title: Longitudinal change of HBsAg in HBeAg-negative patients with genotype B or C infection.
abstract: OBJECTIVE
  Quantitative HBsAg has been recognized to assist in the management of chronic hepatitis B virus (HBV) infection. However, its role in disease monitoring of HBeAg-negative patients remains unclear. We aimed to investigate the longitudinal HBsAg change in HBeAg-negative carriers with HBV genotype B or C infection.
  
  
  METHODS
  This is a retrospective cohort study conducted in a university hospital. Treatment-naïve HBeAg-negative carriers followed for more than 3 years were recruited. Their hepatitis activities were categorized by longitudinal HBV-DNA levels into high viral-load (HVL: HBV-DNA >/ =2000 IU/mL persistently), low viral-load (LVL: HBV-DNA <2000 IU/mL persistently) and fluctuated viral-load (FVL: HBV-DNA between HVL and LVL). The baseline and end-of-follow-up (EOF) HBsAg levels were quantified for analyses.
  
  
  RESULTS
  We recruited 187 patients with a median follow-up of 8 years. LVL patients had a significantly lower HBsAg at baseline and EOF and a significantly greater annualized HBsAg decline compared with the FVL and HVL. The longitudinal HBsAg change was independent of genotype B or C. The lower baseline HBsAg level predicted the HBsAg decline and HBsAg loss, whereas the higher baseline HBV-DNA predicted the hepatitis flare. A baseline HBsAg <50 IU/mL predicted subsequent HBsAg loss with a sensitivity of 82% and specificity of 67%. The annualized HBsAg decline appeared non-linear, and accelerated as the HBsAg level lowered (0.054, 0.091, 0.126 log(10) IU/mL in patients with baseline HBsAg >1000, 100-999, <100 IU/mL, respectively, P for trend= .014).
  
  
  CONCLUSIONS
  In genotype B or C HBeAg-negative carriers, baseline HBsAg levels correlate with future disease activities and help to predict HBsAg decline or loss. Inactive carriers with lower baseline HBsAg levels have a greater and accelerating HBsAg decline over time, regardless of HBV genotypes.
authors: Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
authors: Tung-Hung
authors: TH
authors: Su
authors: Chun-Jen
authors: CJ
authors: Liu
authors: Tai-Chung
authors: TC
authors: Tseng
authors: Chen-Hua
authors: CH
authors: Liu
authors: Hung-Chih
authors: HC
authors: Yang
authors: Chi-Ling
authors: CL
authors: Chen
authors: Pei-Jer
authors: PJ
authors: Chen
authors: Jia-Horng
authors: JH
authors: Kao
authors: Ding-Shinn
authors: DS
authors: Chen
mesh_terms: D000328:Adult; D004279:DNA, Viral / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D006514:Hepatitis B Surface Antigens / Q000097:blood*; D006513:Hepatitis B e Antigens / Q000097:blood*; D006515:Hepatitis B virus / Q000235:genetics* / Q000502:physiology*; D019694:Hepatitis B, Chronic / Q000097:blood* / Q000276:immunology / Q000821:virology*; D006801:Humans; D008103:Liver Cirrhosis / Q000097:blood / Q000473:pathology / Q000821:virology; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D013997:Time Factors
chemical_list: D004279:DNA, Viral; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens