The acute effects of ethanol on acetanilide disposition in normal subjects, and in patients with liver disease.

Abstract

upon Tyne.1 The effects of single doses (25 g and 50 g) oral ethanol on the disposition of acetanilide (50 mg/kg metabolic active mass) has been studied in normal subjects, and in patients with chronic non-alcoholic liver disease. 2 In normal subjects, ethanol produced a dose-dependent increase in acetanilide half-life, and a decrease in acetanilide clearance. There was a significant correlation (rs = 0.71, P < 0.01) between the 90 min blood ethanol concentration and the reduction in acetanilide clearance. 3 In patients with liver disease, ethanol produced a similar proportional change in acetanilide half-life and clearance, but these were less consistent. Moreover, liver disease itself was associated with an increase in acetanilide half-life, and a reduction in clearance. 4 It is concluded that single oral doses of ethanol, comparable to those consumed during social drinking, may inhibit some forms of microsomal oxidation and thus have important clinical implications.

The metabolism of 7‐ethoxycoumarin in human liver microsomes and the effect of primary biliary cirrhosis: implications for studies of drug metabolism in liver disease.

“…Chronic ethanol exposure has been shown in man to cause a reduction in the activity of at least one monooxygenase, aryl hydrocarbon hydroxylase, and this may be unrelated to the degree of liver damage (Brodie et al, 1981). Acute ethanol consumption has also been shown to impair microsomal oxidation both in normal subjects and people with liver disease (McKay et al, 1982). It is therefore possible that in alcoholic cirrhotics, lower microoxygenase activity may be partly related to continued alcoholism rather than liver disease alone.…”