title: Quantitative hepatitis B surface antigen analysis in hepatitis B e antigen-positive nucleoside-naive patients treated with entecavir.
abstract: BACKGROUND
  Entecavir is a potent nucleoside analogue for treating chronic hepatitis B (CHB). Quantitative hepatitis B surface antigen (qHBsAg) levels are predictive of response to interferon-α in CHB treatment; however, the clinical utility of qHBsAg in nucleoside/nucleotide analogue-based CHB therapy is not fully characterized. This study assessed changes in qHBsAg in patients treated with entecavir in the Phase III study ETV-022.
  
  
  METHODS
  This retrospective post hoc analysis included nucleoside/nucleotide-naive, hepatitis B e antigen (HBeAg)-positive patients receiving entecavir (0.5 mg daily) in ETV-022 who had samples available for qHBsAg analysis through week 48. qHBsAg, HBV DNA and alanine aminotransferase levels were assessed for the overall patient cohort, for cohorts with or without HBeAg loss or HBsAg loss by week 48, and by HBV genotype.
  
  
  RESULTS
  Overall, 95 patients from ETV-022 had available samples for qHBsAg analysis through week 48. In all cohorts, 48 weeks of entecavir therapy resulted in effective HBV DNA suppression. In the overall cohort, qHBsAg declined by -0.92 log10 IU/ml through week 48. The decline in qHBsAg was more pronounced in patients with subsequent HBeAg loss or HBsAg loss, and in patients infected with HBV genotype D or A. On-treatment qHBsAg changes did not correlate with changes in HBV DNA; no on-treatment or baseline factor was found to be predictive of HBeAg loss or HBsAg loss.
  
  
  CONCLUSIONS
  Through 48 weeks of entecavir therapy, qHBsAg declined predominantly in those patients who achieved seroclearance of HBeAg or HBsAg. However, unlike with interferon-α-based therapy, early qHBsAg decline was not predictive of serological response at year 1 of entecavir treatment.
authors.affiliation: University of California, San Diego School of Medicine, San Diego, CA, USA. rgish@ucsd.edu.
authors.forename: Robert G
authors.initials: RG
authors.lastname: Gish
authors.forename: Ting-Tsung
authors.initials: TT
authors.lastname: Chang
authors.forename: Ching-Lung
authors.initials: CL
authors.lastname: Lai
authors.forename: Robert A
authors.initials: RA
authors.lastname: de Man
authors.forename: Adrian
authors.initials: A
authors.lastname: Gadano
authors.forename: Cyril
authors.initials: C
authors.lastname: Llamoso
authors.forename: Hong
authors.initials: H
authors.lastname: Tang
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use*; D004279:DNA, Viral; D005260:Female; D005838:Genotype; D006147:Guanine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D006514:Hepatitis B Surface Antigens / Q000276:immunology*; D006513:Hepatitis B e Antigens / Q000276:immunology*; D006515:Hepatitis B virus / Q000235:genetics / Q000276:immunology*; D019694:Hepatitis B, Chronic / Q000188:drug therapy* / Q000276:immunology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D013997:Time Factors; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: D000998:Antiviral Agents; D004279:DNA, Viral; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens; C413685:entecavir; D006147:Guanine