CIDEIM; 1994. <br />6. Fonseca DM, Keyghobadi N, Malcolm CA, Mehmet C, Schaffner F, Mogi M, et al. Emerging vectors in the Culex pipiens complex. Science. 2004;303:1535-8. <br />7. Suárez-Rubio M, Suárez M. The use of the copepod Mesocyclops longisetus as a biological control agent for Aedes aegypti in Cali, Colombia. J Am Mosq Control Assoc. 2004;20:401-4. <br />8. De la Fuente J. Zoología de los artópodos Madrid: McGraw-Hill Interamericana; 1994. <br />9. Batra CP, Mittal PK, Adak T, Ansari MA. Efficacy of IGR compound Starycide 480 SC (Triflumuron) against mosquito larvae in clear and polluted water. J Vector Borne Dis. 2005;42:109-16. <br />10. Darriet F, Carnevale P, Robert V. Laboratory and field evaluation of the activity of an ecdysoid-type insect growth inhibitor, Triflumuron (OMS-2015), on Culex quinquefasciatus, Anopheles gambiae and Aedes aegypti. Geneva: World Health Organization; 1985. <br />11. Regis L, Silva-Filha MH, Nielsen-LeRoux C, Charles JF. Bacteriological larvicides of dipteran disease vectors. Trends Parasitol. 2001;17:377-80. <br />12. Instituto Geográfico Agustín Codazzi. Diccionario geográfico de Colombia. Segunda edición. Tomo I. Bogotá: Subdirección de Investigación y Divulgación Geográfica; 1980. <br />13. Ministerio de la Protección Social. SIVIGILA, Sistema Nacional de Vigilancia en Salud Pública. Prevención y control del dengue. Informe Ejecutivo Semanal. 2001 Semana epidemiológica No. 42. Octubre 14 al 20 de 2001. <br />14. Ministerio de la Protección Social. SIVIGILA, Sistema Nacional de Vigilancia en Salud Pública. Comportamiento por regiones del dengue en el 2001. 2002 Semana Epidemiológica No. 2. Enero 06 a 12 de 2002. <br />15. Laguado J, Alvis N, Máttar S. Investigación de un brote de fiebre de origen desconocido en una localidad colombiana del Caribe. Colombia Médica 2005;36:254-62. <br />16. IDEAM-Estación Base Aérea Marco Fidel Suárez. Valores diarios de precipitación, humedad relativa y temperatura. Bogotá, D.C.: Instituto de Hidrología, Meteorología y Estudios Ambientales (IDEAM); 2005. <br />17. Sih A. Antipredator responses and the perception of danger by mosquito larvae. Ecology. 1986;67:434-41. <br />18. Satizábal Rengifo ME. Control biológico de Aedes aegypti (Diptera: Culicidae) con Mesocyclops longisetus (Copepoda: Cyclopoida) en sumideros de la ciudad de Cali, Colombia (tesis). Cali: Universidad del Valle; 1999. <br />19. Morales CA. Evaluación de la eficacia de triflumurón (ingrediente activo de Starycide®) en el control de larvas de Aedes aegypti y Culex spp. en sumideros de Cali, Colombia. Salud Pública-Bayer. 2002;17:66-71. <br />20. Centers for Disease Control and Prevention. Pictorial keys to arthropods, reptiles, birds and mammals of public health significance. U.S. Departament of health & human services-CDC. Disponible en: <a href="http://www.cdc.gov/nceh/ehs/Pictorial_Keys.htm">http://www.cdc.gov/nceh/ehs/Pictorial_Keys.htm</a> <br />21. Lane R. Neotropical Culicidae. Dixinae, Chaoborinae and Culicinae, tribes Anophelini, Toxorhynchitini and Culicini (Genus Culex only). Sao Paulo: University of Sao Paulo;1953. 22. Prieto AV, Suárez MF, González R. Suceptibilidad de dos poblaciones de Aedes aegypti (Diptera:Culicidae) de Cali (Valle, Colombia) a Temefos (Abate®) y Triflumuron (Starycide®). Revista Colombiana de Entomología. 2002;28:175-8. <br /> <br /><br /> <br />
oai:oai.revistabiomedica.org:article/94
2010-01-26T13:58:56Z
biomedica:ARTI
Mosquitos (Diptera: Culicidae) in the small village where a human case of Venezuelan equine encephalitis was recorded
Mosquitos (Diptera: Culicidae) en el caserío de Chingalé, Santander, donde se registró un caso humano de encefalitis equina venezolana
Ferro, María Cristina
Olano, Victor Alberto
Ahumada, Martha
Weaver, Scott
virus de la encefalitis equina venezolana
encefalitis por arbovirus
Culex
Colombia
Encephalitis virus
Venezuelan equine
encephalitis
arbovirus
Culex
Colombia
Introduction. The enzootic focus of subtype ID of Venezuelan equine encephalitis (VEE) virus in the Central Magdalena region (central Colombia) occasionally produces human cases. The report of a VEE infection in a three-year-old girl in the small village of Chingalé, municipality of Puerto Wilches, Santander, motivated this study.Objective. The village of Chingalé was evaluated as the probable site of infection.Materials and methods. In June 2005, mosquitoes were collected with CDC light traps in and outside of dwellings in the village. Trinidad traps were placed in nearby vegetation, and hamsters were used as sentinel animals near homes.Results. One hundred and seven samples, consisting of 14,423 mosquitoes of 35 species were collected. The relative abundance of incriminated vectors of subtype ID of VEE, Culex (Melanoconion) pedroi and Cx. (Mel.) ocossa, was generally low (<4%), but both species were more frequent outside of dwellings than indoors. Cx. (Mel.) ocossa was collected in CDC traps and was more frequent indoors,whereas Cx. (Mel.) pedroi was found in the Trinidad traps. In addition, Psorophora confinnis was present, recognized as a potential vector of the epidemo/epizootic subtype. Mansonia indubitans, another recognized vector, was present at high frequency within dwellings. The exposed hamsters did not become infected.Conclusion. The child may have been infected in or near her home, although the epidemiologic cycle of the virus was not demonstrated within the village of Chingalé. Possibly, infected Culex mosquitoes of the subgenus Melanoconion carried the virus into the village from a neighboring habitat.
Introducción. El foco enzoótico del subtipo ID del virus de la encefalitis equina venezolana en la región del Magdalena Medio produce esporádicamente casos en humanos. El registro de un caso en una niña de tres años en el caserío de Chingalé, municipio de Puerto Wilches, Santander, motivó este estudio.Objetivo. Evaluar el caserío de Chingalé como probable sitio de infección.Materiales y métodos. En junio de 2005 se recolectaron mosquitos con trampas de luz CDC dentro y fuera de las casas; también se colocaron trampas Trinidad y hámster centinela alrededor de las viviendas.Resultados. En 107 muestreos se recolectaron 14.423 mosquitos distribuidos en 35 especies. La abundancia relativa de los posibles vectores del subtipo ID del virus de la encefalitis equina venezolana encontrados, Culex (Melanoconion) pedroi y Cx. (Mel) ocossa, en general, fue baja (<4%). Estas dos especies fueron más frecuentes en el exterior de las viviendas que en los dormitorios: Cx. ocossa en las trampas CDC y Cx. pedroi en las Trinidad. C. ocossa fue más frecuente en las viviendas. Además, este estudio detectó Psorophora confinis, considerado posible vector de subtipos epidemo/epizoóticos y una alta frecuencia de Mansonia indubitans en las viviendas. Los hámster expuestos no se infectaron.Conclusiones. La niña pudo infectarse en su casa o cerca de ella, aunque el ciclo epidemiológico del virus no tiene lugar en el casco urbano de Chingalé. Posiblemente ocurre en un lugar cercano y Culex (Melanoconion) infectados llevan el virus al caserío, en donde algunos mosquitos incursionaron a alimentarse.
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/94
10.7705/biomedica.v28i2.94
Biomedica; Vol. 28 No. 2 (2008); 234-244
Biomédica; Vol. 28 Núm. 2 (2008); 234-244
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/94/92
/*ref*/Weaver SC, Ferro C, Barrera R, Boshell J, Navarro JC. Venezuelan equine encephalitis. Annu Rev Entomol. 2004;49:141-74. <br />2. Weaver S. Recurrent emergence of Venezuelan equine encephalomyelitis. In: Scheld WM, Hughes J, editors. Emerging infections I. Washington, D.C.: ASM Press; 1998. p. 27-42. <br />3. Groot H. The health and economic impact of Venezuelan equine encephalitis (VEE). En: Proceedings of the Workshop-Symposium on Venezuelan equine encephalitis virus. Sci Pub No. 243. Washington, D.C.: PAHO; 1972. p. 7-16. <br />4. Sudia WD. Arthropod vectors of epidemic Venezuelan equine encephalitis. En: Proceedings of the Workshop-Symposium on Venezuelan equine encephalitis Virus. Sci Pub No. 243. Washington, D.C.: PAHO; 1972. p. 157 69. <br />5. Weaver SC, Anishchenko M, Bowen R, Brault AC, Estrada-Franco JG, Fernandez Z, et al. Genetic determinants of Venezuelan equine encephalitis emergence. Arch Virol Suppl. 2004;18:43-64. <br />6. Jhonson KM, Shelokov A, Peralta PH, Dammin GJ, Young NA. Recovery of Venezuelan equine encephalomyelitis virus in Panama. A fatal case in man. Am J Trop Med Hyg. 1968;17:432-40. <br />7. Ferro C, Boshell J, Moncayo AC, González M, Ahumada ML, Kang W, et al. Natural enzootic vectors of Venezuelan equine encephalitis virus, Magdalena Valley, Colombia. Emerg Infect Dis. 2003;9:49-54. <br />8. Anishchenko M, Bowen RA, Paessler S, Austgen L, Greene IP, Weaver SC. Venezuelan encephalitis emergence mediated by a phylogenetically predicted viral mutation. Proc Natl Acad Sci USA. 2006;103:4994-9. <br />9. Brault AC, Powers AM, Holmes EC, Woelk CH, Weaver SC. Positively charged amino acid substitutions in the E2 envelope glycoprotein are associated with the emergence of Venezuelan equine encephalitis virus. J Virol. 2002;76:1718-30. <br />10. Oberste MS, Fraire M, Navarro R, Zepeda C, Zarate ML, Ludwig GV, et al. Association of Venezuelan equine encephalitis virus subtype IE with two equine epizootics in Mexico. Am J Trop Med Hyg. 1998;59:100-7. <br />11. Walton TE, Alvarez O Jr, Buckwalter RM, Johnson KM. Experimental infection of horses with enzootic and epizootic strains of Venezuelan equine encephalomyelitis virus. J Infect Dis. 1973;128:271-82. <br />12. Dickerman RW, Cupp EW, Groot H, Morales-Alarcón A, Cura E, Dickerman AW, et al. Actividad del virus de la encefalitis equina venezolana en el norte de Colombia, abril y mayo de 1983. Bol Of Sanit Panam. 1987;103:1-9. <br />13. Sanmartin C, Trapido H, Barreto P, Lesmes CI. Isolations of Venezuelan and Eastern Equine Encephalomyelitis viruses from sentinel hamsters exposed in the Pacific lowlands of Colombia. Am J Trop Med Hyg. 1971;20:469-73. <br />14. Groot H, Morales A, Romero M, Ferro C, Prías E, Vidales H, et al. Estudios de arbovirosis en Colombia en la década de 1970. Biomédica 1996;16:331-44. <br />15. Barrera R, Ferro C, Navarro JC, Freier J, Liria J, Salas R, et al. Contrasting sylvatic foci of Venezuelan equine encephalitis virus in Northern South America. Am J Trop Med Hyg. 2002;67:324-34. <br />16. Groot H, Morales A, Vidales H. Virus isolations from forest mosquitoes in San Vicente de Chucurí, Colombia. Am J Trop Med Hyg. 1961;10:397-402. <br />17. Mesa F, Cárdenas J, Villamil LC. Las encefalitis equinas en la salud pública. Bogotá: Facultad de Medicina Veterinaria y de Zootecnia, Universidad Nacional de Colombia; 2005. <br />18. Davies JB. A small mosquito trap for use with animal or carbon dioxide baits. Mosq News. 1971;31:441-3. <br />19. Lumsden WH. A trap for insects biting small vertebrates. Nature. 1958;181:819-20. <br />20. Service M. Mosquito ecology: Field sampling methods. 2nd ed. London: Chapman & Hall; 1993. p. 988. <br />21. Lane J. Neotropical Culicidae. Vol.1 y 2. Sao Paulo: University of Sao Paulo; 1953. <br />22. Cova-García P.Mosquitos de Venezuela. Tomos 1 y 2. Caracas: Ministerio de Sanidad y Asistencia Social; 1966. <br />23. Faran ME, Linthicum K. A handbook of the Amazonian species of Anopheles (Nyssorhynchus) (Diptera: Culicidae). Mosq Syst. 1981;13:1-81. <br />24. Sallum MA, Forattini OP. Revision of the Spissipes section of Culex (Melanoconion) (Diptera: Culicidae). J Am Mosq Control Assoc. 1996;12:517-600. <br />25. Pecor JE, Mallanpalli VI, Harbach RE, Peyton El. Catalog and illustrated review of the subgenus Melanoconion of Culex (Diptera: Culicidae). Contrib Am Entomol Inst. 1992;27:1-228<br />26. Bulla L. An index of evenness and its associated diversity measure. Oikos. 1994;70:167-71. <br />27. Morales A, Romero M, Olano VA, Calvache D. Demostración del virus de la encefalitis equina venezolana tipo enzoótico en la hemolinfa de mosquitos Psorophora confinnis infectados por vía oral. Biomédica. 1982;2:111-7. <br />28. Morales A, Romero M, Olano VA. Transmisión experimental del virus de la encefalitis equina venezolana subgrupo ID tipo enzoótico por Psorophora confinnis a ratones. Biomédica.1983;3:10-4. <br />29. Ortiz D, Aischenko M, Waver SC. Susceptibility of Psorophora confinnis (Diptera : Culicidae) to infection with epizootic (Subtype IC) and enzootic (Subtype ID) Venezuelan equine encephalitis viruses. J Med Entomol. 2005;42:857-63. <br />30. Turell MJ, Jones JW, Sardelis MR, Dohm DJ, Coleman RE, Watts DM, et al. Vector competence of Peruvian mosquitoes (Diptera:Culicidae) for epizootic and enzootic strains of Venezuelan equine encephalomyelitis virus. J Med Entomol. 2000;37:835-9. <br />31. Mendez W, Liria J, Navarro JC, Garcia, CZ, Freier JE, Salas R, et al. Spatial dispersion of adult mosquitoes (Diptera: Culicidae) in a sylvatic focus of Venezuelan equine encephalitis virus. J Med Entomol. 2001:38:813-21. <br />32. Galindo P, Grayson MA. Culex (Melanoconion) aikenii: natural vector in Panamá of endemic Venezuelan encephalitis. Science. 1971;172:594-5. <br />33. Bowen GS, Calisher CH. Virological and serological studies of Venezuelan equine encephalomyelitis in humans. J Clin Microbiol. 1976;4:22-7. <br />34. Weaver SC, Salas R, Rico-Hesse R, Ludwig GV, Oberste MS, Boshell J, et al. Re-emergence of epidemic Venezuelan equine encephalomyelitis in South America. VEE Study Group. Lancet. 1996;348:436-40. <br />35. Sanmartin-Barberi C, Groot H, Osorno-Mesa E. Human epidemic in Colombia caused by the Venezuelan equine encephalomyelitis virus. Am J Trop Med Hyg. 1954;3:283-93. <br />36. Forattini OP. Entomología médica. Vol. 3. Sao Paulo: Editora da Universidade de Sao Paulo; 1965. p. 416. <br />
oai:oai.revistabiomedica.org:article/95
2010-01-26T14:05:22Z
biomedica:ARTI
Pediculosis prevalence and associated risk factors in a nursery school, Bogotá, Colombia
Prevalencia y factores asociados a la pediculosis en niños de un jardín infantil de Bogotá
Moncada, Ligia Inés
Rios, Sandra Milena
Fernández, Julián Alfredo
Rivas, Fabio
Sáenz, María Luz
Pediculus
infestaciones por piojos/epidemiología
prevalencia
factores de riesgo
preescolar
condiciones sociales
Pediculus
lice Infestations/epidemiology
prevalence
risk factors
child
preschool
social conditions
Introduction.Pediculosis is one of the most important chronic infestations in schoolchildren worldwide. Infestations show a high prevalence among the poorest children in developing countries, and it is associated with substandard hygienic practices.Objective.The prevalence was estimated and seasonality described of a Pediculus infestation of seven months duration in a nursery school. Associations were explored among the standards of hygienic practices and hair characteristics.Materials and methods.One hundred and seventy-eight nursery school children between the ages of 3 months to 5 years, from the nursery school located at National University of Colombia, Bogotá, were participants in the study. The children were examined for presence of Pediculus humanus infestation each month for seven months. The lengths and thicknesses of hair were measured at the first examination. A survey requesting information on socioeconomic and hygienic practices was provided to the caretakers of the children. Prevalence rates with 95% confidence intervals were estimated for each explored association, and also to describe the differences of prevalences between age groups in each period.Results.The highest prevalence was found in the children between the ages of 4 and 5 years, at the beginning of the school year. A positive association was indicated between Pediculus infestation and hair longer than 11.5 cm [prevalence rate (PR)=2.0; 95% confidence interval (CI): 0.82-4.8], washing the hair less than three times a week (PR=1.58; 95%CI: 0.58-4.7), as well as sharing cleaning implements (PR=1.31; 95%CI: 38-4.46) and living with more than five people at home (PR=2.04; 95%CI: 0.8-5.06). Due to the limited size of the sample, none of the associations found were statistically significant.Conclusion.Pediculus infestation has a high prevalence in children of the nursery school studied. This infestation is associated with substandard hygienic practices, living with more than five people at home and the length of hair.
Introducción. La pediculosis es una de las infestaciones crónicas más importante en escolares en el mundo.Objetivo. Estimar la prevalencia y describir la estacionalidad de la pediculosis durante siete meses en un jardín infantil y explorar su asociación con las variables socioeconómicas, las prácticas de higiene y las características del cabello.Materiales y métodos. Ciento setenta y ocho niños entre 3 y 60 meses de edad del jardín infantil de la Universidad Nacional de Colombia participaron en el estudio. En cada niño se exploró la presencia de Pediculus humanus mensualmente por siete meses y se midió el grosor y la longitud del cabello al comienzo del seguimiento. Se realizó una encuesta a los cuidadores de los sujetos de estudio sobre prácticas higiénicas y condiciones socio-económicas.Se estimaron las razones de prevalencia con su respectivo IC95% para cada una de las asociaciones exploradas y, también, para describir las diferencias en las prevalencias por grupo de edad en cada uno de los periodos de corte.Resultados. Se encontraron mayores prevalencias en el grupo de edad entre 48 y 59 meses, al principio del año escolar. Estos resultados sugieren una asociación positiva entre la pediculosis y tener una longitud del cabello mayor de 11,5 cm [razón de prevalencia (RP)=2,0; intervalo de confianza (IC) del 95%: 0,82-4,8], el bañarse la cabeza menos de tres veces a la semana (RP=1,58; IC95% 0,58-4,7), el compartir implementos de aseo (RP=1,31; IC95% 0,38- 4,46) y el vivir más de cinco personas en la casa (RP=2,04; IC95% 0,8-5,06). Dado el número limitado de la muestra estudiada, ninguna de las asociaciones fue estadísticamente significativa.Conclusión. La infestación por P. humanus capitis tiene altas prevalencias en los escolares del jardín. Esta infestación se encuentra asociada a las malas prácticas higiénicas, a convivir con más de cinco personas en la casa y a la longitud del cabello.
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/95
10.7705/biomedica.v28i2.95
Biomedica; Vol. 28 No. 2 (2008); 245-251
Biomédica; Vol. 28 Núm. 2 (2008); 245-251
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/95/93
/*ref*/Castex M, Suárez S, De la Cruz M. Presencia de pediculosis en convivientes con niños positivos a Pediculus capitis (Anoplura: Pediculidae). Rev Cubana Med Trop. 2000;52:225-7. <br />2. Piquero-Casals V, Pérez M, Quintero I, Ramírez B, Piquero-Martín J. Epidemiología de la Pediculosis capi-tis en escolares del Distrito sanitario No. 3 en Caracas, Venezuela. Dermatol Venez. 2004;42:19-22. <br />3. Araújo A, Ferreira LF, Guidon N, Maues Da Serra Freire N, Reinhard KJ, Dittmar K. Ten thousand years of head lice infection. Parasitol Today. 2000;16:269. <br />4. Downs AM, Stafford K, Coles GC. Head lice: Prevalence in school children and insecticide resistance. Parasitol Today. 1999;15:1-4. <br />5. Schenone H, Saavedra T, Rojas A. Infestación por Pediculus humanus capitis. Un prolongado problema de salud pública. Bol Chile Parasitol. 1986;41:16-20. <br />6. Borges R, Mendes J. Epidemiological aspects of head lice in children attending day care centers urban and rural schools in Uberlándia, central Brazil. Mem Inst Oswaldo Cruz. 2002;97:189-92. <br />7. Catalá S, Junco L, Vaporaky R. Pediculus capitis infestation according to sex and social factors in Argentina. Rev Saude Publica. 2005;39:438-43. <br />8. Slonka GF, Fleissner ML, Berlin J, Puleo J, Harrod EK, Schultz MG. An epidemic of Pediculosis capitis. J Parasitol. 1977;63:377-83. <br />9. Rasmussen JE. Pediculosis and the pediatrician. Pediatr Dermatol. 1984;2:74-9. <br />10. Satyamoorthy TS, Sachdeva NL, Kabra SC, Ganguly SS. A prevalence study of pediculus humanus capitis infestation among children in a slum area of Pune. Indian Journal of Community Medicine. 1987;12:209-17. <br />11. Fang P, Chung W, Kuo C, Hsu H, Chow C. Present status of head louse ( Pediculus capitis) infestation among school children in Yunlin County, Taiwan. Khaosiung J Med Sci. 1991;7:151-9. <br />12. Calderón-Arguedas O, Solano M, Sánchez C. El problema de la pediculosis capitis en escolares del área metropolitana de San José, Costa Rica. Parasitol Latinoam. 2003;58:177-80. <br />13. Castro DC, Abrahamovich AH, Cicchino AC, Rigoni A, Raffaeli C, De Barrio A. Prevalencia y estacionalidad de la Pediculosis capitis en la población infanto-juvenil de la región sanitaria, Buenos Aires, Argentina. Rev Saúde Pública. 1994;28:295-9. <br />14. Boyle P. Pilot study of the prevalence of head lice infestation in a population of Saudi Arabian Children. Fam Pract. 1987;4:138-42. <br />15. Ogunrinade AF, Oyejide CO. Pediculosis capitis among rural and urban school children in Nigeria. Trans R Soc Trop Med Hyg. 1984;78:590-2. <br />16. Sagua H, Rivera AM, Zamora M, Neira I, Araya J, Maluenda R. Epidemiological study of Pediculosis capitis and scabies in school children from Antofagasta, Chile, 1995. Bol Chil Parasitol. 1997;52:33-6. <br />17. Speare R, Buettner PG. Hard data needed on head lice transmission. Int J Dermatol. 2000;39:877-8. <br />
oai:oai.revistabiomedica.org:article/96
2010-01-26T14:12:01Z
biomedica:ARTI
Concordance between thick blood smear, immunochromatography and polymerase chain reaction for malaria diagnosis
Concordancia entre gota gruesa, inmunocromatografía y reacción en cadena de la polimerasa para el diagnóstico de malaria
Montoya, Astrid Elena
Menco, José
Osorio, Natalia
Zuluaga, Maria Alejandra
Duque, Juliana
Torres, Giovanny
Restrepo, Marcos
Plasmodium
malaria/diagnóstico
técnicas y procedimientos diagnósticos
valor diagnóstico de las pruebas
sensibilidad y especificidad
reacción en cadena de la polimerasa
Plasmodium
malaria/diagnosis
diagnostic techniques and procedures
predictive value of tests
sensitivity and specificity
polymerase chain reaction
Introduction. The rapid and effective diagnosis of malaria is the determining condition for an appropriate treatment and control of the disease.Objective. The sensitivity, specificity and the positive and negative predictive values were evaluated in cases of suspected malaria in Colombia in a comparison of a rapid diagnostic test. the PCR test and the thick blood smear-the traditional gold standard.Materials and methods. A group of 100 patients with symptoms compatible with malaria, were included in the study. They were selected from the following Colombian regions: Urabá, Córdoba, lower Cauca, and relatively fewer from other malaria endemic areas of Colombia including the provinces of Valle, Chocó in the central west of Colombia and Vichada to the east. To each patient the following three tests were performed: the rapid OptiMAL® test, the PCR identification and the thick blood smear. The PCR amplified specific DNA sequences with primers designed to identify the genus Plasmodium, and the two species present in Colombia, P. falciparum and P. vivax.Results. The sensitivity of the rapid test versus the thick smear, for the diagnosis of both species of Plasmodium was 93.9% (95% CI: 87-100%) and the specificity was 94.3% (95% CI:.253 85-100%). The PCR compared with the thick smear showed a sensitivity of 100% (95% CI: 99-100%) and a specificity of 97.1% (95% CI: 90-100%).Conclusions. The sensitivity and specificity of the three tests did not present statistically significant differences. However, the thick blood smear was recommended as the standard test, mainly due to its low cost.
Introducción. El diagnóstico oportuno y efectivo del paludismo, o malaria, son condiciones determinantes para hacer un tratamiento adecuado de la enfermedad y un control de la misma.Objetivo. Se evaluó la concordancia de la sensibilidad, especificidad, valor diagnóstico positivo y negativo de una prueba rápida y de la reacción en cadena de la polimerasa (PCR), con la prueba estándar, la gota gruesa, para el diagnóstico de la malaria.Materiales y métodos. Se analizó una población de 100 pacientes con signos y síntomas indicativos de paludismo, procedentes de las zonas de Urabá, Córdoba, Bajo Cauca y de otras regiones de Colombia, como Valle, Chocó y Vichada, todas áreas endémicas de la enfermedad.A cada paciente se le practicó una gota gruesa, la prueba rápida OptiMAL® y la amplificación a través de una PCR de secuencias de ADN específicas para género y paraPlasmodium falciparum y Plasmodium vivax.Resultados. La sensibilidad de la prueba rápida frente a la gota gruesa, para el diagnóstico de ambas especies de Plasmodium fue de 93,85% (IC95% 87,23-100) y la especificidad de 94,29% (IC95% 85,17-100).La PCR comparada con la gota gruesa mostró una sensibilidad de 100% (IC95% 99,23-100) y una especificidad de 97,14% (IC95% 90,19-100).Conclusiones. Estos hallazgos muestran que la sensibilidad y especificidad de la prueba rápida y la PCR para el diagnóstico de malaria son comparables con el examen al microscopio de la gota gruesa, recomendada por su eficacia y bajo costo.
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/96
10.7705/biomedica.v28i2.96
Biomedica; Vol. 28 No. 2 (2008); 252-261
Biomédica; Vol. 28 Núm. 2 (2008); 252-261
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/96/94
/*ref*/World Health Organization. World Malaria Report. RBM/WHO/ UNICEF. Geneva: WHO; 2005. <br />2. Hay SI, Guerra CA, Tótem AJ, Noor AM, Snow RW. The global distribution and population at risk of malaria past, present and future. Lancet Infect Dis. 2004; 4:327-36. <br />3. Dirección Seccional de Salud de Antioquia. Eventos de vigilancia epidemiológica. Revista Epidemiológica de Antioquia. 2006;28:39-40. <br />4. Instituto Nacional de Salud. Tablas de notificación semanal obligatoria. Semana 52 de 2006. Consultado: agosto de 2007. Disponible en: <a href="http://www.ins.gov.co/pdf/vcsp/Tablas/2006/2006_semana_52.pdf">http://www.ins.gov.co/pdf/vcsp/Tablas/2006/2006_semana_52.pdf</a> <br />5. Aron JL. Malaria epidemiology and detectability. Trans R Soc Trop Med Hyg. 1982;76:595-601. <br />6. Ndao M, Bandyayera E, Kokoskin E, Gyorkos TW, MacLean JD, Ward BJ. Comparison of blood smear, antigen detection, and nested- PCR methods for screening refugees from regions where malaria is endemic after a malaria outbreak in Quebec, Canada. J Clin Microbiol. 2004;42:2694-700. <br />7. Perandin F, Manca G, Piccolo A, Calderaro A, Galati L, Ricci L, et al. Identification of Plasmodium falciparum, P. vivax, P. ovale and P. malariae and detection of mixed infection in patients with imported malaria in Italy. New Microbiol. 2003;26:91-100. <br />8. Barat L, Chipipa J, Kolczak M, Sukwa T. Does the availability of blood slide microscopy for malaria at health centers improve the management of persons with fever in Zambia? Am J Trop Med Hyg. 1999; 60:1024-30. <br />9. Garcia M, Marlborough D, Leafasia J, Rieckmann KH.Immunochromatographic test for malaria diagnosis. Lancet. 1996;347:1549. <br />10. Craig MH, Sharp BL. Comparative evaluation of four techniques for the diagnosis of Plasmodium falciparum infections. Trans R Soc Trop Med Hyg. 1997;91:279-82. <br />11. Stow NW, Torrens JK, Walker J. An assessment of the accuracy of clinical diagnosis, local microscopy, and a rapid immunochromatographic card test in comparison with expert microscopy in the diagnosis of malaria in rural Kenya. Trans R Soc Trop Med Hyg. 1999;93:519-20. <br />12. Moody A. Rapid diagnostic tests for malaria parasites. Clin Microbiol Rev. 2002;15:66-78. <br />13. Coleman RE, Maneechai N, Rachapaew N, Kumpitak C, Soyseng V, Mille RS, et al. Field evaluation of the ICT Malaria Pf/Pv immunochromatographic test for the detection of asymptomatic malaria in a Plasmodium falciparum/vivax endemic area in Thailand. Am J Trop Med Hyg. 2002;66 :379-83. <br />14. World Health Organization. Malaria rapid diagnosis, making it work meeting. Informal consultation on field trials and quality assurance on malaria rapid diagnostic test. 20-23 January 2003. World Health Organization, Regional Office for the Western Pacific. Geneva: WHO; 2003. <br />15. Palmer CJ, Lindo JF, Klaskala WI, Quesada JA, Kaminsky R, Baum MK, et al. Evaluation of the OptiMAL test for rapid diagnosis of Plasmodium vivax and Plasmodium falciparum malaria. J Clin Microbiol. 1998;36:203-6.. <br />16. Iqbal J, SherA, Hira PR, Al-Owaish R. Comparison of the OptiMAL test with PCR for diagnosis of malaria in immigrants. J Clin Microbiol. 1999;37:3644-6. <br />17. Piper R, Lebras J, Wentworth L, Hunt-Cooke A, Houze S, Chiodini P, et al. Immunocapture diagnostic assays for malaria using Plasmodium lactate dehydrogenase (pLDH). Am J Trop Med Hyg. 1999; 60: 109-18. <br />18. Iqbal J, Muneer A, Khalid N, Ahmed MA. Performance of the OptiMAL test for malaria diagnosis among suspected malaria patients at the rural health centers. Am J Trop Med Hyg. 2003;68:624-8. <br />19. Palmer CJ, Bonilla JA, Bruckner DA, Barnett ED, Millar NS, Haseeb MA, et al. Multicenter study to evaluate the OptiMAL test for rapid diagnosis of malaria in U.S hospitals. J Clin Microbiol. 2003;41:5178-82. <br />20. Kolaczinski J, Mohammed N, Ali I, Ali M, Khan N, Ezard N, et al. Comparison of the OptiMAL rapid antigen test with field microscopy for the detection of Plasmodium vivax and P. falciparum: considerations for the application of the rapid test in Afghanistan. Ann Trop Med Parasitol. 2004;98:15-20. <br />21. Kain KC, Lanar DE. Determination of genetic variation within Plasmodium falciparum by using enzymatically amplified DNA from filter paper disks impregnated with whole blood. J Clin Microbiol. 1991;29:1171-4. <br />22. Kain KC, Brown AE, Mirabelli L, Webster HK. Detection of Plasmodium vivax by polymerase chain reaction in a field study. J Infect Dis. 1993;168:1323-6. <br />23. Roper C, Elhassan IM, Hviid L, Giha H, Richardson W, Babiker H, et al. Detection of very low level Plasmodium falciparum infections using the nested polymerase chain reaction and a reassessment of the epidemiology of unstable malaria in Sudan. Am J Trop Med Hyg. 1996;54:325-31. <br />24. Tan TM, Nelson JS, Ng HC, Ting RC, Kara UA. Direct PCR amplification and sequence analysis of ex-trachromosomal Plasmodium DNA from dried blood spots. Acta Trop. 1997;68:105-14. <br />25. Tham JM, Lee SH, Tan TM, Ting RC, Kara UA. Detection and species determination of malaria parasites by PCR: comparison with microscopy and with ParaSight-F and ICT Malaria Pf tests in a clinical environment. J Clin Microbiol.1999;37:1269-73. 26. Fischer A, Lejczak C, Lambert C, Servais J, Makombe N, Rusine J, et al. Simple DNA extraction method for dried blood spots and comparison of two PCR assays for diagnosis of vertical human immunodeficiency virus type 1 transmission in Rwanda. J Clin Microbiol. 2004;42:16-20. <br />27. Altschul SF, Madden TL, Schaffer A, Zhang J, Zhang Z, Miller W, et al. Gapped BLAST and PSI-BLAST: a new generation of protein database search programs. Nucleic Acids Res. 1997;25:3389-402. <br />28. Saiki RK, Scharf S, Faloona F, Mullis KB, Horn GT, Erlich HA, et al. Enzymatic amplification of beta-globin genomic sequences and restriction site analysis for the diagnosis of sickle-cell anemia. Biotechnology. 1992;24,476-80. <br />29. Morassin B, Fabre R, Berry A, Magnaval JF. One years experience of polymerase chain reaction as a routine method for the diagnosis of imported malaria. Am J Trop Med Hyg. 2002;66:503-8. <br />30. Mendoza NM, Montoya R, García M, Padilla JC, Bruzón LO, Mendoza E, et al. Evaluación de campo de una prueba rápida para el diagnóstico de malaria. Biomédica. 2001;21:313-9. <br />31. Ferro BE, González IJ, de Carvajal F, Palma GI, Saravia N. Performance of OptiMAL ® in the Diagnosis of Plasmodium vivax and Plasmodium falciparum infection in malaria referral center in Colombia. Mem Inst Oswaldo Cruzi. 2002;97:731-5. <br />32. van den Broek I, Hill O, Gordillo F, Angarita B, Hamade P, Counihan H, et al. Evaluation of three rapid tests for diagnosis of P. falciparum and P. vivax malaria in Colombia. Am J Trop Med Hyg. 2006;75:1209-15. <br />33. Londoño B, Carmona J, Blair S. Comparación de los métodos Optimal ® y gota gruesa para el diagnóstico de malaria en una zona endémica sin epidemia. Biomédica.2002;22:466-75. <br />34. Humar A, Harrington MA, Pillai D, Kain KC. ParaSightTM-Ftest compared with the polymerasechain reaction and microscopy for the diagnosis of P. falciparum malaria in travelers. Am J Trop Med Hyg. 1997;56:44-8. <br />35. Tjitra E, Suprianto S, McBroom J, Currie BJ, Anstey NM. Persistent ICT Malaria Pf/Pv panmalarial and HRP2 antigen reactivity after treatment of Plasmodium falciparum malaria is associated with gametocytemia and results in false-positive diagnosis of P. vivax in convalescence. J Clin Microbiol. 2001;39:1025-31. <br /> <br />
oai:oai.revistabiomedica.org:article/97
2010-01-26T14:29:49Z
biomedica:ARTI
Characterizing the CD3 epsilon chain from the New World primate Aotus nancymaae
Caracterización de la cadena CD3 épsilon en el primate del nuevo mundo Aotus nancymaae
Vernot, Jean Paul
del Castillo, Hernando
sistema inmune
receptores del antígeno de célula T
antígenos CD3
proteínas adaptadoras transductoras de señales
immune system
receptors
antigen
T-cell
CD3 antigens
adaptor proteins
signal transducing
Introduction. The T-cell receptor (TCR)-associated complex, CD3 (d, g, e) and z-chains are essential transmembrane proteins for signal transduction during T cell activation and immune response, as well as during thymocyte development.Objective. This work established the CD3ε-chain primary structure for the New World owl monkey Aotus nancymaae.Materials and methods. Total RNA was isolated from peripheral blood mononuclear cells; CD3ε molecule was amplified, cloned and sequenced.Results. The CD3ε amino acid sequence was deduced for the owl monkey Aotus nancymaae.It has an identity for nucleotide and amino acid sequences with the human counterpart of 84% and 76%, respectively. As described in other species, the Aotus CD3-e molecule is very variable in the extracellular region and greatly conserved in the intracellular domain. Even though high variability occurs in the CD3ε-extracellular domain, the subregions involved in ectodomain folding are conserved.Conclusions. The primary structure suggested that the Aotus protein has a functional role similar to that of humans, and that the initial T-cell activation steps are also similar. However, the great variation observed in CD3ε-extracellular region in humans in contrast to the Aotus (especially in areas that are surface-exposed) indicated that some monoclonal antibodies against the human CD3 complex will not recognize these Aotus determinants.
Introducción. El complejo asociado al receptor de las células T está constituido por las moléculas CD3 (δ, γ, ε) y las cadenas ζ, todas proteínas transmembrana esenciales para la transducción de señales durante la activación del linfocito y la respuesta inmune, así como durante el desarrollo de los timocitos.Objetivo. En este trabajo se buscaba determinar la estructura primaria de la cadena CD3ε, en el mono del nuevo mundo, Aotus nancymaae.Materiales y métodos. A partir del ARN total obtenido de células mononucleares de sangre periférica, se amplificó la molécula de CD3ε, luego se clonó en un vector y, finalmente, se secuenció.Resultados. Se presenta la secuencia deducida de aminoácidos de la cadena CD3ε de A. nancymaae. Se estableció una identidad de 84% y de 76% en la secuencia nucleotídica y la de aminoácidos, respectivamente, con su contraparte humana. La molécula de Aotus muestra bastante variabilidad en la región extracelular y bastante conservación en la intracelular.Están conservadas subregiones del ectodominio que son importantes para el plegamiento de la molécula, así como para la asociación con las otras cadenas del complejo.Conclusiones. La estructura primaria determinada aquí sugiere que la proteína de Aotus tiene una funcionalidad similar y que los pasos iniciales de activación de la célula T se suceden como en los humanos; por otra parte, la gran variabilidad encontrada en el ectodominio, permite explicar por qué algunos anticuerpos monoclonales dirigidos contra el complejo CD3 de humano no reconocen estas estructuras en el Aotus.
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/97
10.7705/biomedica.v28i2.97
Biomedica; Vol. 28 No. 2 (2008); 262-270
Biomédica; Vol. 28 Núm. 2 (2008); 262-270
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/97/95
/*ref*/Collins WE. The owl monkey as a model for malaria. En: Baer JF, Weller RE, Kakoma J, editors. Aotus the owl monkey. San Diego: Academic Press; 1994. p. 217-44. <br />2. Gynsin J. Animal models: primates. En: Sherman IW, editor. Malaria: parasite biology, pathogenesis and pro-tection. Washington, DC: ASM Press; 1998. p. 419-39. <br />3. Stowers AW, Miller L H. Are trials in new world monkeys on the critical path for blood-stage malaria vaccine development? Trends Parasitol. 2001;17:415-9. <br />4. Vogel TU, Evans DT, Urvater JA, OConnor DH, Hughes AL, Watkins DI. Major histocompatibility complex class I genes in primates: co-evolution with pathogens. Immunol Rev. 1999;167:327-37. <br />5. Bontrop RE, Otting N, de Groot NG, Doxiadis GG. Major histocompatibility complex class II polymorphisms in primates. Immunol Rev. 1999;167:339-50. <br />6. Heppner DG, Cummings JF, Ockenhouse C, Kester KE, Lyon JA, Gordon DM. New world monkey efficacy trials for malaria vaccine development: critical path or detour? Trends Parasitol. 2001;17:419-25. <br />7. Cantrell D. T cell antigen receptor signal transduction pathways. Annu Rev Immunol. 1996;14:259-74. <br />8. Germain RN, Štefanová I. The dynamics of T cell receptor signaling: complex orchestration and key roles of tempo and cooperation. Annu Rev Immunol. 1999;17:467-522. <br />9. Zamoyska R, Basson A, Filby A, Legname G, Lovatt M, Seddon B. The influence of the src-family kinases, Lck and Fyn, on T cell differentiation, survival and activation. Immunol Rev. 2003;191:107-18. <br />10. Pitcher LA, van Oers NS. T-cell receptor signal transmission: who gives an ITAM? Trends Immunol. 2003;24:554-60. <br />11. Werlen G, Palmer E. The TCR signalosome: a dynamic structure with expanding complexity. Curr Opin Immunol. 2002;14:299-305. <br />12. Pan Q, Brodeur JF, Drbal K, Dave VP. Different role for mouse and human CD3ä/å heterodimer in preT cell receptor (preTCR) function: Human CD3d/e heterodimer restores the defective preTCR function in CD3g- and CD3 gd-deficient mice. Mol Immunol. 2006;43:1741-50. <br />13. Gil D, Schamel WW, Montoya M, Sánchez-Madrid F, Alarcón B. Recruitment of Nck by CD3 reveals a ligand-induced conformational change essential for T cell receptor signaling and synapse formation. Cell. 2002;109:901-12. <br />14. Alarcón B, Gil D, Delgado P, Schamel WW. Initiation of TCR signaling: regulation within CD3 dimers. Immunol Rev. 2003;191:38-46. <br />15. Gil D, Schrum AG, Alarcón B, Palmer E. T cell receptor engagement by peptide-MHC ligands induces a conformational change in the CD3 complex of thymocytes. J Exp Med. 2005;201:517-22. <br />16. Gold DP, Puck JM, Pettey CL, Cho M, Coligan J, Woody JN, et al. Isolation of cDNA clones encoding the 20K non-glycosylated polypeptide chain of the human T-cell receptor/T3 complex. Nature. 1986;321: 431-4. <br />17. Gold DP, Clevers H, Alarcon B, Dunlap S, Novotny J, Williams AF, et al. Evolutionary relationship between the T3 chains of the T-cell receptor complex and the immunoglobulin supergene family. Proc Natl Acad Sci USA. 1987;84:7649-53. <br />18. Uda A, Tanabayashi K, Mukai R, Yachi M, Nam KH, Yamada A. CD3 polymorphism in cynomolgus monkeys (Macaca fascicularis). J Med Primatol. 2001;30:141-7. <br />19. Clevers H, Dunlap S, Saito H, Georgopoulos K, Wileman T, Terhorst C. Characterization and expression of the murine CD3-e gene. Proc Natl Acad Sci USA. 1988;85:8623-7. <br />20. Clevers HC, Dunlap S, Wileman TE, Terhorst C. Human CD3-e gene contains three miniexons and is transcribed from a non-TATA promoter. Proc Natl Acad Sci USA. 1988;85:8156-60. <br />21. Tunnacliffe A, Olsson C, Buluwela L, Rabbitts TH. Organization of the human CD3 locus on chromosome 11. Eur J Immunol. 1988;18:1639-42. <br />22. Pinzón-Charry A, Vernot JP, Rodríguez R, Patarroyo ME. Proliferative response of peripheral blood lymphocytes to mitogens in the owl monkey Aotus nancymae. J Med Primatol. 2003;32:31-8. <br />23. Montoya GE, Vernot JP, Patarroyo ME. Comparative analysis of CD45 proteins in primate context: owl monkeys vs humans. Tissue Antigens. 2004;64:165-72. <br />24. Vernot JP, Pérez-Quintero LA, Perdomo-Arciniegas AM, Quijano S, Patarroyo ME. Herpesvirus saimiri immortalization of Aotus T lymphocytes specific for an immunogenically modified peptide of Plasmodium falciparum merozoite surface antigen 2. Immunol Cell Biol. 2005;83:67-74. <br />25. Niño-Vásquez JJ, Vogel D, Rodríguez R, Moreno A, Patarroyo ME, Pluschke G, et al. Sequence and diversity of DRB genes of Aotus nancymaae, a primate model for human malaria parasites. Immunogenetics. 2000;51:219-30. <br />26. Díaz D, Naegeli M, Rodríguez R, Niño-Vásquez JJ, Moreno A, Patarroyo ME, et al. Sequence and diversity of MHC DQA and DQB genes of the owl monkey Aotus nancymaae. Immunogenetics. 2000;51:528-37. <br />27. Montoya GE, Vernot JP, Patarroyo ME. Partial characterization of the CD45 phosphatase cDNA in the owl monkey ( A. vociferans). Am J Primatol. 2002;57:1-11. <br />28. Rost B, Sander C. Prediction of protein secondary structure at better than 70% accuracy. J Mol Biol. 1993;232:584-99. <br />29. Rost B, Fariselli P, Casadio R. Topology prediction for helical transmembrane proteins at 86% accuracy. Protein Sci. 1996;5:1704-18. <br />30. Sun ZYJ, Kim KS, Wagner G, Reinherz EL. Mechanisms contributing to T cell receptor signaling and assembly revealed by the solution structure of an ectodomain fragment of the CD3 eg heterodimer. Cell. 2001;105:913-23. <br />31. Arnett KL, Harrison SC, Wiley DC. Crystal structure of a human CD3-ed dimer in complex with a UCHT1 single-chain antibody fragment. Proc Natl Acad Sci USA. 2004;101:16268-73. <br />32. Kjer-Nielsen L, Dunstone MA, Kostenko L, Ely LK, Beddoe T, Mifsud N, et al. Crystal structure of the human T cell receptor CD3ε g heterodimer complexed to the therapeutic mAb OKT3. Proc Natl Acad Sci USA. 2004;101:7675-80. <br />33. Salmerón A, Sánchez-Madrid F, Ursa MA, Fresno M, Alarcón B. A conformational epitope expressed upon association of CD3-e with either CD3-d or CD3-g is the main target for recognition by anti-CD3 monoclonal antibodies. J Immunol. 1991;147:3047-52 <br />34. Liu YY, Wang Z, Thomas J, Goodwin KJ, Stavrou S, Neville DM Jr. Polymorphisms of CD3ε in cynomolgus and rhesus monkeys and their relevance to anti-CD3 antibodies and immunotoxins. Immunol Cell Biol. 2007;85:357-62. <br />35. Call ME, Pyrdol J, Wiedmann M, Wucherpfennig KW. The organizing principle in the formation of the T cell receptor-CD3 complex. Cell. 2002;111:967-79. <br />36. Call ME, Wucherpfennig KW. Molecular mechanisms for the assembly of the T cell receptor–CD3 complex. Mol Immunol. 2004;40:1295-305. <br />37. Pitcher LA, Mathis MA, Young JA, DeFord LM, Purtic B, Wulfing C, et al. The CD3 ge/de signaling module provides normal T cell functions in the absence of the TCR z immunoreceptor tyrosine-based activation motifs. Eur J Immunol. 2005;35:3643-54. <br />38. Lysechko TL, Ostergaard HL. Differential src family kinase activity requirements for CD3z phosphorylation/ ZAP70 recruitment and CD3ε phosphorylation. J Immunol. 2005;174:7807-14. <br />39. Davis MM. A new trigger for T cells. Cell. 2002;110: 285-7 <br />40. Szymczak AL, Workman CJ, Gil D, Dilioglou S, Vignali KM, Palmer E, et al. The CD3 proline-rich sequence, and its interaction with Nck, is not required for T cell development and function. J Immunol. 2005;175:270-5. <br /> <br />
oai:oai.revistabiomedica.org:article/98
2010-01-26T14:37:32Z
biomedica:ARTI
Prevalence of epithelial squamous cell abnormalities and associated factors in women of a rural town of Colombia
Prevalencia de anormalidades de células epiteliales y factores asociados en mujeres de un municipio rural colombiano
Arbeláez, María Patricia
Grisales, Hugo
Vanegas, Ángela Patricia
Gaviria, Ángela M.
Castaño, Jorge
Mora, Martín Alonso
Borrero, Mauricio
Rojas, Carlos
Sanchez, Gloria I.
neoplasias del cuello uterino/epidemiología
células epiteliales
frotis vaginal
citología
neoplasia intraepitelial del cuello uterino/prevención y control
Colombia
uterine cervical neoplasms/epidemiology
epithelial cells
cervical cancer
vaginal smears
cytology
control and prevention
cervical intraepithelial neoplasia/prevention and control
Colombia
Introduction. In spite of implementation of cytology-based cervical cancer screening in Colombia, mortality rates remain stable. The description of factors associated to cervical pre-neoplasic lesions is needed to establish strategies for mortality prevention.Objective. The prevalence of epithelial squamous cell abnormalities was determined to explore the association of cytology abnormalities with described risk factors. Materials and methods. This population-based, cross-sectional study included 739 women randomly selected by age. A validated face-to-face questionnaire and conventional cervical cytology were used to collect the information. To establish the association between cervical abnormalities and some qualitative variables, the independent chi squared test was used. We also calculated prevalence ratio with their 95% confidence intervals. A logistic regression model was used to explore variables that potentially explain cytology abnormalities.Results. The prevalence of squamous cell abnormality was 15.8%. Among women with abnormal cytology, 10% presented atypical squamous cells of undetermined significance, 3.9% low grade squamous intra-epithelial lesion and 1.9% high grade squamous intra-epithelial lesion. The adjusted logistical regression analysis showed that history of sexual transmitted disease, two or more sexual partners during entire life and previous abnormal cytology were associated with cytology abnormalities.Conclusion. The relation of epithelial squamous cell abnormalities with sexual behavior history reflexes the link between human papiloma virus infection and cervical cancer pre-neoplasic lesions. The frequency of use and knowledge about the purpose of cytology were factors that suggested other diagnostic limitations such as quality of cervical cytology or barriers to access health care. These latter factors may be the underlying basis for the high cervical cancer mortality rates.
Introducción. A pesar de la existencia de los programas de tamización basados en la citología, las tasas de cáncer de cuello uterino permanecen estables en Colombia. La descripción de los factores asociados a las lesiones precursoras de cáncer de cuello uterino es necesaria para establecer estrategias para su prevención.Objetivo. Determinar la prevalencia de las anormalidades de células epiteliales escamosasy su asociación con los factores de riesgo descritos.Materiales y métodos. Estudio transversal de población en 739 mujeres, seleccionadas en forma aleatoria. La información se recolectó mediante la citología y un cuestionario previamente validado. La medida de asociación fue la razón de prevalencia con su respectivo intervalo de confianza del 95%. Las variables de confusión fueron controladas en un modelo de regresión logística multivariado.Resultados.La prevalencia del evento fue de 15,8%. Entre las mujeres con citología anormal, 10% presentó células escamosas atípicas de significado indeterminado; 3,9%, lesión escamosa intraepitelial de bajo grado, y 1,9%, lesión escamosa intraepitelial de alto grado.La regresión logística ajustada sugiere que los antecedentes de enfermedades de transmisión sexual, una citología anormal y tener dos o más parejas regulares/ocasionales durante la vida se asocian con la presencia del evento.Conclusiones. La relación de anormalidades de células escamosas con conducta sexual refleja la asociación entre el virus del papiloma humano y lesiones preneoplásicas de cáncer de cuello uterino. El uso frecuente y el adecuado conocimiento sobre la citología, sugiere que aspectos tales como las dificultades con la calidad de la citología o el acceso al diagnóstico y tratamiento, pudieran explicar las altas tasas de cáncer de cuello uterino.
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/98
10.7705/biomedica.v28i2.98
Biomedica; Vol. 28 No. 2 (2008); 271-283
Biomédica; Vol. 28 Núm. 2 (2008); 271-283
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/98/96
/*ref*/Yang BH, Bray FI, Parkin DM, Sellors JW, Zhang ZF. Cervical cancer as a priority for prevention in different world regions: an evaluation using years of life lost. Int J Cancer. 2004;109:418-24. <br />2. Parkin DM, Bray F. The burden of HPV-related cancers. Vaccine. 2006;24(Suppl.3):S11-25. <br />3. Piñeros M, Ferlay J, Murillo R. Cancer incidence estimates at the national and district levels in Colombia. Salud Pública Mex. 2006;48:455-65. <br />4. Piñeros M, Cendales R, Murillo R, Wiesner C, Tovar S. Pap test coverage and related factors in Colombia, 2005. Rev Salud Pública (Bogotá). 2007;9:327-41. <br />5. Walboomers JM, Jacobs MV, Manos MM, Bosch FX, Kummer JA, Shah KV, et al. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J Pathol. 1999;189:12-9. <br />6. Burchell AN, Winer RL, de Sanjose S, Franco EL. Chapter 6: Epidemiology and transmission dynamics of genital HPV infection. Vaccine. 2006;24 (Suppl. 3):S52-61. <br />7. Moscicki AB, Schiffman M, Kjaer S, Villa LL. Updating the natural history of HPV and anogenital cancer. Vaccine. 2006;24(Suppl.3):S42-51. <br />8. Solomon D, Davey D, Kurman R, Moriarty A, OConnor D, Prey M, et al. The 2001 Bethesda System: terminology for reporting results of cervical cytology. JAMA. 2002;287:2114-9. <br />9. Kitchener HC, CastlePE, Cox JT. Achievements and limitations of cervical cytology screening. Vaccine. 2006;24(Suppl.3):S63-70. <br />10. Almonte M, Ferreccio C, Winkler JL, Cuzick J, Tsu V, Robles S, et al. Cervical screening by visual inspection, HPV testing, liquid-based and conventional cytology in Amazonian Peru. Int J Cancer. 2007;121:796-802. <br />11. Goldie SJ, Kim JJ, Kobus K, Goldhaber-Fiebert JD, Salomon J, Oshea MK, et al. Cost-effectiveness of HPV 16, 18 vaccination in Brazil. Vaccine. 2007;25:6257-70. <br />12. Arbyn M, Sasieni P, Meijer CJ, Clavel C, Koliopoulos G, Dillner J. Clinical applications of HPV testing: A summary of meta-analyses. Vaccine. 2006;24(Suppl.3):S78-89. <br />13. Herrero R, Hildesheim A, Bratti C, ShermanME, Hutchinson M, Morales J, et al. Population-based study of human papillomavirus infection and cervical neoplasia in rural Costa Rica. J Natl Cancer Inst. 2000;92:464-74. <br />14. Hosmer DW, Lemeshow S. Applied Logistic Regression. New York: Wiley Interscience, John Wiley & Sons, Inc; 2000. <br />15. Lazcano-Ponce E, Herrero R, Muñoz N, Cruz A, Shah K, Alonso P, et al. Epidemiology of HPV infection among Mexican women with normal cervical cytology. Int J Cancer. 2000;91:412-20. <br />16. Molano M, Posso H, Weiderpass E, van den Brule AJ, Ronderos M, Franceschi S, et al. Prevalence and determinants of HPV infection among Colombian women with normal cytology. Br J Cancer. 2002;87: 324-33. <br />17. Ferreccio C, Prado RB, Luzoro AV, Ampuero SL, Snijders PJ, Meijer CJ, et al. Population-based prevalence and age distribution of human papillomavirus among women in Santiago, Chile. Cancer Epidemiol Biomarkers Prev. 2004;13:2271-6. <br />18. Molano M, van den Brule AJ, Posso H, Weiderpass E, Ronderos M, Franceschi S, et al. Low grade squamous intra-epithelial lesions and human papillomavirus infection in Colombian women. Br J Cancer. 2002;87:1417-21. <br />19. Stoler MH, Schiffman M. Interobserver reproducibility of cervical cytologic and histologic interpretations: realistic estimates from the ASCUS-LSIL Triage Study. JAMA. 2001;285:1500-5. <br />20. Confortini M, Carozzi F, Dalla Palma P, Ghiringhello B, Parisio F, Prandi S, et al. Interlaboratory reproducibility of atypical squamous cells of undetermined significance report: a national survey. Cytopathology. 2003;14:263-8. <br />21. Castellsague X, Bosch FX, Munoz N. The male role in cervical cancer. Salud Pública Mex. 2003;45 (Suppl.3):S345-53. <br />22. Profamilia. Encuesta Nacional de Demografía y Salud-ENDS 2005. Consultado: 16 de agosto de 2007. Disponible en: <a href="http://www.profamilia.org.co/encuestas/01encuestas/2005resultados_generales.htm">http://www.profamilia.org.co/encuestas/01encuestas/2005resultados_generales.htm</a> <br />23. Paavonen J, Jenkins D, Bosch FX, Naud P,Salmeron J, Wheeler CM, et al. Efficacy of a prophylactic adjuvanted bivalent L1 virus-like-particle vaccine against infection with human papillomavirus types 16 and 18 in young women: an interim analysis of a phase III double-blind, randomized controlled trial. Lancet. 2007;369:2161-70. <br />24. Ault KA, Future II Study Group. Effect of prophylactic human papillomavirus L1 virus-like-particle vaccine on risk of cervical intraepithelial neoplasia grade 2, grade 3, and adenocarcinoma in situ: a combined analysis of four randomized clinical trials. Lancet. 2007;369:1861-8. <br />25. Hildesheim A, Herrero R, Wacholder S, RodríguezAC, Solomon D, Bratti MC, et al. Effect of human papillomavirus 16/18 L1 viruslike particle vaccine among young women with preexisting infection: a randomized trial. JAMA. 2007;298:743-53. <br />26. Markowitz LE. HPV vaccines prophylactic, not therapeutic. JAMA. 2007;298:805-6. <br />27. Hanisch R, Gustat J, Hagensee ME, Baena A, Salazar JE, Castro MV, et al. Knowledge of Pap screening and human papillomavirus among women attending clinics in Medellin, Colombia. Aceptado. Int J Gynecol Cancer. 2007. doi: 10.1111/j.1525- 1438.2007.01131. <br />28. Flores Y, Bishai D, Lazcano E, Shah K, Lorincz A, Hernández M, et al. Improving cervical cancer screening in Mexico: results from the Morelos HPV Study. Salud Pública Mex. 2003;45(Suppl.3):S388-98. <br />
oai:oai.revistabiomedica.org:article/99
2010-01-26T14:43:56Z
biomedica:ARTI
Resistance profiles to fluoroquinolones in clinical isolates of Gram positive cocci
Perfiles de resistencia a fluoroquinolonas en aislamientos clínicos de cocos Gram positivos provenientes de hospitales colombianos, 1994-2004
Arias, César A.
Hidalgo, Marylin
Reyes, Jinnethe
Cárdenas, Ana María
Díaz, Lorena
Ríncon, Sandra
Vanegas, Natasha
Díaz, Paula Lucía
Castañeda, Elizabeth
fluoroquinolonas
Streptococcus pneumoniae
Staphylococcus aureus
Enterococcus
resistencia microbiana a los medicamentos
Colombia
fluoroquinolones
Streptococcus pneumoniae
Staphylococcus aureus
Enterococcus
drug resistance
microbial
Colombia
Introduction. Fluoroquinolones are broad spectrum antibiotics commonly used in the treatment of infections.Objective. Resistance profiles of coccus bacteria to fluoroquinolones were evaluated in isolates of Streptococcus pneumoniae, Staphylococcus aureus, coagulase negative staphylococci and Enterococcus spp. The samples were recovered from Colombian hospitals between 1994 and 2004.Materials and methods. The minimal inhibitory concentration of ciprofloxacin, moxifloxacin and gatifloxacin was determined in 270 clinical isolates of S. pneumoniae, 348 of S. aureus, 176 of coagulase negative staphylococci and 123 of coagulase-negative enterococci. The minimal inhibitory concentration of levofloxacin was also determined in all isolates of methicillin-resistant S. aureus. An agar diffusion susceptibility test with disks of levofloxacin and ofloxacin was also applied to all isolates of S. pneumoniae.Results. A total of 269 (99.6%) isolates of S. pneumoniae were susceptible to moxifloxacin and gatifloxacin. For levofloxacin and ofloxacin, resistance in S. pneumoniae was found in 1.5% and 8.9% of isolates, respectively. The ciprofloxacin minimal inhibitory concentration was >4 µg/ml in 15.9% of pneumococcal isolates. The rates of resistance to ciprofloxacin, gatifloxacin and moxifloxacin in the 348 S. aureus isolates were 55.4%, 54.9% and 52.6%, respectively; increasing to 92.3%, 91.3% and 87.5%, respectively in methicillin resistant isolates. Resistance to levofloxacin was found in 91.8% of MRSA isolates. The rates of resistance to ciprofloxacin, gatifloxacin and moxifloxacin in coagulase negative staphylococci and vancomycin-susceptible enterococci were between 25.6% and 31.8%. All vancomycin-resistant enterococci were resistant to all fluroquinolones tested.Conclusion. The newer fluoroquinolones have maintained effective activity against clinical isolates of S. pneumoniae. The rates of fluoroquinolone resistance in S. aureus were very high, particularly in methicillin resistant isolates (approaching 100%).
Introducción. Las fluoroquinolonas son antibióticos de amplio espectro comúnmente utilizados en el manejo de infecciones.Objetivo. Determinar los patrones de resistencia a fluoroquinolonas en aislamientos colombianos de Streptococcus pneumoniae, Staphylococcus aureus, estafilococos coagulasa negativa y enterococos de centros hospitalarios colombianos, recolectados entre 1994 y 2004.Materiales y métodos. Se realizó la determinación de concentraciones inhibitorias mínimas frente a ciprofloxacino, moxifloxacino y gatifloxacino a 270 aislamientos clínicos de S. pneumoniae, 348 de S. aureus, 176 de estafilococos coagulasa negativa y 123 de enterococos.Para los aislamientos de S. aureus resistentes a la meticilina se determinó la concentración inhibitoria mínima frente a levofloxacino y para aislamientos de S. pneumoniae se realizó la prueba de difusión en agar con discos de ofloxacino y levofloxacino.Resultados. Doscientos sesenta y nueve (99,6%) aislamientos de S. pneumoniae fueron susceptibles a gatifloxacino y moxifloxacino; para levofloxacino y ofloxacino la resistencia fue del 1,5% y 8,9%, respectivamente. El 15,9% de S. pneumoniae tuvo una concentración inhibitoria mínima ³ ³³ ³³4 µg/ml frente a ciprofloxacino. Las prevalencias de resistencia para ciprofloxacino, gatifloxacino y moxifloxacino en los 348 aislamientos de S. aureus fueron 55,4%, 54,9% y 52,6%, y en S. aureus resistentes a meticilina, fueron 92,3%, 91,3% y 87,5% y 91,8% para levofloxacino. En estafilococos coagulasa negativa y enterococos susceptibles a vancomicina se observaron tasas de resistencia entre 25,6% y 31,8%. Todos los aislamientos de enterococos resistente a vancomicina fueron resistentes a los compuestos evaluados.Conclusión. Los aislamientos colombianos de S. pneumoniae mantienen susceptibilidad a las fluoroquinolonas de última generación. La resistencia a fluoroquinolonas es alta en S. aureus, especialmente en aislamientos resistentes a la meticilina (cercana al 100%).
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/99
10.7705/biomedica.v28i2.99
Biomedica; Vol. 28 No. 2 (2008); 284-294
Biomédica; Vol. 28 Núm. 2 (2008); 284-294
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/99/97
/*ref*/Lesher GY, Froelich EJ, Gruett MD, Bailey JH, Brundage RP. 1,8-Naphthyridine derivates: a new class of chemotherapeutic agents. J Med Pharm Chem. 1962;5:1063-5. <br />2. Hopper DC. New uses for new and old quinolones and challenge of resistance. Clin Infect Dis. 2000;30:243-54. <br />3. Hooper DC. Fluoroquinolone resistance among Gram-positive cocci. Lancet Infect Dis. 2002;2:530-8. <br />4. Saravolatz LD, Leggett J. Gatifloxacin, gemifloxacin, and moxifloxacin: the role of 3 newer fluoroquinolones. Clin Infect Dis. 2003;37:1210-5. <br />5. Jacoby GA. Mechanisms of resistance to quinolones. Clin Infect Dis. 2005;41:S120-6. <br />6. Schmitz FJ, Higgins PG, Mayer S, Fluit AC, Dalhof A. Activity of quinolones against Gram positive cocci: Mechanisms of drug action and bacterial resistance. Eur J Clin Microbiol Infect Dis. 2002;21:647-59. <br />7. Tran JH, Jacoby GA. Mechanism of plasmid-mediated quinolone resistance. Proc Natl Acad Sci USA. 2002;99: 5638-42. <br />8. Ruiz J. Mechanisms of resistance to quinolones: target alterations, decreased accumulation and DNA gyrase protection. J Antimicrob Chemother. 2003;51:1109-17. <br />9. Arsene S, Leclercq R. Role of a qnr-like gene in the intrinsic resistance of Enterococcus faecalis to fluoroquinolones. Antimicrob Agents Chemother. 2007;51:3254-8. <br />10. Arias CA, Reyes J, Zuñiga M, Cortés L, Cruz C, Rico CL, et al. Multicentre surveillance of antimicrobial resistance in enterococci and staphylococci from Colombian hospitals, 2001-2002. J Antimicrob Chemother. 2003;51:59-68. <br />11. Álvarez C, Cortés J, Arango A, Correa C, Leal A, Grupo para el Control de la Resistencia Bacteriana en Bogotá. Antimicrobial resistance in intensive care units in Bogotá, Colombia, 2001-2003. Rev Salud Pública (Bogotá). 2006;8(Suppl.1):86-101. <br />12. Grupo de Microbiología. Streptococcus pneumoniae aislamientos invasores. Consultado: 19 de septiembre 2006.Disponible en: <a href="http://www.ins.gov.co/pdf_investiga/Microbiologia_spn_005.pdf">http://www.ins.gov.co/pdf_investiga/Microbiologia_spn_005.pdf</a>. <br />13. Organización Panamericana de la Salud. Programa de Vigilancia de los serotipos y resistencia antimicrobiana de Streptococcus pneumonaie y Haemophilus influenzae. Manual de Procedimientos. Consultado: 3 de marzo de 2006. Disponible en:http://www.paho.org/Spanish/AD/THS/EV/LABS-manual-vigilancia-serotipos.pdf. <br />14. Agudelo CI, Moreno J, Sanabria OM, Ovalle MV, Di Fabio JL, Castañeda E, et al. Streptococcus pneumoniae: evolución de los serotipos y los patrones de susceptibilidad antimicrobiana en aislamientos invasores en 11 años de vigilancia en Colombia (1994- 2004). Biomédica. 2006;26:234-49. <br />15. Martineau F, Picard FJ, Lansac N, Ménard C, Roy PH, Ouellette M, et al. Correlation between the resistance genotype determined by multiplex PCR assays and the antibiotic susceptibility patterns of Staphylococcus aureus and Staphylococcus epidermidis. Antimicrob Agents Chemother. 2000;44: 231-8. <br />16. Dutka-Malen S, Evers S, Courvalin P. Detection of glycopeptide resistance genotypes and identification to the species level of clinically relevant enterococci by PCR. J Clin Microbiol. 1995;33:24-7. <br />17. Woodford N, Egelton CM, Morrison D. Comparison of PCR with phenotypic methods for the speciation of enterococci. Adv Exp Med Biol. 1997;418:405-8. <br />18. Reyes J, Hidalgo M, Díaz L, Rincón S, Moreno J, Vanegas N, et al. Characterization of macrolide resistance in Gram-positive cocci from Colombian hospitals: a countrywide surveillance. Int J Infect Dis. 2007;11:329-36. <br />19. Cruz C, Moreno J, Renzoni A, Hidalgo M, Reyes J, Schrenzel J, et al. Tracking methicillin-resistant Staphylococcus aureus clones in Colombian hospitals over 7 years (1996-2003): emergence of a new dominant clone. Int J Antimicrob Agents. 2005;26:457-62. <br />20. Clinical and Laboratory Standards Institute. Performance Standards for Antimicrobial Susceptibility Testing: Fifteenth Informational Supplement. M7-A6 Methods for dilution antimicrobial susceptibility test for bacteria that grow aerobically: Approved Standard. Sixth Edition. Wayne, Pennsylvania: CLSI; 2005. <br />21. Clinical and Laboratory Standards Institute. Performance Standards for Antimicrobial Susceptibility Testing: Fifteenth Informational Supplement. M2-A8 Performance standards for antimicrobial disk susceptibility test; Approved standard. Eighth edition. Wayne, Pennsylvania: CLSI; 2005. <br />22. López H, Sader H, Amábile C, Pedreira W, Muñoz-Bellido JL, García-Rodríguez JA, et al. in vitro activity of moxifloxacin against respiratory pathogens in Latin America. Rev Esp Quimioter. 2002;15:325-34 <br />23. Adam HJ, Schurek KN, Nichol KA, Hoban CJ, Baudry TJ, Laing DJ, et al. Molecular characterization of increasing fluoroquinolone resistance in Streptococcus pneumoniae in Canada 1997 to 2005. Antimicrob Agents Chemother. 2007;51:198-207. <br />24. Song JH, Jung SI, Ko KS, Kim NY, Son JS, Chang HH, et al. High prevalence of antimicrobial resistance among clinical Streptococcus pneumoniae isolates in Asia (an ANSORP study). Antimicrob Agents Chemother. 2004;48:2101-7. <br />25. Ip M, Chau SSL, Chi F, Cheuk ES, Ma H, Lai RW, et al. Longitudinally tracking fluoroquinolone resistance and its determinants in penicillin-susceptible and non-susceptible Streptococcus pneumoniae isolates in Hong Kong, 2000-2005. Antimicrob Agents Chemother. 2007; 51:2192-4. <br />26. Pérez-Trallero E, Fernández-Mazarrasa C, García-Rey C, Bouza E, Aguilar L, García-de-Lomas J, et al. Spanish Surveillance Group for Respiratory Pathogens. Antimicrobial susceptibilities of 1,684 Streptococcus pneumoniae and 2,039 Streptococcus pyogenes isolates and their ecological relationships: results of a 1-year (1998-1999) multicenter surveillance study in Spain. Antimicrob Agents Chemother. 2001;45: 3334-40. <br />27. Mandell LA, Bartlett JG, Dowell SF, File TM, Musher DM, Whitney C, et al. Update of practice guidelines for the management of community-acquired pneumonia in immunocompetent adults. Clin Infect Dis. 2003;37: 1405-33. <br />28. Ambrose PG, Bast D, Doern GV, Iannini PB, Jones RN, Klugman KP, et al. Fluoroquinolone-resistant Streptococcus pneumoniae, an emerging but unrecognized public health concern: is it time to resight the goalposts? Clin Infect Dis. 2004;39:1554-6. <br />29. Fuller JD, Low D. A review of Streptococcus pneumoniae infection treatment failures associated with fluoroquinolone resistance. Clin Infect Dis. 2005;41: 118-21. <br />30. Legg JM, Bint AJ. Will pneumococci put quinolones in their place? J Antimicrob Chemother. 1999;44:425-7. <br />31. Niederman MS. Challenges in the management of community-acquired pneumonia: the role of quinolones and moxifloxacin. Clin Infect Dis. 2005;41:S158-66. <br />32. Dobay O, Rozgonyi F, Ghidán A, Matuz M, Nagy K, Amyes SG. The first steps towards fluoroquinolone resistance in Hungarian pneumococci. J Chemother. 2006;18:624-7. <br />33. Dias R, Louro D, The Antimicrobial Resistance Surveillance Program in Portugal, Caniça M. Antimicrobial susceptibility of invasive Streptococcus pneumoniae isolates in Portugal over an 11-Year Period. Antimicrob Agents Chemother. 2006;50:2098-105. <br />34. Jones ME, Blosser-Middleton RS, Thornsberry C, Karlowsky JA, Sahm DF. The activity of levofloxacin and other antimicrobials against clinical isolates of Streptococcus pneumon iae collected worldwide during 1999-2002. Diagn Microbiol Infect Dis. 2003;47:579- 86. <br />35. Ho PL, Yung RW, Tsang DN, Que TL, Ho M, Seto WH. Increasing resistance of Streptococcus pneumoniae to fluoroquinolones: results of a Hong Kong multicentre study in 2000. J Antimicrob Chemother. 2001; 48:659-65. <br />36. Richter SS, Heilmann KP, Beekmann SE, Miller NJ, Rice CL, Doern GV. The molecular epidemiology of Streptococcus pneumoniae with quinolone resistant mutations. Clin Infect Dis. 2005;40:225-35. <br />37. Karlowsky JA, Jones ME, Draghi DC, Thornsberry C, Sahm DF, Volturo GA. Prevalence and antimicrobial susceptibilities of bacteria isolated from blood cultures of hospitalized patients in the United States in 2002. Ann Clin Microbiol Antimicrob. 2004;10:3-7. <br />38. Canton R, Morosini M, Enright MC, Morrissey I. Worldwide incidence, molecular epidemiology and mutations implicated in fluoroquinolone-resistant Streptococcus pneumoniae: data from the global PROTEKT surveillance programme. J Antimicrob Chemother. 2003;52:944-52. <br />39. Andrews J, Ashby J, Jevons G, Marshall T, Lines N, Wise R. A comparison of antimicrobial resistance rates in Gram-positive pathogens isolated in the UK from October 1996 to January 1997 and October 1997 to January 1998. J Antimicrob Chemother. 2000;45: 285-93. <br />40. El Kholy A, Baseem H, Hall GS, Procop GW, Longworth DL. Antimicrobial resistance in Cairo, Egypt 1999-2000: a survey of five hospitals. J Antimicrob Chemother. 2003;51:625-30. <br />41. Decousser JW, Pina P, Picot F, Delalande C, Pangon B, Courvalin P, et al. Frequency of isolation and antimicrobial susceptibility of bacterial pathogens isolated from patients with bloodstream infections: a French prospective national survey. J Antimicrob Chemother. 2003;51:1213-22. <br />42. Blumberg HM, Rimland D, Carroll DJ, Terry P, Wachsmuth IK. Rapid development of ciprofloxacin resistance in methicillin-susceptible and methicillin-resistant Staphylococcus aureus. J Infect Dis. 1991; 163:1279-85. <br />43. Zangrillo A, Landoni G, Fumagalli L, Bove T, Bellotti F, Sottocorna O, et al. Methicillin-resistant Staphylococcus species in a cardiac surgical intensive care unit: a 5-year experience. J Cardiothorac Vasc Anesth. 2006;20:31-7. <br />44. Klevens M. Changes in the epidemiology of methicillin-resistant Staphylococcus aureus in intensive care units in US hospitals, 1992-2003 . Clin Infect Dis. 2006;42: 389-91. <br />45. Reynolds R, Potz N, Colman M, Williams A, Livermore D, MacGowan A, et al. Antimicrobial susceptibility of the pathogens of bacteraemia in the UK and Ireland 2001-2002: the BSAC Bacteraemia Resistance Surveillance Programme. J Antimicrob Chemother. 2004;53:1018-32. <br />46. Andrade SS, Sader HS, Jones RN, Pereira AS, Pignatari AC, Gales AC. Increased resistance to first-line agents among bacterial pathogens isolated from urinary tract infections in Latin America: time for local guidelines? Mem Inst Oswaldo Cruz. 2006;101:741-8. <br />47. Deshpande LM, Fritsche TR, Moet GJ, Biedenbach DJ, Jones RN. Antimicrobial resistance and molecular epidemiology of vancomycin-resistant enterococci from North America and Europe: a report from the SENTRY antimicrobial surveillance program. Diagn Microbiol Infect Dis. 2007;58:163-70. <br />48. Aires De Sousa M, Miragaia M, Sanches IS, Avila S, Adamson I, Casagrande ST, et al. Three-year assessment of methicillin-resistant Staphylococcus aureus clones in Latin America from 1996 to 1998. J Clin Microbiol. 2001;39:2197-205. <br />49. Weber SG, Gold HS, Hooper DC, Karchmer AW, Carmeli Y. Fluoroquinolones and the risk for methicillin-resistant Staphylococcus aureus in hospitalized patients. Emerg Infect Dis. 2003;9:1415-22. <br />50. Loo VG, Poirier L, Miller MA, Oughton M, Libman MD, Michaud S, et al. A predominantly clonal multi-institutional outbreak of Clostridium difficile-associated diarrhea with high morbidity and mortality. N Engl J Med. 2005;8;353:2442-9. <br />51. Sanders CC. Mechanisms responsible for cross-resistance and dichotomous resistance among the quinolones. Clin Infect Dis. 2001;32(Suppl.1):S1-8. <br />52. Rodríguez-Martínez JM. Mechanisms of plasmid-mediated resistance to quinolones. Enferm Infecc Microbiol Clin. 2005;23:25-31. <br />53. Álvarez CA, Barrientes OJ, Leal AL, Contreras GA, Barrero L, Rincón S, et al. Community-associated methicillin-resistant Staphylococcus aureus, Colombia. Emerg Infect Dis. 2006;12:2000-1. <br />
oai:oai.revistabiomedica.org:article/100
2010-01-26T00:29:32Z
biomedica:EDUC
Haga usted el diagnóstico Segunda parte
Knudson, Ángelica
Motta, Adriana
Sopó, Leticia
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
250
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/100
10.7705/biomedica.v28i2.100
Biomedica; Vol. 28 No. 2 (2008); 295-297
Biomédica; Vol. 28 Núm. 2 (2008); 295-297
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/100/98
/*ref*/Mok WY. Nature and Identification of Exophiala werneckii. J Clin Microbiol. 1982;16:976-8.<br />2. Pegas JR, Criado PR, Lucena SK, de Oliveira MA. Tinea nigra: report of two cases in infants. Pediatr Dermatol. 2003;20:315-7.<br />3. Schwartz RA. Superficial fungal infections. Lancet. 2004;364:1173-82..297<br />4. Severo LC, Bassanesi MC, Gonder AT. Tinea nigra: report of four cases observed in Rio Grande do Sul (Brazil) and a review of Brazilian literature. Mycopathologia. 1994;126:157-62.<br />5. Perez C, Colella MT, Olaizola C, Hartung de Capriles C, Magaldi S, Mata-Essayag S. Tinea nigra: report of twelve cases in Venezuela. Mycopathologia. 2005;160:235-8.<br />6. Uezato H, Gushi M, Hagiwara K, Kayo S, Hosokawa A, Nonaka S. A case of tinea nigra palmaris in Okinawa, Japan. J Dermatol. 2006;33:23-9.<br />7. Dixon DM, Polak-Wyss A. The medically important dematiaceous fungi and their identification. Mycoses. 1991;34:1-18.<br />8. McGinnis MR, Schell WA, Carson J. Phaeoannellomyces and the Phaeococcomycetaceae, new dematiaceous blastomycete taxa. Sabouraudia. 1985;23:179-88.<br />9. Arango M, Castañeda E. Micosis humanas. Procedimientos diagnósticos. Exámenes directos. Segunda edición. Medellín, Bogotá, D.C.: Corporación para Investigaciones Biológicas, Instituto Nacional de Salud; 2003.<br />10. McGinnis MR. Chromoblastomycosis and phaeohypho-mycosis: new concepts, diagnosis, and mycology. JAm Acad Dermatol. 1983;8:1-16.<br />11. Revankar SG. Dematiaceous fungi. Mycoses. 2007;50:91-101.
oai:oai.revistabiomedica.org:article/101
2010-01-26T14:50:28Z
biomedica:BREV
In vitro effect of caffeine on internal mammary artery rings used in cardiac revascularization surgery
Acción in vitro de la cafeína en anillos de arteria mamaria interna utilizada en cirugía de revascularización cardiaca
Echeverry, Darío
Montes, Félix R.
Delgadillo, Alexandra
Beltrán, Marcela
Buitrago, Lorena
cafeína/uso terapéutico
revascularización miocárdica
vasodilatación
aorta
ateroesclerosis
endotelio
acetilcolina
caffeine/therapeutic use
myocardial revascularization
vasodilation
aorta
atherosclerosis
endothelium
acetylcholine
Introduction. The vasodilator effect of caffeine in animal models arteries has been demostrated previously. However, studies with the same methodology using human arteries in vitro have not been performed.Objectives. The in vitro vasoactive effects of caffeine was evaluated on human internal mammary arteries.Materials and methods. Internal mammary artery rings were used (n=20). Endothelial function was evaluated with acetylcholine at a concentration of 3.16x10 -6 M, nitroglycerine at cumulative concentrations of 10 –11 M to 10 –4 M and caffeine with cumulative concentrations of 10 –8 M to 10 –4 M.Results. Nitroglycerin produced a maximum relaxation percentage of 87.4±12.3%, caffeine a percentage of 86.9±21.0% in arteries with functional endothelium, and of 71.6±28.6% in arteries with endothelial dysfunction. No differences were detected among the three groups ( p=0.289).Similarly, no differences were found between EC 50 in arteries with functional endothelium (1.66x10 -5 ±1.57x10 -5 M) and dysfunctional arteries (7.8 x10 -5 ±14.6 x10 -5 M). Nitroglycerine proved more potent than caffeine (EC 50 = 4.3 x10 -9 ±4.4x10 -9 M) ( p=0.013).Conclusions. Although nitroglycerin was a more potent vasodilator, caffeine had a strong arterial vasodilator effect regardless of endothelial function in human arteries.
Introducción. El efecto vasodilatador de la cafeína en las arterias de modelos animales ya ha sido demostrado. Se desconocen estudios con la misma metodología in vitro utilizando arterias humanas.Objetivos. Evaluar los efectos vasoactivos in vitro de la cafeína en la arteria mamaria interna de humanos.Materiales y métodos. Se utilizaron 80 anillos de arteria mamaria interna (n=20 pacientes).La funcionalidad del endotelio se evaluó con acetilcolina a una concentración de 3,16x10-6M, de nitroglicerina con dosis acumulativas de 10 -11 M a 10 -4 M y de cafeína con concentraciones acumulativas de 10 -8 M a 10-4 M.Resultados. La nitroglicerina indujo un porcentaje máximo de relajación de 87,4±12,3%, la cafeína, de 86,9±21,0% en arterias con endotelio funcional y de 71,6±28,6% en arterias con disfunción endotelial. No se encontraron diferencias entre los tres grupos ( p=0,289). Tampoco se encontraron diferencias en la EC 50 en arterias con endotelio funcional (1,66x10 -5 ±1,57x10 -5 M) y arterias disfuncionales (7,75x10 -5 ±14,64x10 -5 M). La nitroglicerina resultó más potente que la cafeína (EC 50 = 4,30x10 -9 ±4,35x10 -9 M) ( p=0,013).Conclusiones. Aunque la nitroglicerina fue un vasodilatador más potente, la cafeína tuvo un fuerte efecto vasodilatador arterial in vitro independientemente de la funcionalidad del endotelio en arterias humanas.
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/101
10.7705/biomedica.v28i2.101
Biomedica; Vol. 28 No. 2 (2008); 298-304
Biomédica; Vol. 28 Núm. 2 (2008); 298-304
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/101/99
/*ref*/Ascherio A, Chen H, Schwarzschild MA, Zhang SM, Colditz GA, Speizer FE. Caffeine, postmenopausal estrogen, and risk of Parkinson´s disease. Neurology. 2003;60:790-5. <br />2. Bruce MS, Lader M. Caffeine abstention in the management of anxiety disorders. Psychol Med. 1989;19: 211-4. <br />3. Klag MJ, Wang NY, Meoni LA, Brancati FL, Cooper LA, Liang KY, et al. Coffee intake and risk of hypertension: the Johns Hopkins Precursors Study. Arch Intern Med. 2002;162:657-62. <br />4. James JE. Critical review of dietary caffeine and blood pressure: A relationship that should be taken more seriously? Psychosom Med. 2004;66:63-71. <br />5. Temple ME, Luzier AB, Kazierad DJ. Homocysteine as a risk factor for atherosclerosis. Ann Pharmacother. 2000;34:57-65. <br />6. Brugada P, Gursoy S, Brugada J, Andries E. Investigation of palpitations. Lancet. 1993;341:1254-8. <br />7. Grobbee DE, Rimm EB, Giovannucci E, Colditz G, Stampfer M, Willett W. Coffee, caffeine, and cardio-vascular disease in men. N Engl J Med. 1990;323:1026- 32. <br />8. Tverdal A, Stensvold I, Solvoll K, Foss PO, Lund-Larsen P, Bjartveit K. Coffee consumption and death from coronary heart disease in middle aged Norwegian men and women. BMJ. 1990;300:566-9. <br />9. Wilson PW, Garrison RJ, Kannel WB, McGee DL, Caselli WP. Is coffee consumption a contributor to cardiovascular disease? Insights from the Framingham Study. Arch Intern Med. 1989;149:1169-72. <br />10. Woodward M, Tunstall-Pedoe H. Coffee and tea consumption in the Scottish Heart Health Study follow up: conflicting relations with coronary risk factors, coronary disease, and all cause mortality. J Epidemiol Community Health. 1999;53:481-7. <br />11. Corti R, Binggeli C, Sudano I, Spieker L, Hanseler E, Ruschitzka F, et al. Coffee acutely increases sym-pathetic nerve activity and blood pressure indepen-dently of caffeine content role of habitual versus non-habitual drinking. Circulation. 2002;106:2935-40. <br />12. Vanhoutte PM, Perrault LP, Vilaine JP. Endothelial dysfunction and vascular disease. In: Rubanyi GM and Dzau VJ Eds. The endothelium in clinical practice. Source and target of novel therapies. New York: Marcel Dekker, Inc.; 1997. p. 265-89.. 13. Furchgott RF, Zawadzki JV. The obligatory role of endothelial cells in the relaxation of smooth muscle by acetylcholine. Nature. 1980;288:373-6. <br />14. Habib JB, Bossaller C, Wells S, Williams C, Morriset JD, Henry PD. Preservation of endothelium-dependent vascular relaxation in cholesterol fed rabbit by treatment with the calcium blocker PN200110. Cir Res. 1986;58:305-9. <br />15. Hatano Y, Mizumoto K, Yoshiyama T, Yamamoto M, Iranami H. Endothelium-dependent and -indepen-dent vasodilation of isolated rat aorta induced by caf-feine. Am J Physiol. 1995;269:H1679-84. <br />16. Watanable C, Yamamoto H, Hirano K, Kobayashi S, Kanaide H. Mechanisms of caffeine- induced contraction and relaxation of rat aortic smooth muscle. J Physiol.1992;456:193-213. <br />17. Sekiguchi F, Miyake Y, Kashimoto T, Sunano S. Unaltered caffeine-induced relaxation in the aorta of stroke-prone spontaneously hypertensive rats (SHRSP). J Smooth Muscle Res. 2002;38:11-22. <br />18. Ahn HY, Karaki H, Urakawa N. Inhibitory effects of caffeine on contractions and calcium movement in vascular and intestinal smooth muscle. Br J Pharmacol. 1988;93:267-74. <br />19. Huraux C, Makita T, Montes F, Szlam F, Levy JH. A comparative evaluation of the effects of multiple vasodilators on human internal mammary artery. Anes-thesiology. 1998;88:1654-9. <br />20. Tsuda A, Kenichi A, Huraux C, et al. The in vitro reversal of histamine - induced vasodilatation in the human internal mammary artery. Anesth Analg. 2001;93:1453-9. <br />21. He G, Buxton BF, Rosenfeldt FL, Wilson A, Angus JA. Weak beta-adrenoreceptor mediated relaxation in the human internal mammary artery. J Thorac Cardiovasc Surg. 1989;97:259-66. <br />22. Umemura T, Ueda K, Nishioka K, Hidaka T, Takemoto H, Nakamura S, et al. Effects of acute administration of caffeine on vascular function. Am J Cardiol. 2006;98: 1538-41. <br />23. Riksen NP, Franke B, van den Broek P, Smits P, Rongen GA. The 1976C>T polymorphism in the adenosine A2A receptor gene does not affect the vasodilator response to adenosine in humans in vivo. Pharmacogenet Genomics. 2007;17:551-4. <br />24. Daly JW. Mechanisms of action of caffeine. En: Garattini S, editor. Caffeine, coffee and health. New York: Raven Press, Ltd.; 1993. p. 97-150. <br />25. Pincomb GA, Lovallo WR, McKey BS, Sung BH, Passey RB, Everson SA, et al. Acute blood pressure elevations with caffeine in men with bordenline systemic hypertension. Am J Cardiol. 1996;77:270-4. <br />26. Vlachopoulos Ch, Hirata K, O´Rourke MF. Pressure- altering agents affect central aortic pressures more than is apparent from upper limb measurements in hypertensive patientes: role of arterial wave reflections. Hypertension. 2001;38:1456-60. 27. Vlachopoulos Ch, Hirata K, Stefanadis C, Toutouzas P, O´Rourke MF. Caffeine increases aortic stiffness in hypertensive patients. Am J Hypertens. 2003;16:63-6. <br />28. Thuringer D, Sauve R. A patch-clamp study of the Ca2+ mobilization from internal store in bovine aortic endothelium cells. I. Effects of caffeine on intracellular Ca 2+ stores. J Membr Biol. 1992;130:125-37. <br />29. Bryson SE, Rodger IW. Effects of phosphodiesterase inhibitors on normal and chemically-skinned isolated airway smooth muscle. Br J Pharmacol. 1987;92:673-81. <br />30. Shahid M, Rodger W. Chronotropic and inotropic actions of amrinone, carbazeran and isobutylmethyl xan-thine: role of phosphodiesterase inhibition. Br J Pharmacol. 1989; 98:291-301. <br />31. Van der Bet V, Beny JL. Mechanisms controlling caffeine- induced relaxation of coronary artery of the pig. Br J Pharmacol. 1991;103:1877-82. <br />32. Martin C, Dacquet C, Mironneau C, Mironneau J. Caffeine-induced inhibition of calcium channel current in cultured smooth muscle cells from pregnant rat myo-metrium. Br J Pharmacol. 1989;98:493-8. <br />33. Nishikori K, Maeno H. Close relationship between adenosine 3,5-monophosphate-dependent endog-enous phosphorylation of a specific protein and stimu-lation of calcium uptake in rat uterine microsomes. J Biol Chem. 1979;254:6099-106. <br />34. Ahn HY, Karaki H, Urakawa N. Inhibitory effects of caffeine on contractions and calcium movement in vas-cular and intestinal smooth muscle. Br J Pharmacol. 1988;93:267-74. <br />35. López-Jaramillo P, González MC, Palmer RMJ, Moncada S. The crucial role of physiological Ca 2a concentrations in the production of endothelial nitric oxide and the control of vascular tone. Br J Pharmacol. 1990;101:489-93. <br />36. Cox MM. Biosignaling. In: Lehninger AL, Nelson DL, Cox MM, Lehninger AL, editors. Principles of Biochem-istry. New York: Worth Publishers; 2000. p. 411-61 <br />37. Ignarro LJ, Burke TM, Wood M, Wolin S, Kadowitz PJ. Association between cyclic GMP accumulation and acetylcholine-elicited relaxation of bovine intrapulmonary artery. J Pharmacol Exp Ther. 1984;228:682-90. <br /> <br />
oai:oai.revistabiomedica.org:article/102
2010-01-26T14:56:31Z
biomedica:BREV
Preliminary evaluation of maggot (Diptera: Calliphoridae) therapy as a potential treatment for leishmaniasis ulcers
Evaluación preliminar en un modelo animal de la terapia con larvas de Lucilia sericata para el tratamiento de la leishmaniasis cutánea
Arrivillaga, Jazzmin
Rodríguez, Jaime
Oviedo, Milagros
leishmaniasis
cutaneous/therapy
therapies
investigational
debridement
larva
Ulcer
Introduction. Maggot debridement therapy has been widely used for treating a variety of scarred-over soft-tissue wounds. Published accounts record several illnesses in which treatment with larval therapy has promoted injury healing in conjunction with infection by bacterial pathogens resistant to conventional antibiotics.Objective. An initial test of the maggot therapy was developed for cutaneous injuries produced by Leishmania amazonensis.Materials and methods. An experimental design based on an animal model with three replicates in Mesocricetus aureatus (Rodentia: Muridae) was used to evaluate size variation lesion before and after after larval therapy with Lucilia sericata maggots. The criteria used for therapy evaluation were lesion size, maggot application time, and presence or absence of edema and secretions.Results. Effective scarring and wound healing was observed after therapy with L. sericata larvae, i.e. 80% to 100% lesion area reduction after 12 hours.Conclusion. The preliminary results suggest that fly maggots of L. sericata have a potential use as natural medical and veterinary alternative therapy for the cutaneous leishmaniasis.
Introducción. La terapia con larvas ha sido ampliamente utilizada para el tratamiento de lesiones ulcerativas de la piel; existen registros de enfermedades, como podopatía diabética, osteomielitis y úlceras varicosas, en las cuales el uso de la terapia con larvas ha promovido la cicatrización de la lesión en presencia de patógenos bacterianos resistentes a los antibióticos convencionales.Objetivo. Realizar una prueba piloto de terapia con larvas de Lucilia sericata sobre lesiones cutáneas producidas por Leishmania amazonensis.Materiales y métodos. En el presente trabajo se empleó un diseño experimental en animales ( Mesocricetus aureatus, tres réplicas) con la finalidad de analizar las variaciones del tamaño de la lesión por leishmaniasis antes y después de la terapia con larvas de L. sericata, utilizando criterios para la evaluación de la terapia tales como tamaño de la lesión, tiempo de aplicación y presencia de edema y secreción.Resultados. Indican una cicatrización efectiva y curación de las lesiones localizadas después de la terapia con larvas de L. sericata (80% a 100% de reducción del área de la lesión en 12 horas).Discusión. Los resultados preliminares indican que las larvas de moscas L. sericata son de uso potencial como terapia natural alternativa médica y veterinaria para la leishmaniasis cutánea.
Instituto Nacional de Salud
2008-06-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/102
10.7705/biomedica.v28i2.102
Biomedica; Vol. 28 No. 2 (2008); 305-310
Biomédica; Vol. 28 Núm. 2 (2008); 305-310
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/102/100
/*ref*/Berman JD, Grogl M. Leishmania mexicana: chemistry and biochemistry of sodium stibogluconate (Pentostam). Exp Parasitol. 1988;67:96-103. <br />2. Herwald BT, Berman JD. Recommendations for treating leishmaniasis with sodium stibogluconate (pentostam) and review of pertinent clinical studies. Am J Trop Med Hyg. 1992;46:296-306. <br />3. Scorza JV, Morales C, Petit Y, Vásquez L, Rojas E, Scorza JV. Síntesis de un complejo antimonial pentavalente (Ulamina) y su aplicación experimental para el tratamiento de leishmaniasis cutánea localizada en Venezuela. Bol Malariol San Amb. 2006;1:59-65. <br />4. Bofante R, Barroeta S. Leishmanias y leishmaniasis en América con especial referencia en Venezuela. Barquisimeto: Editorial Lara; 2002. p. 270 <br />5. Brenzan MA, Nakamura CV, Pardo Dias Filho B, Ueda-Nakamura T, Young MC, Aparacio Garcia Cortz D. Antileishmanial activity of crude extract and courin from Calophyllum brasiliense leaves against Leishmania amazonensis. Parasitol Res. 2007;101:715-22. <br />6. Fitzpatrick M. Tiny "surgeons" prove surprisingly effective. JAMA. 2000;284:2306-7. <br />7. Sherman RA, Sherman J, Gilead L, Lipo M, Mumcuoglu KY. Maggot debridement therapy in out-patients. Arch Phys Med Rehabil. 2001;82:1226-9. <br />8. Sherman RA, Wyle F, Vulpe M. Maggot therapy for treating pressure ulcers in spinal cord injury patients. J Spinal Cord Med. 1995;18:71-4. <br />9. Sherman RA. A new dressing design for use with maggot therapy. Plast Reconstr Surg. 1997;100:451-6. <br />10. Sherman RA. Maggot debridement in modern medicine. Infect Med. 1998;15:651-6. <br />11. Sherman RA, Wyle FA. Low-cost, low-maintenance rearing of maggots in hospitals, clinics and schools. Am J Trop Med Hyg. 1996;54:38-41. <br />12. Thomas S, Andrews AM, Hay NP, Bourgoise S. The anti-microbial activity of maggot secretions: results of a preliminary study. J Tissue Viability. 1999;9:127-32. <br />13. Guevara P, Rojas E, González N, Scorza JV, Añez N, Valera M, et al. Presence of Leishmania braziliensis in blood samples from cured patients to different stages of immunotherapy. Clin Diagn Lab Immunol. 1994;1: 385-9. <br />14. Juárez E. Evaluación en sueros de la quimioterapia específica, por las técnicas de ELISA, PCR e hibridación de pacientes con leishmaniasis cutánea del Estado Trujillo (Tesis). Trujillo: Núcleo Universitario "Rafael Rangel"-Universidad de Los Andes; 2004. p. 72. <br />15. Ministerio de Ciencia y Tecnología. Código de Bioética y Bioseguridad. Caracas: Editorial MCT; 2002. p. 35. <br />16. Thomas S, Jones M. Maggots and the battle against MRSA. Bridgend: SMTL.; 2000. p. 123-40. <br />17. Mumcuoglou KY, Miller J, Mumcuoglu M, Friger M, Tarshis M. Destruction of bacteria in the digestive tract of the maggot of Lucilia sericata (Diptera: Calliphoridae). J Med Entomol. 2001;38:161-6. <br />18. Erdmann GR, Bromel M, Gassner G, Freeman TP, Fischer A. Antibacterial activity demonstrated by culture filtrates of Proteus mirabilis isolated from screwwork (Cochliomyia homivorax) (Diptera: Calliphoridae). J Med Entomol. 1984;21:159-64. <br />19. Erdmann GR, Khalil SK. Isolation and identification of two antibacterial agents produced by a strain of Proteus mirabilis isolated from larvae of the screwworm (Cochliomyia hominovorax) (Diptera: Calliphoridae). J Med Entomol. 1986;23:208-11. <br />20. Parnés A, Lagan KM. Larval therapy in wound management: A review. Int J Clin Pract. 2007;61:488-93. <br />21. Horobin AJ, Pritchad DL, Shakesheff LM. How do larvae of Lucilia sericata iniciate human wound healing. Eur Cell Mater. 2002;4(Suppl.2):70-1. <br />22. Daeschlein G, Mumcuoglu KY, Assadian O, Hoffmeister B, Kramer A. In vitro antibacterial activity of Lucilia sericata maggot secretions. Skin Pharmacol Physiol. 2007;20:112-5. <br />23. Figueroa L, Flores J, Rodríguez S. Método de cultivo de larvas de moscas Lucilia sericata para terapia larval. Parasitol Latinoam. 2007;62:79-82. <br />24. Anderson GS. Minimum and maximum development rates of some forensically important Calliphoridae (Diptera). J Forensic Sci. 2000;45:824-32. <br />25. Talari S, Sadr F, Doroodgar A, Talari M, Gharabagh A. Wound myasis caused by Lucilia sericata. Arch Iranian Med. 2004;2:128-9. <br /> <br />
oai:oai.revistabiomedica.org:article/103
2016-11-22T10:32:54Z
biomedica:IMAG
Diagnosis of leptospirosis by dark-field microscopy of blood samples and culture
Diagnóstico de leptospirosis de muestras de sangre y cultivo por observación en microscopio de campo oscuro
Agudelo-Flórez, Piedad
Restrepo, Marcos
Moreno, Natalí
leptospirosis/diagnóstico
Leptospira
microscopía
leptospirosis/diagnosis
Leptospira
microscopy
Leptospirosis, one of the most extended zoonosis in the world is considered a reemergent disease. It is produced by the pathogenic species of the genus Leptospira. There are approximately 13 of 17 species described up to date. These species are indistinguishable morphologically and their taxonomic classification is done by molecular methods. Leptospirosis presents with multiple unspecific clinical symptoms that make it difficult to confirm the case. To verify the diagnoses, the medical personnel need to know how to recognize the clinical manifestations for leptospirosis and to corroborate a good diagnostic suspicion, in addition to ordering the appropriate tests to the laboratory for: 1) dark field microscopy visualization of the bacteria in blood samples, urine or postmortem tissues which need to use special stains like silver stain or immunofluorescence; 2) having positive culture for leptospirosis from blood, urine, CSF or of tissues postmortem; 3) having an increase (fourfold rise) of the tires in microagglutination test from two serum samples taken with an interval of 15 days apart, 4) an elevated unique title (>1:400) using microagglutination for serological diagnosis or IgM detection test, and 5) positive PCR assay in blood, urine, CSF or tissues postmortem. Due to the fact that the first two tests for diagnosis needs a trained personnel for Leptospiras visualization, we would like to present to the medical community reference images of Leptospira species that can be observed by dark field microscopy from as blood as cultures. It is necessary to have methods for leptospirosis in the public health laboratories; additionally, to have qualified personnel to realize them. This will allow confirming a clinical diagnosis with symptoms that resemble other endemic diseases in Colombia, like dengue and malaria.
La leptospirosis, una de las zoonosis más extendidas en el mundo, es considerada una enfermedad reemergente, producida por especies patógenas del género Leptospira que comprende, aproximadamente, 13 de las 17 especies descritas hasta el momento; éstas son indistinguibles morfológicamente y su clasificación taxonómica se hace por métodos moleculares. La leptospirosis se presenta con múltiples síntomas inespecíficos y para llegar a la definición de caso confirmado, el personal médico debe, además de reconocer las manifestaciones clínicas que coinciden con leptospirosis, confirmar la sospecha diagnóstica de la enfermedad por laboratorio, bien sea por: 1) observación al microscopio de campo oscuro de la bacteria en muestras de sangre u orina, o en tejidos obtenidos post mórtem y, en este caso, se usan coloraciones especiales de plata o inmunofluorescencia; 2) cultivo positivo (sangre, orina, líquido cefalorraquídeo o muestras post mórtem); 3) incremento o alza cuádruple de los títulos por microaglutinación en sueros pareados tomados con un intervalo de 15 días; 4) título alto único (>1:400) utilizando diagnóstico serológico por microaglutinación o pruebas que detecten IgM, o 5) resultado positivo de la prueba de reacción en cadena de la polimerasa en sangre, orina, líquido cefalorraquídeo o muestras de tejidos post mórtem. Debido a que las dos primeras formas de diagnóstico requieren de un personal experto para la visualización de Leptospira spp., nos proponemos presentar a la comunidad médica imágenes de referencia de Leptospira spp. que se observan en el microscopio de campo oscuro provenientes de muestras de sangre o de cultivo. Se necesita disponer de métodos de diagnóstico para leptospirosis en los laboratorios de salud pública, además de personal capacitado para realizarlos, lo cual permite confirmar el diagnóstico clínico de una etiología que como ésta, presenta síntomas comunes a otras enfermedades endémicas en Colombia, como son el dengue y el paludismo.
Instituto Nacional de Salud
2008-03-01
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
application/pdf
application/pdf
https://revistabiomedica.org/index.php/biomedica/article/view/103
10.7705/biomedica.v28i1.103
Biomedica; Vol. 28 No. 1 (2008); 7-9
Biomédica; Vol. 28 Núm. 1 (2008); 7-9
2590-7379
0120-4157
spa
https://revistabiomedica.org/index.php/biomedica/article/view/103/101
https://revistabiomedica.org/index.php/biomedica/article/view/103/488
2caee2047e9ebd24553f12ebf05eb588