The activity of LCAT (the controlling enzyme for cholesterol esterification in plasma) is known to be reduced in alcoholic cirrhosis, while little is known about early stage (liver steatosis) alcoholics. In this study, LCAT activity was assayed by Stokke and Norum's method, before and after a 15-day sobriety period, in liver steatosis and in cirrhosis alcoholics. Before alcohol withdrawal, LCAT activity was depressed in both groups. After the sobriety period, LCAT activity was significantly raised in liver steatosis patients, but was still lower than in controls; in cirrhosis patients, it was increased, but not significantly. According to our results, LCAT activity impairment in alcoholic liver disease is sustained by both the hypothesized mechanisms, alcohol-related metabolic disorders and lowered LCAT-enzyme production, but to different degrees, depending on the stage of the disease. In liver steatosis, metabolic disorders play a major role, as a liver-impairment-induced decrease in LCAT production seems rather unlikely, and increased LCAT activity is more likely to be sustained by metabolic normalisation than by any recovery of the damaged liver. However, the lack of improvement in about 20% of patients, and the fairly wide scattering of individual data, suggest a minor LCAT production impairment in liver steatosis too. In cirrhosis, the major role seems to be played by a permanent decrease in LCAT production, as no significant rise in LCAT activity was observed after alcohol withdrawal. However the restored LCAT activity observed in some patients could be related to improvement in the metabolic disorder, thus confirming the effectiveness of this mechnism in cirrhosis too.(ABSTRACT TRUNCATED AT 250 WORDS)