Search resultsModerate alcohol consumption increases oxidative stress in patients with chronic hepatitis C
Title
Moderate alcohol consumption increases oxidative stress in patients with chronic hepatitis C
Publication type
Journal Article
Year of Publication
2003
Authors
Journal
Hepatology
Volume
38
Issue
1
Pagination
42 - 49
Date published
2003
ISBN
02709139 (ISSN)
Keywords
4 hydroxynonenal, 4 hydroxynonenal antibody, Adult, Aged, alcohol, alcohol consumption, Alcohol Drinking, aldehydes, antibody titer, Arachidonic Acid, arachidonic acid hydroperoxide, arachidonic acid hydroperoxide antibody, article, Autoantibodies, Biological Markers, cardiolipin, Cardiolipins, chronic hepatitis, controlled study, disease marker, evolution, Female, hepatitis C, Hepatitis C virus, Hepatitis C, Chronic, human, human serum albumin, human tissue, Humans, hydrogen peroxide, Immunoglobulin G, lipid peroxidation, liver biopsy, liver disease, liver fibrosis, liver injury, liver necrosis, major clinical study, male, malonaldehyde, Malondialdehyde, malondialdehyde antibody, Middle Aged, oxidative stress, oxidized cardiolipin, oxidized cardiolipin antibody, priority journal, Serum Albumin, unclassified drug
Abstract
The mechanisms by which alcohol consumption worsens the evolution of chronic hepatitis C (CHC) are poorly understood. We have investigated the possible interaction between hepatitis C virus (HCV) and ethanol in promoting oxidative stress. Circulating IgG against human serum albumin (HSA) adducted with malondialdehyde (MDA-HSA), 4-hydroxynonenal (HNE-HSA), or arachidonic acid hydroperoxide (AAHP-HSA) and against oxidized cardiolipin (Ox-CL) were evaluated as markers of oxidative stress in 145 CHC patients with different alcohol consumption, 20 HCV-free heavy drinkers (HD) without liver disease, and 50 healthy controls. Anti-MDA IgG was increased in CHC patients irrespective of alcohol intake as well as in the HD group. CHC patients with moderate alcohol intake (< 50 g ethanol/d), but not HD, also had significantly higher values of anti-AAHP-HSA, anti-HNE-HSA, and anti-Ox-CL IgG (P < .05) than controls. A further elevation (P < .001) of these antibodies was evident in CHC patients with heavy alcohol intake (>50 g ethanol/d). Anti-AAHP and anti-Ox-CL IgG above the 95th percentile in the controls were observed in 24% to 26% of moderate and 58% to 63% of heavy drinkers but only in 6% to 9% of the abstainers. The risk of developing oxidative stress during CHC was increased 3-fold by moderate and 13- to 24-fold by heavy alcohol consumption. Heavy drinking CHC patients had significantly more piecemeal necrosis and fibrosis than abstainers. Diffuse piecemeal necrosis was 4-fold more frequent among alcohol-consuming patients with lipid peroxidation-related antibodies than among those without these antibodies. In conclusion, even moderate alcohol consumption promotes oxidative stress in CHC patients, suggesting a role for oxidative injury in the worsening of CHC evolution by alcohol.