title: Treatment of pegylated interferon-α2a in chronic hepatitis B patients demonstrating a spontaneous decline in HBV DNA after acute exacerbation.
abstract: BACKGROUND
  Acute exacerbation (AE) in chronic hepatitis B (CHB) is usually followed by a spontaneous decline in HBV DNA levels. The subsequent treatment is controversial. In this study, we evaluated the efficacy and safety of pegylated interferon-α2a (PEG-IFN-α2a) for such CHB patients.
  
  
  METHODS
  A total of 74 hepatitis B e antigen (HBeAg)-positive patients with a spontaneous HBV DNA decline (by >2 log10 IU•ml(-1), compared with baseline levels before antiviral treatment) after AE (alanine aminotransferase [ALT]: 10-30-fold the upper limit of normal [ULN], total bilirubin [TBIL]: 2-20 mg•dl(-1), prothrombin time activity >60%) were included. In total, 22 patients (group A) received PEG-IFN-α2a treatment (180 µg•kg(-1)•week(-1), when ALT was <10 ULN and TBIL<2 mg•dl(-1)) for 48 weeks, with 48 weeks of treatment-free follow-up. Twenty-one patients (group B) selected continual entecavir therapy. Thirty-one patients (group C, control group) received routine liver-protective drugs.
  
  
  RESULTS
  At week 96, virological response rates were 90.5%, 100% and 48%, and ALT normalization rates were 81%, 95% and 40% for groups A, B and C, respectively. HBeAg seroconversion rates were 71.4%, 45% and 32% in groups A, B and C, respectively. A high hepatitis B surface antigen (HBsAg) loss rate was observed in PEG-IFN-α2a-treated patients, while no entecavir-treated patients achieved HBsAg loss. Group A patients suffered from typical PEG-IFN therapy-related adverse events. No severe adverse event was observed in any groups.
  
  
  CONCLUSIONS
  PEG-IFN-α2a is effective and safe for treating CHB patients demonstrating a spontaneous decline in HBV DNA after AE, and yields an increased likelihood of HBsAg loss.
authors.affiliation: The Department of Infectious Disease, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, PR China.
authors.forename: Qingxian
authors.initials: Q
authors.lastname: Cai
authors.forename: Fengjuan
authors.initials: F
authors.lastname: Chen
authors.forename: Xiaoqiong
authors.initials: X
authors.lastname: Shao
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Zhang
authors.forename: Zhixin
authors.initials: Z
authors.lastname: Zhao
authors.forename: Zhiliang
authors.initials: Z
authors.lastname: Gao
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D000998:Antiviral Agents / Q000627:therapeutic use*; D001663:Bilirubin / Q000097:blood; D015415:Biomarkers / Q000097:blood; D018450:Disease Progression; D005260:Female; D006147:Guanine / Q000031:analogs & derivatives / Q000627:therapeutic use; D006514:Hepatitis B Surface Antigens / Q000097:blood; D006513:Hepatitis B e Antigens / Q000097:blood; D006515:Hepatitis B virus / Q000187:drug effects* / Q000502:physiology; D019694:Hepatitis B, Chronic / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy* / Q000276:immunology; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use*; D008099:Liver / Q000187:drug effects / Q000473:pathology / Q000821:virology; D008297:Male; D008875:Middle Aged; D011092:Polyethylene Glycols / Q000627:therapeutic use*; D011379:Prognosis; D011446:Prospective Studies; D011517:Prothrombin Time; D011994:Recombinant Proteins / Q000627:therapeutic use; D012075:Remission, Spontaneous; D016896:Treatment Outcome; D019562:Viral Load / Q000187:drug effects*
chemical_list: D000998:Antiviral Agents; D015415:Biomarkers; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens; D016898:Interferon-alpha; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; C413685:entecavir; D006147:Guanine; D000410:Alanine Transaminase; C100416:peginterferon alfa-2a; D001663:Bilirubin