Higuera-de la Tijera MF, Pérez-Hernández JL, Servín-Caamaño AI, Serralde-Zúñiga AE, Cruz-Palacios A, Abdo-Francis JM, Bernal-Sahagún F, Salas-Gordillo F

Idioma: Español
Referencias bibliográficas: 42
Paginas: 215-221
Archivo PDF: 101.53 Kb.

RESUMEN

El alcohol es una toxina hepática directa. 10 a 20% de los alcohólicos desarrollarán hepatitis alcohólica; esto implica una interacción compleja entre factores facilitadores y comorbilidades como el género, factores hereditarios e inmunidad. La hepatitis alcohólica se origina por la ingesta abundante de etanol, aunado a un consumo del mismo por tiempo prolongado; se puede manifestar por esteatosis moderada a severa; en general, esta última con elevado índice de mortalidad. Varios órganos son capaces de metabolizar el etanol; sin embargo, el hígado es el que posee los sistemas enzimáticos más específicos. Dentro de la fisiopatología, el Factor de Necrosis Tumoral-alfa juega un papel importante en el desarrollo del daño hepático inducido por etanol. La hepatitis alcohólica se asocia con un amplio espectro de manifestaciones clínicas. Para estimar el pronóstico disponemos del índice discriminatorio de Maddrey, la escala de Glasgow, el MELD y el modelo de Lille. En el tratamiento de la hepatitis por alcohol se han utilizado diversos medicamentos, cuyos objetivos principales son: controlar el infiltrado inflamatorio, bloquear el proceso inmunológico y evitar la progresión a la fibrosis, esto con la finalidad de aumentar la supervivencia.

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