Hepatitis B surface antigen Quantification: Why and How to u…

682256

Author: [email protected]
Date: 2011-07-04 05:59 +800
To: hbv_research
Subject: Viral level is an indicator of long-term outcome of hepatitis B virus e antigen-negative carriers with persistently normal serum alanine aminotransferase levels

J Viral Hepat. 2011 Jul;18(7):e191-9. doi: 10.1111/j.1365-2893.2010.01427.x. Epub 2011 Jan 11.



Viral level is an indicator of long-term outcome of hepatitis B virus e antigen-negative carriers with persistently normal serum alanine aminotransferase levels.



Nakazawa T, Shibuya A, Takeuchi A, Shibata Y, Hidaka H, Okuwaki Y, Takada J, Tanaka Y, Watanabe M, Minamino T, Sakurai K, Koizumi W.




Source

Department of Gastroenterology, Kitasato University East Hospital, Sagamihara Nakazawa Medical Clinic, Sagamihara Department of Clinical Laboratory, Kitasato University East Hospital, Sagamihara, Japan.




Abstract

Summary.  The association between viral level and the long-term outcomes of hepatitis B virus (HBV) carriers who test negative for hepatitis B virus e antigen (HBeAg) but have persistently normal serum alanine aminotransferase levels (PNALT) remains unclear. We examined hepatocarcinogenesis, hepatitis reactivation, predictive factors and the time course of HBV DNA levels during follow-up in 104 HBeAg-negative Japanese carriers with PNALT. During a mean follow-up period of 6.4 ± 3.4 years, 5 patients (4.8%) had hepatocarcinogenesis and 14 (13.5%) had hepatitis reactivation. At 5 and 10 years, the cumulative rates of hepatocarcinogenesis were 2.4% and 9.9%, while those of hepatitis activation were 13.7% and 15.5%, respectively. An HBV DNA level of ≥5 log(10)  copies/mL was the sole predictor of hepatocarcinogenesis with a univariate analysis. An HBV DNA level of ≥5 log(10)  copies/mL and an alanine aminotransferase (ALT) level of >20 to ≤40 IU/L were independent predictors of hepatitis reactivation in a Cox model. Because there was no association between hepatocarcinogenesis and ALT activity, the HBV DNA level was considered an essential predictor. In addition, the baseline HBV DNA level was related to the future level and was not subject to wide fluctuations. Our results showed that an HBV DNA level of ≥5 log(10)  copies/mL predicts subsequent hepatocarcinogenesis and hepatitis reactivation in HBeAg-negative carriers with PNALT. As the baseline HBV DNA level reflects the future level, appropriate clinical management according to the viral level is expected to decrease future risk.



© 2011 Blackwell Publishing Ltd.




PMID: 21692932 [PubMed - in process]

Subject: Hepatitis B surface antigen Quantification: Why and How to use it in 2011 - A Core Group Report

J Hepatol. 2011 Jun 27. [Epub ahead of print]



Hepatitis B surface antigen Quantification: Why and How to use it in 2011 - A Core Group Report.



Chan HL, Thompson A, Martinot-Peignoux M, Piratvisuth T, Cornberg M, Brunetto MR, Tillmann HL, Kao JH, Jia JD, Wedemeyer H, Locarnini S, Janssen HL, Marcellin P; for the Good Practice in using sAg in Chronic Hepatitis B Study Group (GPs-CHB Study Group).




Source

Department of Medicine and Therapeutics and Institute of Digestive Disease, The Chinese University of Hong Kong.




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 tend 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.



Copyright © 2011. Published by Elsevier B.V.


PMID: 21718667 [PubMed - as supplied by publisher]





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