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Alcohol changes the progression of hepatitis C virus (HCV)-related chronic liver disease and may affect the outcome of interferon therapy. The ethanol intake of 245 patients with biopsy-proven chronic hepatitis C with or without cirrhosis, its interaction with laboratory and histological parameters common to alcohol and HCV-mediated liver damage, and its effects on therapy were evaluated. The results show that 60-70% of subjects regularly consumed alcohol (median intake >40 g/day in about 30%). Less than 50% stopped drinking after being diagnosed as having liver disease. Ethanol intake affected: fibrosis, especially in women, HCV RNA levels, which were significantly lower in abstainers than in drinkers (0.6 +/- 0.3 vs 6.9 +/- 5.9 Eq/ml x10(6); P < 0.01), and response to interferon therapy. The number of responders decreased as ethanol intake increased. There were less abstainers than drinkers among non-responders (10.7% vs 63.1% respectively; P < 0.001). Data indicate that alcohol will induce and worsen liver damage and, in subjects with chronic liver disease who continue to drink, adversely affect their response to treatment.

Background: Ethanol abuse and liver cirrhosis cause a reduction of glutathione blood levels; liver cirrhosis induces an alteration of the plasma amino acid pattern. We evaluated whether or not ethanol abuse affects amino acid levels, particularly those that are involved in metabolizing glutathione in the plasma and erythrocytes of chronic alcohol abusers with or without liver cirrhosis., Methods: We studied 10 chronic alcohol abusers without liver cirrhosis, 10 with alcoholic cirrhosis, 10 affected by hepatitis C virus-related cirrhosis, and 10 healthy subjects. Glutathione, y-glutamyl-cysteine, and cysteine were determined by fluorescent HPLC, glutamic acid, glycine, and other free amino acids by cation exchange chromatography both in the plasma and erythrocytes of all studied subjects., Results and Conclusions: In both alcoholics and cirrhotics, we found a significant increase of plasma-aromatic amino acid and methionine levels, whereas glutathione was significantly reduced. The erythrocytes of these patients showed a significant increase of cysteine, glutamic acid, and glycine; gamma-glutamylcysteine was normal; and glutathione and other free amino acids were significantly decreased. Data suggest that, independent of liver cirrhosis, ethanol abuse affects the metabolism of amino acids and glutathione in both the plasma and the erythrocytes.

Glutathione (GSH) is a principal cellular scavenger of free radicals. Chronic alcohol abuse, as well as liver disease, induces a decrease of hepatic GSH. We evaluated the effect of GSH administration (2.4 g day-1 in saline i.v. for 15 days) on the concentration of GSH in plasma and erythrocytes and on liver function tests, including galactose and antipyrine tests. We studied 40 alcoholic cirrhotic patients: 22 treated with GSH (10 persistent alcohol abusers and 12 weaning from alcohol during the study) and 18 treated with saline only (8 persistent alcohol abusers and 10 abstainers). Treatment with GSH improved the concentration of GSH in plasma and erythrocytes only in abstainers from alcohol; it did not affect liver function tests or galactose clearance. Persistent alcohol consumption significantly prolonged antipyrine metabolism; GSH administration counteracted this effect.

α-Gluthathione-S-transferascs (α-GSTs) are enzymes involved in the cellular detoxifying processes; elevated circulating α-GSTs activity is considered to be an early index of liver damage. Glutathione (GSH) is the substrate for α-GST action. The aims of our study were: (1) to evaluate plasma GSH levels and α-GST activity in chronic alcohol abusers with or without liver cirrhosis; (2) to define the relationship between these two biochemical parameters; (3) to establish their clinical relevance in patients with alcohol abuse and/or liver damage. We studied 69 subjects (18 healthy subjects and 51 chronic alcohol abusers: 29 without liver cirrhosis and 22 with). Plasma α-GST activity was determined on baseline samples and every following day for a total of 10 days in five alcoholics by HEPKIT (Alpha-Biotech, Biotrin International, Dublin, Ireland). GSH was determined on all subjects' baseline samples by fluorescent high-performance liquid chromatography. Alcohol intake was evaluated in all patients by determining blood-alcohol concentrations. Significant increases in plasma α-GSTs were observed in 9/29 (31%) alcoholics and 3/22 (13.6%) cirrhotics irrespective of their alcohol intake. GSH was significantly lower than normal values (P < 0.001) in all alcoholics with or without cirrhosis (controls 10.4 ± 4.8; alcoholics without cirrhosis 3.9 ± 1.4; alcoholics with cirrhosis 3.3 ± 1.6). No correlation was observed between plasma α-GST and GSH levels. Our data indicate that: (1) α-GST activity does not correlate with GSH levels in the plasma; (2) α-GSTs do not have clinical relevance as markers of recent alcohol intake; (3) in cirrhotics, α-GST does not provide more information than other liver function tests. However, plasma α-GST determination may be useful in selecting a subgroup of alcoholics in whom routine biochemical markers of liver damage are within reference ranges. [ABSTRACT FROM AUTHOR]