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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

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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