[Alcoholic hepatopathy]

To extensively discuss clinical features, laboratory data and pathology findings associated with alcoholic hepatitis as well as the new insights into pathogenesis and the appropriate therapy.

Review of current literature.

Acetaldehyde gives rise to neoantigens by complexing with various proteins, which, in turn, favors the appearance of autoantibodies. Antibodies against the hepatic lipoprotein and a number of hepatocyte surface glycoproteins have been detected in alcoholic hepatitis. Experimental studies have shown that acetaldehyde and malonyldialdehyde form highly immunogenic aggregates (MAA adducts). Antibody titers are usually higher in patients with more advanced disease, which argues for a major etiologic role. HLA antigens such as B8, DR3, DR4, which are usually associated with autoimmune diseases, are more frequently observed in alcoholic hepatitis patients.

Despite the above, it is still questionable whether alcoholic hepatitis pathogenesis is autoimmune in origin. Why do only 15-20% of subjects who have long been abused alcohol develop hepatitis? What are the predisposing factors? What events trigger the immunologic reactivity? If MAA adducts play a role, why are not all the alcohol abusers affected by hepatitis? Transplantation outcome in well selected patients with alcoholic hepatitis is as good as--or even better than--the one reported for patients with different types of hepatitis.