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Serum HBsAg kinetics in clinical prediction
[url=]Wen-Juei Jeng[/url]
, [url=]Yun-Fan Liaw[/url][url=]Correspondence information about the author Yun-Fan Liaw[/url]Email the author Yun-Fan Liaw
Liver Research Unit, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taipei, Taiwan
We read with great interest the review article “The role of quantitative hepatitis B surface antigen revisited” by Cornberg et al. in the Journal of Hepatology [1]. Indeed, it is a comprehensive update. However, the role of hepatitis B surface antigen (HBsAg) quantification in the prediction of spontaneous or antiviral therapy related HBsAg seroclearance and relapse after cessation of nucleos(t)ide analog (NUC) therapy was not well addressed. The studies mentioned in the review used an HBsAg level <100 IU/ml as a predictor for remote (6–10 years) HBsAg seroclearance but two studies on short-term prediction of HBsAg seroclearance within 1–3 years were not mentioned.
One longitudinal study showed that serum HBsAg level ≤200 IU/ml had a negative predictive value for HBsAg seroclearance of 100% and 92% at 1 and 3 years, respectively, and the positive predictive value increased from 36% at 1 year and 49% at 3 year to 97% and 100%, respectively if combined with a ≥1 log10 IU/ml reduction in the preceding 2 years [2]. Another large case-control study also showed that HBsAg level <200 IU/ml was predictive of HBsAg seroclearance within 3 years and a patient with HBsAg <200 IU/ml and a 0.5 log10 IU/ml HBsAg decline in the next year may predict HBsAg seroclearance in 3 years with a sensitivity of 74% and a specificity of 89.4% [3]. Obviously, prediction of spontaneous HBsAg seroclearance within a much shorter period of 1–3 years is more desirable and useful in daily clinical practice.
Stronger HBsAg decline during NUC therapy associated with higher pretherapy alanine aminotransferase (ALT) was briefly mentioned in the review. Actually, patients with pretherapy ALT over 5× upper limit of normal (ULN) showed greater HBsAg decline not only at an ALT-level dependent manner but also at an alpha-fetoprotein (AFP) level-dependent manner, in which AFP dominated over ALT as a more powerful factor for early “rapid HBsAg decline” [4]. These findings are important because “rapid HBsAg decline” >0.5 log10 IU/ml by month 6 or >1 log10 IU/ml by month 12 of NUC therapy were found to be predictors for HBsAg seroclearance [5], and HBsAg decline ≥75% by week 24 of adefovir/tenofovir therapy was also predictive for HBsAg seroclearance [6]. A most recent study further showed that hepatitis flares (ALT >5× ULN) during pegylated interferon and tenofovir combination therapy in HBeAg positive patients was associated with HBsAg decline >1 log10 by week 12, which was an independent factor for HBsAg loss [7]. More studies on this issue are ongoing.
The issue of stopping NUC therapy in HBeAg-negative patients has attracted more and more attention in recent years. Studies have shown the lower the HBsAg level at the end of NUC therapy, the less chance of clinical relapse [[8], [9], [10]]. HBsAg <100 IU/ml seems to be the best predictive level but no consensus has been reached. This is also applicable in patients with liver cirrhosis who had discontinued NUC therapy, as such patients were included in these studies [[8], [9], [10]].
In conclusion, HBsAg quantification has a wide range of clinical applications. It is anticipated that the role of HBsAg kinetics in the natural course and during antiviral therapy in patients with chronic hepatitis B will remain a hot issue to be explored.
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