title: Hepatic Steatosis as a Predictive Factor of Antiviral Effect of Pegylated Interferon Therapy in Patients With Hepatitis B.
abstract: OBJECTIVE
  This study sought to evaluate the impact of hepatic steatosis, a common hepatocyte change in nonalcoholic fatty liver disease, upon response to pegylated interferon (PEG-IFN) therapy in patients with chronic hepatitis B (CHB).
  
  
  METHODS
  Eighty-nine consecutive CHB patients from the Affiliated Hospital of Hangzhou Normal University receiving 48 weeks of PEG-IFN therapy were enrolled in this study, and 56 patients were followed up for 48 weeks among subjects with completed therapy. Baseline characteristics, end-of-treatment response (ETR), and sustained viral response (SVR) to PEG-IFN therapy were evaluated. Univariate analysis and multivariate logistic regression were applied to find independent factors of hepatic steatosis and PEG-IFN treatment failure.
  
  
  RESULTS
  Steatosis was present in 34.5% (31 of 89) of liver biopsy samples. ETR to PEG-IFN therapy was 56.17% (50 of 89) at 48 weeks, and SVR to PEG-IFN therapy was 57.6% (32 of 56) at 96 weeks. There was no significant difference in ETR between the patients with hepatic steatosis and those without hepatic steatosis at 48 weeks (P > .05), whereas SVR was higher in patients without hepatic steatosis than in those with hepatic steatosis at 96 weeks (P < .05). Multivariate analysis showed that the sustained response rate was independently associated with steatosis, fibrosis, aspartate aminotransferase, C-reactive protein, and ferritin. Hepatic steatosis was a prediction factor with the sustained response.
  
  
  CONCLUSIONS
  Hepatic steatosis may be a predictive factor of response to PEG-IFN therapy in patients with CHB.
authors.affiliation: Department of Liver Diseases, The Affiliated Hospital of Hangzhou Normal University, Hangzhou 310015, China.
authors.forename: L
authors.initials: L
authors.lastname: Gong
authors.affiliation: Department of Liver Diseases, The Affiliated Hospital of Hangzhou Normal University, Hangzhou 310015, China.
authors.forename: J
authors.initials: J
authors.lastname: Liu
authors.affiliation: Department of Liver Diseases, The Affiliated Hospital of Hangzhou Normal University, Hangzhou 310015, China.
authors.forename: J
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Liver Diseases, The Affiliated Hospital of Hangzhou Normal University, Hangzhou 310015, China.
authors.forename: G Q
authors.initials: GQ
authors.lastname: Lou
authors.affiliation: Department of Liver Diseases, The Affiliated Hospital of Hangzhou Normal University, Hangzhou 310015, China. Electronic address: qunpingshihz@sina.com.
authors.forename: J P
authors.initials: JP
authors.lastname: Shi
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use*; D001219:Aspartate Aminotransferases / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D005234:Fatty Liver / Q000150:complications*; D005260:Female; D005293:Ferritins / Q000032:analysis; D005500:Follow-Up Studies; D019694:Hepatitis B, Chronic / Q000150:complications / Q000188:drug therapy*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D011092:Polyethylene Glycols / Q000627:therapeutic use*; D011446:Prospective Studies; D011994:Recombinant Proteins / Q000627:therapeutic use
chemical_list: D000998:Antiviral Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D002097:C-Reactive Protein; D005293:Ferritins; D001219:Aspartate Aminotransferases; C417083:peginterferon alfa-2b