title: Determinants of spontaneous surface antigen loss in hepatitis B e antigen-negative patients with a low viral load.
abstract: Loss of hepatitis B surface antigen (HBsAg) usually indicates the cure of hepatitis B virus (HBV) infection. In spontaneous hepatitis B e antigen (HBeAg) seroconverters, lower serum HBsAg and HBV DNA levels have been shown to be associated with HBsAg loss over time. However, little is known about their impacts on HBsAg loss in HBeAg-negative patients with limited viral replication. A total of 688 HBeAg-negative patients with baseline serum HBV DNA levels <2000 IU/mL were enrolled in Taiwan. The relationships of HBsAg and HBV DNA levels with subsequent HBsAg loss were investigated. In a mean follow-up of 11.6 years, the average annual rate of HBsAg loss was 1.6%. Baseline HBsAg and HBV DNA levels were inversely associated with subsequent HBsAg loss. When compared to patients who had HBsAg levels >1000 IU/mL, the rates of HBsAg loss were significantly higher in patients with HBsAg levels of 100-999, 10-99, and <10 IU/mL, with hazard ratios of 2.5 (95% confidence interval [CI], 1.6-4.0), 2.8 (95% CI, 1.6-5.0), and 13.2 (95% CI, 8.1-21.5), respectively. Multivariate analysis showed that HBsAg level, but not HBV DNA, remained as an independent factor. The adjusted hazard ratio of HBsAg loss was 13.2 (95% CI, 7.8-22.1) for HBsAg level <10 versus ≥ 1000 IU/mL. When compared to HBV DNA level by receiver operating characteristic curve analysis, HBsAg level served as a better predictor of both 5-year and 10-year HBsAg loss.
  
  
  CONCLUSIONS
  In HBeAg-negative patients with HBV genotype B or C infection who have HBV DNA level <2000 IU/mL, HBsAg level <10 IU/mL is the strongest predictor of HBsAg loss.
authors.affiliation: Division of Gastroenterology, Department of Internal Medicine, Buddhist Tzu Chi General Hospital Taipei Branch, Taipei, Taiwan.
authors.forename: Tai-Chung
authors.initials: TC
authors.lastname: Tseng
authors.forename: Chun-Jen
authors.initials: CJ
authors.lastname: Liu
authors.forename: Hung-Chih
authors.initials: HC
authors.lastname: Yang
authors.forename: Tung-Hung
authors.initials: TH
authors.lastname: Su
authors.forename: Chia-Chi
authors.initials: CC
authors.lastname: Wang
authors.forename: Chi-Ling
authors.initials: CL
authors.lastname: Chen
authors.forename: Stephanie Fang-Tzu
authors.initials: SF
authors.lastname: Kuo
authors.forename: Chen-Hua
authors.initials: CH
authors.lastname: Liu
authors.forename: Pei-Jer
authors.initials: PJ
authors.lastname: Chen
authors.forename: Ding-Shinn
authors.initials: DS
authors.lastname: Chen
authors.forename: Jia-Horng
authors.initials: JH
authors.lastname: Kao
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D006528:Carcinoma, Hepatocellular / Q000175:diagnosis / Q000453:epidemiology / Q000821:virology; D015331:Cohort Studies; D004279:DNA, Viral / Q000378:metabolism; D005260:Female; D005500:Follow-Up Studies; D006513:Hepatitis B e Antigens / Q000235:genetics / Q000378:metabolism*; D006515:Hepatitis B virus / Q000235:genetics / Q000254:growth & development / Q000302:isolation & purification*; D019694:Hepatitis B, Chronic / Q000175:diagnosis* / Q000453:epidemiology / Q000821:virology*; D006801:Humans; D015994:Incidence; D008103:Liver Cirrhosis / Q000175:diagnosis / Q000453:epidemiology / Q000821:virology; D008113:Liver Neoplasms / Q000175:diagnosis / Q000453:epidemiology / Q000821:virology; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D011379:Prognosis; D016016:Proportional Hazards Models; D012008:Recurrence; D019562:Viral Load / Q000502:physiology*; D014766:Viremia / Q000175:diagnosis / Q000453:epidemiology / Q000821:virology; D014779:Virus Replication / Q000502:physiology
chemical_list: D015415:Biomarkers; D004279:DNA, Viral; D006513:Hepatitis B e Antigens