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2002, Número 5

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Gac Med Mex 2002; 138 (5)


Mecanismos celulares y bioquímicos involucrados en la fisiopatogenia de la púrpura trombocitopénica autoinmune

Domínguez-García MV, Rodríguez-Moyado H

Idioma: Español
Referencias bibliográficas: 123
Paginas: 461-472
Archivo PDF: 69.62 Kb.


RESUMEN

La púrpura trombocitopénica autoinmune (PTA) es un síndrome causado por la destrucción excesiva de plaquetas recubiertas por autoanticuerpos dirigidos contra antígenos de la membrana plaquetaria. Se ha demostrado que la destrucción de plaquetas se lleva a cabo en los macrófagos del sistema retículo endotelial, pero todavía no se conocen los mecanismos inmunológicos involucrados en la destrucción. El objetivo de este artículo es revisar la información acerca de la fisiopatogenia de esta enfermedad. Ante la dificultad de tener estudios controlados en humanos se ha recurrido a los modelos en animales de laboratorio. Entre estos modelos están los ratones (NZW X BXSB) F1 con púrpura autoinmune, y los llamados ratones “Harrington” con púrpura inmune. Los estudios en humanos sugieren que existen diferencias en la patogénesis de la PTA aguda y crónica, particularmente al nivel de células T reactivas; por ejemplo, una elevada actividad de Th (CD4+) con actividad reducida T supresora (CD8+) concomitante en la forma crónica, pero en la forma aguda no se ha encontrado predominio de algún fenotipo especial, e incluso puede haber disminución de CD4+. La proliferación de linfocitos inducida por diferentes mitógenos se encuentra elevada en los pacientes con PTA crónica, pero disminuida en los pacientes con PTA aguda.


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