title: Impact of steatosis on long-term histological outcome in chronic hepatitis C after antiviral therapy.
abstract: OBJECTIVE
  Steatosis is recognized as a cofactor influencing the presence and progression of fibrosis in chronic hepatitis C. It has been reported that antiviral therapy may reduce the progression of fibrosis and leads to regression in chronic hepatitis C patients achieving a sustained virological response (SVR). Whether steatosis might affect the long-term histological outcome of antiviral therapy remains unclear.
  
  
  METHODS
  One-hundred and sixty-one consecutive patients (genotype 1, n=76; genotype 2, n=73) receiving interferon-alpha2b and ribavirin were analysed. Ninety patients had paired biopsies with a mean interval of 29.1 +/- 7.1 months.
  
  
  RESULTS
  Variables associated with baseline steatosis were higher body mass index (> or = 25, P=0.002) and higher fibrosis stage (> or = 2, P=0.019). Neither the presence nor the severity of steatosis was associated with SVR. Evaluation of paired biopsies showed no different distribution of steatosis evolution between patients with and without SVR (P=0.374). Among patients achieving a SVR, there was a significant difference in fibrosis changes between those with grade 0 or 1 steatosis and with grade 2 or 3 steatosis at post-treatment biopsy (-0.6 +/- 1.2 vs 0.3 +/- 1.3, P=0.041), whereas changes in histological activity index did not differ (-3.7 +/- 2.6 vs -4.0 +/- 2.9, P=0.740). Stepwise logistic regression analysis showed that SVR (odds ratio [OR]: 16.33, P=0.004) and grade 0 or 1 post-treatment steatosis (OR: 12.82, P=0.018) were independently associated with fibrosis regression.
  
  
  CONCLUSIONS
  In patients with chronic hepatitis C, steatosis not only correlates with advanced fibrosis at baseline but also affects fibrosis regression after antiviral therapy.
authors.affiliation: Division of Hepatogastroenterology, Department of Internal Medicine, Chang Gung Memorial Hospital, Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
authors.forename: Chao-Hung
authors.initials: CH
authors.lastname: Hung
authors.forename: Fang-Ying
authors.initials: FY
authors.lastname: Kuo
authors.forename: Jing-Houng
authors.initials: JH
authors.lastname: Wang
authors.forename: Sheng-Nan
authors.initials: SN
authors.lastname: Lu
authors.forename: Tsung-Hui
authors.initials: TH
authors.lastname: Hu
authors.forename: Chien-Hung
authors.initials: CH
authors.lastname: Chen
authors.forename: Chuan-mo
authors.initials: CM
authors.lastname: Lee
authors.forename: Hock-Liew
authors.initials: HL
authors.lastname: Eng
mesh_terms: D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use*; D001706:Biopsy; D018450:Disease Progression; D005234:Fatty Liver / Q000473:pathology* / Q000821:virology; D005260:Female; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000188:drug therapy* / Q000473:pathology / Q000821:virology; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D008099:Liver; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood; D011994:Recombinant Proteins; D012254:Ribavirin / Q000627:therapeutic use*
chemical_list: D000998:Antiviral Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins; D012254:Ribavirin