Alcoholic liver disease

Citation
L. Lumeng et Dw. Crabb, Alcoholic liver disease, CURR OPIN G, 17(3), 2001, pp. 211-220
Citations number
53
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
CURRENT OPINION IN GASTROENTEROLOGY
ISSN journal
02671379 → ACNP
Volume
17
Issue
3
Year of publication
2001
Pages
211 - 220
Database
ISI
SICI code
0267-1379(200105)17:3<211:ALD>2.0.ZU;2-W
Abstract
Research has substantiated the role of several mechanisms responsible for a lcohol-induced hepatotoxicity. These mechanisms include: oxidative stress a nd lipid peroxidation; immunogenic processes initiated by formation of prot ein adducts of acetaldehyde, other aldehydes and 1-hydroxyethyl radicals; a nd activation of Kupffer cells by endotoxin and subsequent cascade of event s that involved cytokines, chemokines, and adhesion molecules. Increasing e vidence implicates enhanced intestinal permeability caused by alcohol inges tion as the culprit that leads to endotoxemia. While oxidative stress is im portant, the principal source of reactive oxygen species that causes alcoho l-induced liver injury is hotly debated. Potential sources may include cyto chrome P450IIE1, activated Kupffer cells, and mitochondrial electron transf er chain. Apoptosis is likely an important pathway that culminates in hepat ocyte cell death. Abstinence, corticosteroids, and enteral nutrition remain the cornerstones in the treatment of alcoholic hepatitis. The efficacies o f medications such as S-adenosylmethionine and pentoxifylline will need fur ther confirmation by additional randomized trials before they can be recomm ended as standard therapies for alcoholic hepatitis. Curr Opin Gastroentero l 2001, 17:211-220 (C) 2001 Lippincott Williams & Wilkins, Inc.