Literature DB >> 21718667

Hepatitis B surface antigen quantification: why and how to use it in 2011 - a core group report.

Henry Lik-Yuen Chan1, Alex Thompson, Michelle Martinot-Peignoux, Teerha Piratvisuth, Markus Cornberg, Maurizia Rossana Brunetto, Hans L Tillmann, Jia-Horng Kao, Ji-Dong Jia, Heiner Wedemeyer, Stephen Locarnini, Harry L A Janssen, Patrick Marcellin.   

Abstract

Quantitative HBsAg had been suggested to be helpful in management of HBV, but assays were cumbersome. The recent availability of commercial quantitative assays has restarted the interest in quantitative serum hepatitis B surface antigen (HBsAg) as a biomarker for prognosis and treatment response in chronic hepatitis B. HBsAg level reflects the transcriptional activity of cccDNA rather than the absolute amount of cccDNA copies. Serum HBsAg level tends to be higher in hepatitis B e antigen (HBeAg)-positive than HBeAg-negative patients. Among patients with a low HBV DNA (<2000IU/ml), HBsAg <1000IU/ml in genotype D HBV infection and HBsAg <100IU/ml in genotype B/C HBV infection is associated with inactive carrier state in HBeAg-negative patients. The HBsAg reduction by nucleos(t)ide analogues (NA) is not as pronounced as by interferon treatment. On peginterferon treatment, sustained responders tend to show greater HBsAg decline than the non-responders. The optimal on-treatment HBsAg cutoff to predict response needs further evaluation in HBeAg-positive patients, but an absence of HBsAg decline together with a <2 log reduction in HBV DNA at week 12 can serve as stopping rule in HBeAg-negative patients with genotype D HBV infection. A rapid serum HBsAg decline during NA therapy may identify patients who will clear HBsAg in the long-term. There are early reports among Asian patients that an HBsAg level of <100IU/ml might predict lower risk of relapse after stopping NA treatment. In clinical practice, serum HBsAg level should be used together with, but not as a substitute for, HBV DNA.
Copyright © 2011 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

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Year:  2011        PMID: 21718667     DOI: 10.1016/j.jhep.2011.06.006

Source DB:  PubMed          Journal:  J Hepatol        ISSN: 0168-8278            Impact factor:   25.083


  92 in total

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