title: Combination of oxidative stress and steatosis is a risk factor for fibrosis in alcohol-drinking patients with chronic hepatitis C.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Medical Sciences, University "Amedeo Avogadro" of East Piedmont, Novarra, Italy.
authors.forename: Matteo
authors.initials: M
authors.lastname: Vidali
authors.forename: Giuseppa
authors.initials: G
authors.lastname: Occhino
authors.forename: Alessandra
authors.initials: A
authors.lastname: Ivaldi
authors.forename: Cristina
authors.initials: C
authors.lastname: Rigamonti
authors.forename: Massimo
authors.initials: M
authors.lastname: Sartori
authors.forename: Emanuele
authors.initials: E
authors.lastname: Albano
mesh_terms: D000328:Adult; D000368:Aged; D000428:Alcohol Drinking / Q000009:adverse effects* / Q000378:metabolism / Q000473:pathology; D000888:Antibodies, Anti-Idiotypic / Q000276:immunology*; D001706:Biopsy; D018450:Disease Progression; D005234:Fatty Liver / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D005260:Female; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology*; D015227:Lipid Peroxidation; D008103:Liver Cirrhosis / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000276:immunology*; D011379:Prognosis; D012307:Risk Factors
chemical_list: D000888:Antibodies, Anti-Idiotypic; D007074:Immunoglobulin G