We recently presented preliminary data indicating the presence of antibodies against acetaldehyde adducts in sera of over 70% of alcoholic patients. To assess the respective roles of liver disease and alcohol consumption as well as the specificity of this immune response, 141 patients in various stages of alcoholic and nonalcoholic liver diseases were tested by a hemagglutination assay. Sixty-three (73%) of 86 alcoholics had antibody titers above control levels (p c 0.0001). Alcohol consumption of these individuals was significantly higher (p < 0.001) than that of those alcoholics with normal titers. Twentytwo patients (39%) with nonalcoholic liver diseases also had elevated levels of antibodies against acetaldehyde adducts (p < 0.0005); of these, 8 had primary biliary cirrhosis (7 in Stages I11 and IV), 9 had chronic active hepatitis (6 with cirrhosis) and 5 had acute (virus-or drug-induced) hepatitis. Antibody titers did not correlate with levels of transaminase or alkaline phosphatase activity, nor with bilirubin, and albumin. However, in 52 alcoholics and in nonalcoholic patients with biopsyconfirmed liver disease, the highest titers were seen in the more advanced stages of liver damage. Thus, in addition to alcohol consumption, severity of liver disease may play a role in the appearance of circulating antibodies against acetaldehyde adducts.
Numerous attempts have been made to identify chronic alcohol abusers by clinical or biochemical parameters. In addition to the established alcohol dehydrogenase pathway, chronic ethanol consumption leads to the induction of a hepatic microsomal ethanol-oxidizing system (1) generating increased amounts of the reactive metabolite acetaldehyde. Although acetaldehyde is rapidly oxidized to acetate, detectable amounts of this intermediate accumulate in the blood and liver during ethanol oxidation (2). Several studies have shown that acetalde-