Hepatitis B surface antigen quantification: Why and how to use it in 2011 - A core group report
Journal
Journal of Hepatology
Journal Volume
55
Journal Issue
5
Pages
1121-1131
Date Issued
2011
Author(s)
Chan H.L.-Y.
Thompson A.
Martinot-Peignoux M.
Piratvisuth T.
Cornberg M.
Brunetto M.R.
Tillmann H.L.
Jia J.-D.
Wedemeyer H.
Locarnini S.
Janssen H.L.A.
Marcellin P.
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 (<2000 IU/ml), HBsAg <1000 IU/ml in genotype D HBV infection and HBsAg <100 IU/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 <100 IU/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. ? 2011 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
Subjects
Antiviral treatment; HBsAg; Hepatitis B virus; Peginterferon
SDGs
Other Subjects
alanine aminotransferase; alpha interferon; circular DNA; entecavir; genomic RNA; hepatitis B surface antigen; hepatitis B(e) antigen; lamivudine; nucleoside analog; peginterferon; peginterferon alpha2a; telbivudine; tenofovir; virus DNA; age; alanine aminotransferase blood level; antiviral therapy; chronic hepatitis; clinical practice; codon; disease carrier; disease course; drug efficacy; enzyme immunoassay; genotype; hepadnavirus infection; hepatitis B; human; humoral immunity; immunological tolerance; liver cell; liver cirrhosis; minichromosome; nonhuman; open reading frame; phase 3 clinical trial (topic); point mutation; priority journal; protein blood level; review; sensitivity and specificity; seroconversion; treatment response; viremia; virion; virus DNA cell DNA interaction; virus particle; virus replication; Antiviral Agents; Biological Markers; Hepatitis B e Antigens; Hepatitis B Surface Antigens; Hepatitis B virus; Hepatitis B, Chronic; Humans; Interferon-alpha; Polyethylene Glycols; Prognosis; Recombinant Proteins; Reverse Transcriptase Inhibitors
Type
review