title: Hepatocellular fat accumulation and low serum cholesterol in patients infected with HCV-3a.
abstract: OBJECTIVE
  The aim of this study was to prospectively investigate the prevalence of hepatic steatosis in chronic hepatitis C patients with respect to viral genotype, hepatic iron concentration, total body iron, body mass index, and serum lipid parameters. Furthermore, the effect of hepatitis C virus (HCV) eradication by antiviral therapy on serum cholesterol levels was studied.
  
  
  METHODS
  Hepatocellular fat and hepatic iron were determined in liver biopsies obtained from 137 interferon-naïve patients with chronic hepatitis C (100 men, 37 women, mean age 40.8 +/- 10.7 yr) enrolled in two prospective clinical trials of interferon/ribavirin therapy. Body mass index and fasting cholesterol levels were determined at baseline, during, and after therapy.
  
  
  RESULTS
  Marked steatosis (>20% of fat-containing hepatocytes) was found in 74.5% of patients infected with HCV-3a compared with 17.9% in HCV-1 and 21.7% in HCV-4-infected patients (p < 0.01). Steatosis in HCV-3a-infected patients did not correlate with the body mass index, hepatic iron content, ferritin, or transferrin saturation. At baseline, serum cholesterol was lower in patients infected with HCV-3a (147 +/- 42 mg/dl; p < 0.01) compared with HCV-1 (188 +/- 36) or HCV-4 (172 +/- 35). In contrast to HCV-1- or HCV-4-infected patients, serum cholesterol increased in HCV-3a virological responders at the end of treatment and 6 months after therapy (baseline 146 +/- 38, end of treatment 166 +/- 29, p < 0.05, sustained virological response 200 +/- 34, p < 0.01). However, serum cholesterol remained unchanged in HCV-3a nonresponders.
  
  
  CONCLUSIONS
  Our data suggest that, in addition to inducing steatosis, HCV-3a lowers serum cholesterol. This metabolic effect is fully reversible after successful HCV-3a eradication. This unique property is not shared by other HCV genotypes.
authors.affiliation: Department of Internal Medicine IV, University of Vienna, Austria.
authors.forename: Harald
authors.initials: H
authors.lastname: Hofer
authors.forename: Hans C
authors.initials: HC
authors.lastname: Bankl
authors.forename: Friedrich
authors.initials: F
authors.lastname: Wrba
authors.forename: Petra
authors.initials: P
authors.lastname: Steindl-Munda
authors.forename: Markus
authors.initials: M
authors.lastname: Peck-Radosavljevic
authors.forename: Christoph
authors.initials: C
authors.lastname: Osterreicher
authors.forename: Christian
authors.initials: C
authors.lastname: Mueller
authors.forename: Alfred
authors.initials: A
authors.lastname: Gangl
authors.forename: Peter
authors.initials: P
authors.lastname: Ferenci
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000008:administration & dosage / Q000494:pharmacology; D005234:Fatty Liver / Q000150:complications* / Q000378:metabolism; D005260:Female; D005293:Ferritins / Q000378:metabolism; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics*; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000188:drug therapy / Q000821:virology; D022781:Hepatocytes / Q000378:metabolism*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000008:administration & dosage / Q000494:pharmacology; D007501:Iron / Q000378:metabolism*; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D009752:Nutritional Status; D011092:Polyethylene Glycols / Q000008:administration & dosage / Q000494:pharmacology; D015995:Prevalence; D011446:Prospective Studies; D012367:RNA, Viral / Q000097:blood; D011994:Recombinant Proteins; D012720:Severity of Illness Index; D014168:Transferrin / Q000378:metabolism
chemical_list: D000998:Antiviral Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D008055:Lipids; D012367:RNA, Viral; D011994:Recombinant Proteins; D014168:Transferrin; D011092:Polyethylene Glycols; D005293:Ferritins; D007501:Iron; C100416:peginterferon alfa-2a