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Clinical utility of quantitative HBsAg in natural history and nucleos(t)ide analogue treatment of chronic hepatitis B: new trick of old dog

Authors
  • Tseng, Tai-Chung1, 2, 3
  • Kao, Jia-Horng2, 4, 5, 6
  • 1 Buddhist Tzu Chi General Hospital, Taipei Branch, Division of Gastroenterology, Department of Internal Medicine, Taipei, Taiwan , Taipei (Taiwan)
  • 2 National Taiwan University College of Medicine, National Taiwan University Hospital, Graduate Institute of Clinical Medicine, 7 Chung-Shan South Road, Taipei, 10002, Taiwan , Taipei (Taiwan)
  • 3 Tzu Chi University, School of Medicine, Hualien, Taiwan , Hualien (Taiwan)
  • 4 National Taiwan University College of Medicine, National Taiwan University Hospital, Department of Internal Medicine, Taipei, Taiwan , Taipei (Taiwan)
  • 5 National Taiwan University College of Medicine, National Taiwan University Hospital, Department of Medical Research, Taipei, Taiwan , Taipei (Taiwan)
  • 6 National Taiwan University College of Medicine, National Taiwan University Hospital, Hepatitis Research Center, Taipei, Taiwan , Taipei (Taiwan)
Type
Published Article
Journal
Journal of Gastroenterology
Publisher
Springer Japan
Publication Date
Oct 24, 2012
Volume
48
Issue
1
Pages
13–21
Identifiers
DOI: 10.1007/s00535-012-0668-y
Source
Springer Nature
Keywords
License
Yellow

Abstract

Using commercial quantitative assays, quantitative hepatitis B surface antigen (qHBsAg) has improved our understanding and management of chronic hepatitis B (CHB). The HBsAg level is highest in the immune tolerance phase, starts to decline during the immune clearance phase, and decreases slowly but progressively after hepatitis B e antigen (HBeAg) seroconversion. The HBsAg level is lowest in individuals with an inactive carrier state but higher in those who develop HBeAg-negative hepatitis. It has been shown that a reduction of HBsAg by 1 log IU/mL or more reflects improved host immune control of HBV infection. A combination of HBsAg <1000 IU/mL and HBV-DNA <2000 IU/mL can identify a 3-year inactive state in a genotype D HBeAg-negative carrier population. In the Asian-Pacific region, where HBV genotypes B and C are dominant, HBsAg levels of ≤10–100 IU/mL predict HBsAg loss over time. As to the prediction of disease progression, low-viremic carriers with HBsAg >1000 IU/mL have been shown to be at higher risks of HBeAg-negative hepatitis, cirrhosis, and hepatocellular carcinoma than those with HBsAg <1000 IU/mL. Although qHBsAg has been widely used in CHB patients receiving pegylated interferon therapy, the HBsAg decline is slow and does not correlate with HBV-DNA levels during nucleos(t)ide analogue (NUC) therapy. However, a rapid HBsAg decline during NUC therapy may identify patients who will finally clear HBsAg. A 6- to 12-monthly assessment of HBsAg level could be considered during NUC therapy. Taking these lines of evidence together, qHBsAg can complement HBV-DNA levels to optimize the management of CHB patients in our daily clinical practice.

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