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Serum HBsAg (serum + hbsag)
Selected AbstractsEarly on-treatment prediction of response to peginterferon alfa-2a for HBeAg-negative chronic hepatitis B using HBsAg and HBV DNA levels,HEPATOLOGY, Issue 2 2010Vincent Rijckborst Peginterferon alfa-2a results in a sustained response (SR) in a minority of patients with hepatitis B e antigen (HBeAg),negative chronic hepatitis B (CHB). This study investigated the role of early on-treatment serum hepatitis B surface antigen (HBsAg) levels in the prediction of SR in HBeAg-negative patients receiving peginterferon alfa-2a. HBsAg (Architect from Abbott) was quantified at the baseline and during treatment (weeks 4, 8, 12, 24, 36, and 48) and follow-up (weeks 60 and 72) in the sera from 107 patients who participated in an international multicenter trial (peginterferon alfa-2a, n = 53, versus peginterferon alfa-2a and ribavirin, n = 54). Overall, 24 patients (22%) achieved SR [serum hepatitis B virus (HBV) DNA level < 10,000 copies/mL and normal alanine aminotransferase levels at week 72]. Baseline characteristics were comparable between sustained responders and nonresponders. From week 8 onward, serum HBsAg levels markedly decreased in sustained responders, whereas only a modest decline was observed in nonresponders. However, HBsAg declines alone were of limited value in the prediction of SR [area under the receiver operating characteristic curve (AUC) at weeks 4, 8, and 12 = 0.59, 0.56, and 0.69, respectively]. Combining the declines in HBsAg and HBV DNA allowed the best prediction of SR (AUC at week 12 = 0.74). None of the 20 patients (20% of the study population) in whom a decrease in serum HBsAg levels was absent and whose HBV DNA levels declined less than 2 log copies/mL exhibited an SR (negative predictive value = 100%). Conclusion: At week 12 of peginterferon alfa-2a treatment for HBeAg-negative CHB, a solid stopping rule was established with a combination of declines in serum HBV DNA and HBsAg levels from the baseline. Quantitative serum HBsAg in combination with HBV DNA enables on-treatment adjustments of peginterferon therapy for HBeAg-negative CHB. (HEPATOLOGY 2010) [source] Relationship between serum hepatitis B virus DNA and surface antigen with covalently closed circular DNA in HBeAg-negative patients,JOURNAL OF MEDICAL VIROLOGY, Issue 9 2010L.Y. Lin Abstract Hepatitis B virus (HBV) covalently closed circular DNA (cccDNA) is responsible for viral persistence. This study aimed to investigate the serum surrogate markers for cccDNA and to evaluate the intrahepatic viral events associated with disease activity in HBeAg-negative chronic hepatitis B patients. Thirty-three treatment-naïve patients with a negative HBeAg who had a liver biopsy were studied. Active disease was defined as a serum alanine aminotransferase >40,IU/L and a serum HBV DNA >10,000,copies/ml. This study showed significant correlation between serum HBV DNA and both log cccDNA (r,=,0.41, P,=,0.018) and log total intrahepatic HBV DNA (r,=,0.71, P,<,0.0001). No significant correlation was observed between serum HBsAg and log cccDNA (P,=,0.15) or log total intrahepatic HBV DNA (P,=,0.97). Fourteen and 19 patients had inactive and active disease, respectively. The median log cccDNA and log total intrahepatic HBV DNA (copies/106 cells) were significantly higher in patients with active disease compared with those with inactive disease (4.11 vs. 3.53, P,=,0.03 and 5.46 vs. 4.64, P,<,0.001, respectively). The HBV replicative efficiency, defined as the ratio of serum HBV DNA to cccDNA, was approximately 20% higher in patients with active disease. No significant difference was observed in the HBsAg levels and the ratio of serum HBsAg to cccDNA between the two groups. In conclusion, serum HBV DNA, but not HBsAg, reflects the amount of cccDNA and the replication efficiency of HBV in patients with HBeAg-negative chronic hepatitis B. J. Med. Virol. 82:1494,1500, 2010. © 2010 Wiley-Liss, Inc. [source] Clearance of serum HBsAg and anti-HBs seroconversion following antiviral therapy for chronic hepatitis BJOURNAL OF MEDICAL VIROLOGY, Issue 8 2009Olivier Borgniet Abstract In this study, we have analyzed the evolution of serum HBsAg levels in 16 patients with chronic hepatitis B who showed an HBsAg seroconversion following antiviral therapy. The data showed that the clearance of serum HBsAg is slower than that of serum HBV DNA, which may reflect a slow kinetics of clearance of infected hepatocytes. Interestingly, HBsAg was detectable for a longer time using the Architect assay than with the Bio-Rad assay. As viremia suppression is achieved in most patients under therapy with the new generation of nucleoside analogs, these data suggest that the quantitative monitoring of serum HBsAg may represent a novel tool for the assessment of antiviral therapy efficacy. J. Med. Virol. 81:1336,1342, 2009. © 2009 Wiley-Liss, Inc. [source] Decline of hepatitis B carrier rate in vaccinated and unvaccinated subjects: Sixteen years after newborn vaccination program in TaiwanJOURNAL OF MEDICAL VIROLOGY, Issue 4 2003Hans Hsienhong Lin Abstract Taiwan was an endemic area for hepatitis B virus (HBV) infection, and related liver diseases cause a significant drain of public resources. To control the endemic, a nation-wide newborn vaccination program was started in 1985. We reviewed the results of the annual survey for HBV surface antigen (HBsAg) performed in freshmen class of two high schools in Hualien, eastern Taiwan, from 1991 to 2001. A total of 10,194 students, most of them 15 years old, were tested for serum HBsAg using enzyme immunoassays. There is a significant trend (P,<,0.0001) of decreasing HBsAg carrier rate from 20.3 to 4.4% in males and 14.3% to 2.4% in females, respectively, over 11 years. The HBsAg carrier rate was 16.0,20.3% in students surveyed during 1991,1993 (born more than 6 years before the start of the national vaccination program), which decreased to 7.7,11.9% during 1994,1999 (born 1,6 years before the program). It further declined to 4.7% and 3.4% in 2000 and 2001 (born after the start of the program). The HBsAg carrier rate in male students was significantly higher than that in female students in most of the years. The HBV newborn vaccination program not only successfully prevented most of the perinatal transmission of HBV but also reduced horizontal transmission of HBV to children born up to 6 years before the start of the program. Also, the protection persisted for at least 15 years. J. Med. Virol. 69:471,474, 2003. © 2003 Wiley-Liss, Inc. [source] Five-year follow-up of a hepatitis B virus-positive recipient of hepatitis B surface antigen-positive living donor liver graftLIVER TRANSPLANTATION, Issue 6 2006Shin Hwang The shortage of cadaveric donor organs has led to the use of living donors and marginal cadaveric donors. To date, there have been only 2 reports on the use of hepatitis B surface antigen (HBsAg)-positive liver grafts. Here we describe the 5-yr posttransplantation sequence of a hepatitis B virus (HBV)-positive recipient who received an HBsAg-positive living donor liver graft. A 43-yr-old HBV-positive patient with hepatorenal syndrome received a living donor liver graft in October 2000 from a 27-yr-old HBsAg-positive carrier with no clinical evidence of HBV infection other than the serologic markers. The recipient recovered slowly after liver transplantation (LT). Recipient serum HBsAg was continuously positive despite anti-HBV therapy with high-dose hepatitis B immunoglobulin (HBIG) and lamivudine. The patient was also treated with famciclovir and interferon; to date, a final regimen of lamivudine and adefovir has kept liver function stable for 20 months. The recipient has lived for 64 months after transplantation. The donor has not revealed any clinical evidence of active hepatitis during follow-up. In conclusion, our result implicates that a recipient of liver graft from an HBsAg-positive carrier may survive for a long period following antiviral therapy with lamivudine and adefovir. Considering this living donor case and previously reported cases, the use of an HBsAg-positive cadaveric liver graft may deserve attention when no other donor is available. Liver Transpl 12:993,997, 2006. © 2006 AASLD. [source] | ||||||||||