title: Serum hepatitis B surface antigen levels help predict disease progression in patients with low hepatitis B virus loads.
abstract: Chronic hepatitis B patients with high viral loads are at increased risk of cirrhosis and hepatocellular carcinoma (HCC). In patients with low viral loads, higher hepatitis B surface antigen (HBsAg) levels have been shown to predict HCC development. However, little is known about the difference in risk for other hepatitis B virus (HBV)-related adverse outcomes with varying HBsAg levels. A total of 1,068 Taiwanese hepatitis B e antigen (HBeAg)-negative HBV carriers with serum HBV DNA level <2,000 IU/mL at baseline were followed for a mean duration of 13.0 years. Patients were categorized based on their HBsAg levels, and the relationships between HBsAg level and development of HBeAg-negative hepatitis, hepatitis flare, and cirrhosis were investigated. Of the 1068 patients with low viral loads, 280 developed HBeAg-negative hepatitis, with an annual incidence rate of 2.0%. HBsAg level, but not HBV DNA level, was found to be a risk factor for HBeAg-negative hepatitis. Multivariate analysis showed that the adjusted hazard ratio in patients with an HBsAg level ≥ 1,000 versus <1000 IU/mL was 1.5 (95% confidence interval, 1.2-1.9). The positive correlation was present when evaluating other endpoints, including hepatitis flare and cirrhosis, and remained consistent when the study population was restricted to those with normal alanine aminotransferase (ALT) level at baseline. The annual incidence rate of HBeAg-negative hepatitis was lowered to 1.1% in patients with low levels of HBV DNA, HBsAg, and ALT.
  
  
  CONCLUSIONS
  In HBeAg-negative patients with low viral loads and genotype B or C virus infection, a higher HBsAg level can predict disease progression. HBsAg <1,000 IU/mL in combination with low levels of HBV DNA and ALT help define minimal-risk HBV carriers.
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: Cheng-An
authors.initials: CA
authors.lastname: Hsu
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; D000410:Alanine Transaminase / Q000097:blood; D004279:DNA, Viral / Q000097:blood*; D018450:Disease Progression; D005260:Female; D006514:Hepatitis B Surface Antigens / Q000097:blood*; D006515:Hepatitis B virus / Q000235:genetics*; D019694:Hepatitis B, Chronic / Q000276:immunology / Q000503:physiopathology* / Q000821:virology; D006801:Humans; D008103:Liver Cirrhosis / Q000209:etiology / Q000821:virology; D008297:Male; D008875:Middle Aged; D013624:Taiwan / Q000453:epidemiology; D019562:Viral Load
chemical_list: D004279:DNA, Viral; D006514:Hepatitis B Surface Antigens; D000410:Alanine Transaminase