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2003, Número 2

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Cir Gen 2003; 25 (2)


Mecanismos fisiopatogénicos de la pancreatitis aguda

Gutiérrez VI, Domínguez MA, Acevedo MJJ

Idioma: Español
Referencias bibliográficas: 60
Paginas: 95-102
Archivo PDF: 78.69 Kb.


RESUMEN

Propósito: Análisis de la bibliografía sobre los principales aspectos de la fisiopatología de la pancreatitis aguda.
Obtención de los datos: Revisión de la literatura médica en idioma inglés de 1997 a 2002 (60 citas seleccionadas). Selección de los estudios: Se seleccionaron los artículos más relevantes relacionados con la fisiopatología de la pancreatitis aguda.
Extracción de los datos: Se revisó la literatura médica internacional durante el periodo comprendido de 1997 a 2002 de los estudios de investigación sobre diversos aspectos de la fisiopatología de la pancreatitis aguda. Se utilizó la base de datos MEDLINE del Sistema MEDLARS.
Resultados: La fisiopatología es compleja y no totalmente entendida. Independientemente de la etiología, se cree que el evento inicial es la lesión de la célula acinar mediante la activación intra-acinar de zimógenos inactivos a su forma activa. En los últimos 10 años, se ha investigado el papel de las múltiples vías involucradas en la fisiopatología de la pancreatitis aguda que incluyen al sistema inmune, citocinas, especies reactivas de oxígeno y alteraciones de la microcirculación que llevan al daño local y sistémico.
Conclusión: La pancreatitis aguda es una enfermedad de gravedad variable. Su fisiopatología sigue sin comprenderse completamente, a pesar de los conocimientos actuales sobre la activación intraacinar del tripsinógeno, la producción de citocinas inflamatorias por la misma célula acinar, las alteraciones en la microcirculación con el descubrimiento reciente de la producción local de reninaangiotensina y los efectos de especies reactivas de oxígeno.


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