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Review
. 2013 Jan;48(1):13-21.
doi: 10.1007/s00535-012-0668-y. Epub 2012 Oct 24.

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

Tai-Chung Tseng  1 , Jia-Horng Kao
Affiliations
Review

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

Tai-Chung Tseng et al. J Gastroenterol. 2013 Jan.

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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Figures

Fig. 1
Fig. 1
Pathway of hepatitis B surface antigen (HBsAg) production in the life cycle of hepatitis B virus (HBV) replication. cccDNA covalently closed circular DNA, ER endoplasmic reticulum, PreS2/S mRNA, Pre-S1 mRNA. Adapted from J Hepatol. 2011;55:1121–31
Fig. 2
Fig. 2
HBsAg levels in different phases of chronic HBV infection. HBeAg hepatitis B e antigen, CHB chronic hepatitis B, ALT alanine aminotransferase, Anti-HBe HBe antibody
See this image and copyright information in PMC

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