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http://www.sciencedirect.com/science/article/pii/S0168827811004971
Review
Hepatitis B surface antigen quantification: Why and how to use it in 2011 – A core group report
Henry Lik-Yuen Chan1,  ,  , Alex Thompson2, Michelle Martinot-Peignoux3, Teerha Piratvisuth4, Markus Cornberg5, Maurizia Rossana Brunetto6, Hans L. Tillmann7, Jia-Horng Kao8, Ji-Dong Jia9, Heiner Wedemeyer5, Stephen Locarnini2, Harry L.A. Janssen10, Patrick Marcellin3, †
| 1 | Department of Medicine and Therapeutics and Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong |
| 2 | Victorian Infectious Diseases Reference Laboratory, 10 Wreckyn St., North Melbourne, Victoria 3051, Australia |
| 3 | INSERM U773, Centre de Recherche Biomédicale Bichat-Beaujon (CRB3), Service d’Hépatologie, Université Paris-Diderot, Hopilal Beaujon, Clichy, France |
| 4 | Department of Medicine, Prince of Songkla University, NKC Institute of Gastroenterology and Hepatology, Hat Yai, Songkla, Thailand |
| 5 | Department of Gastroenterology, Hepatology, and Endocrinology, Hannover Medical School, Hannover, Germany |
| 6 | Hepatology Unit, University of Pisa, Italy |
| 7 | Duke Clinical Research Institute, Duke University, Durham, NC, USA |
| 8 | Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan |
| 9 | Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China |
| 10 | Department of Gastroenterology & Hepatology, Erasmus MC University Hospital, Rotterdam, The Netherlands |
Received 26 March 2011; revised 27 May 2011; Accepted 9 June 2011. Available online 28 June 2011.
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.
Abbreviations: Anti-HBe, antibodies to hepatitis B e antigen; ALT, alanine aminotransferase; cccDNA, covalently closed circular DNA; CHB, chronic hepatitis B; HBV, hepatitis B virus; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B surface antigen; NA, nuclet(s)ide analogues; NPV, negative predictive value; ORF, open reading frame; PPV, positive predictive value
Keywords: Hepatitis B virus; HBsAg, Antiviral treatment; Peginterferon
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发表于 2011-10-24 18:24
