Article first published online: 25 JUL 2011
Copyright © 2011 American Association for the Study of Liver Diseases
Volume 54, Issue 2, pages E1–E9, August 2011
How to Cite
Liaw, Y.-F. (2011), Clinical utility of hepatitis B surface antigen quantitation in patients with chronic hepatitis B: A review. Hepatology, 54: E1–E9. doi: 10.1002/hep.24473
Potential conflict of interest: The author has been involved in clinical trials and has served as a global advisory board member for Roche, Bristol-Myers Squibb, Novartis, and Gilead Sciences.
The author thanks the Chang Gung Medical Research Fund for its long-term grant support (SMRPG1005 and BMRPG380061) and Roche Diagnostics (Rotkreuz, Switzerland) for its financial support.
- Issue published online: 25 JUL 2011
- Article first published online: 25 JUL 2011
- Manuscript Accepted: 7 APR 2011
- Manuscript Received: 26 NOV 2010
This clinically relevant review focuses on recent findings concerning hepatitis B surface antigen (HBsAg) quantitation in untreated patients and treated patients with chronic hepatitis B. Recent studies and emerging data have shown that both HBsAg and hepatitis B virus (HBV) DNA levels decline during the natural course of a chronic HBV infection; they are lowest in the inactive phase, which is also characterized by the highest HBsAg/HBV DNA ratio. It has been demonstrated that the combined use of HBsAg and HBV DNA levels might help in the identification of true inactive carriers with high accuracy. Retrospective analyses of HBsAg levels in patients undergoing therapy have suggested a role for HBsAg quantitation in monitoring the response to therapy. In comparison with nucleos(t)ide analogues (NAs), interferon-based therapy results in greater overall declines in serum HBsAg levels. A rapid on-treatment decline in HBsAg levels appears to be predictive of a sustained response. With the aid of HBsAg quantitation, it appears that we can anticipate an individualized approach to tailoring the treatment duration. The proposal of early stopping rules for patients not responding to pegylated interferon (according to a lack of any HBsAg decline) represents a step toward a response-guided approach. The development of stopping rules for patients treated with NAs is desirable for reducing the need for lifelong therapy. However, before stopping rules for antiviral therapy can be applied, we need to learn more about the kinetics of HBsAg declines during the natural history of the infection and as a response to therapy so that we can better define the best timing, the relevant HBsAg cutoff levels, and the best ways to apply these rules in clinical practice. (HEPATOLOGY 2011;)