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Combination of Oxidative Stress and Steatosis Is a Risk Factor for Fibrosis in Alcohol-Drinking Patients With Chronic Hepatitis C

Vidali, Matteo, M.D., Ph.D.1; Occhino, Giuseppa, Ph.D.1; Ivaldi, Alessandra, Ph.D.1; Rigamonti, Cristina, M.D.1,3; Sartori, Massimo, M.D.2; Albano, Emanuele, M.D., Ph.D.1

American Journal of Gastroenterology: January 2008 - Volume 103 - Issue 1 - p 147–153
ORIGINAL CONTRIBUTIONS: LIVER AND BILIARY TRACT
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BACKGROUND AND AIMS Alcohol and HCV have been shown to interact in stimulating hepatic oxidative damage. Thus, we investigated the contribution of oxidative mechanisms in the progression of chronic hepatitis C (CHC) in alcohol consumers.

METHODS An increased IgG reactivity against lipid peroxidation-derived antigens was used as the marker for alcohol-induced oxidative damage in 125 CHC patients.

RESULTS Alcohol intake significantly increased the frequency of the subjects with elevated lipid peroxidation-related IgG. However, no association was evident between oxidative stress markers and the severity of steatosis, necroinflammation, or fibrosis. Multivariate analysis revealed that age (P= 0.014) and hepatic iron content (P= 0.034) were the only independent predictors of fibrosis in these patients. However, the risk of fibrosis in the subjects with both steatosis and oxidative stress-induced immune responses was 6- (OR 6.2, 95% CI 1.2–31.0) and 14-fold (OR 14.6, 95% CI 3.1–68.1) higher than in the subjects with steatosis alone or without steatosis, respectively. Multivariate analysis confirmed that the combination of steatosis and oxidative stress (P= 0.045) was, together with age (P= 0.021) and hepatic iron content (P= 0.027), an independent risk factor for fibrosis in CHC patients with alcohol intake.

CONCLUSIONS These results demonstrate that oxidative stress interacts with steatosis to promote the progression of CHC in alcohol-consuming patients.

1Department of Medical Sciences, University “Amedeo Avogadro” of East Piedmont; 2Gastroenterology Unit, Ospedale Maggiore della Carità, Novara, Italy; and 3IRCCS Fondazione Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, First Division of Gastroenterology, Milan, Italy

Reprint requests and correspondence: Emanuele Albano, Department of Medical Sciences, University “Amedeo Avogadro” of East Piedmont, Via Solaroli 17, 28100 Novara, Italy.

Received June 12, 2007; accepted August 29, 2007.

CONFLICT OF INTERESTGuarantor of the article: Emanuele Albano, M.D., Ph.D.

Specific author contributions: Matteo Vidali played a major role in the planning of the study, performing statistical analysis, and manuscript preparation; G. Occhino, A. Ivaldi, and C. Rigamonti were involved in performing the immunological analysis; M. Sartori collected clinical data and contributed to the statistical analysis and in the writing of the manuscript; and E. Albano supervised the work.

Financial support: This work was supported by grants from the University of East Piedmont, Regional Government of Piedmont, and Italian Ministry for University and Scientific and Technological Research (Research Program: 200401213).

Potential competing interests: None.

© The American College of Gastroenterology 2008. All Rights Reserved.
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