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Conference Paper: Viral Hepatitis (+Antiviral Therapy) HBsAg and HBV DNA levels guiding entecavir cessation in HBeAg-negative chronic hepatitis B

TitleViral Hepatitis (+Antiviral Therapy) HBsAg and HBV DNA levels guiding entecavir cessation in HBeAg-negative chronic hepatitis B
Authors
Keywordshepatitis B
nucleoside analogue
treatment cessation
HBsAg
Issue Date2013
PublisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JGH
Citation
Asian Pacific Digestive Week 2013 & World Congress of Gastroenterology (APDW/WCOG), Shanghai, China, 21-24 September 2013. In Journal of Gastroenterology and Hepatology, 2013, v. 28 n. Suppl. 3, p. 414, abstract no. P1035 How to Cite?
AbstractObjective: The role of hepatitis B surface antigen (HBsAg) and HBV DNA levels in predicting virologic kinetics after nucleoside analogue cessation has not been well-investigated. Methods: Following APASL guidelines, entecavir was stopped in HBeAg-negative patients treated for ≥2 years and undetectable HBV DNA levels on ≥3 separate occasions 6 months apart before treatment cessation. HBsAg and HBV DNA levels were monitored at every 6–12 weeks for 1 year. Entecavir was restarted if virologic relapse (defined HBV DNA >2,000 IU/mL) occurred. Results: 184 patients (mean age 53.9 years, 67.9% male) were recruited. The mean baseline HBsAg level was 2.86 (SD ± 0.56) log IU/mL. Mean duration of entecavir therapy before cessation was 3.06 (SD ± 0.63) years. At the time of writing, 168 (91.3%) and 119 (72.6%) patients have been followed up for 24 and 36 weeks respectively. Cumulative rates of virologic relapse, calculated using the Kaplan-Meier method, were 75.9% and 86.9% at weeks 24 and 36 respectively. Among patients with at least 24 weeks of follow-up, patients without virologic relapse (n = 25), when compared to patients with virologic relapse (n = 143), had a higher probability of undetectable viremia at week 12 off-treatment (64.0% and 18.2% respectively, p < 0.001). Mean HBsAg levels at entecavir commencement, entecavir cessation and the mean rate of HBsAg reduction during entecavir therapy had no association with virologic relapse (p = 0.738, 0.829 and 0.605 respectively). Off-treatment week-12 HBV DNA levels achieved an AUROC of 0.766 (p < 0.001, 95%CI 0.662–0.869) in predicting virologic relapse. Among patients with HBsAg <1,000 and <500 IU/mL at entecavir cessation, week-12 HBV DNA achieved an AUROC of 0.811 (p = 0.004, 95%CI 0.690–0.931) and 0.868 (p = 0.004, 95%CI 0.736–0.993) respectively. Conclusion: The combination of HBsAg levels at treatment cessation and off-treatment HBV DNA levels could predict virologic remission after entecavir cessation.
DescriptionPoster Presentation
Persistent Identifierhttp://hdl.handle.net/10722/201273
ISSN
2015 Impact Factor: 3.322
2015 SCImago Journal Rankings: 1.190

 

DC FieldValueLanguage
dc.contributor.authorSeto, WKWen_US
dc.contributor.authorHui, AJen_US
dc.contributor.authorWong, VWSen_US
dc.contributor.authorWong, GLHen_US
dc.contributor.authorLiu, Ken_US
dc.contributor.authorLai, CLen_US
dc.contributor.authorYuen, RMFen_US
dc.contributor.authorChan, HLYen_US
dc.date.accessioned2014-08-21T07:20:16Z-
dc.date.available2014-08-21T07:20:16Z-
dc.date.issued2013en_US
dc.identifier.citationAsian Pacific Digestive Week 2013 & World Congress of Gastroenterology (APDW/WCOG), Shanghai, China, 21-24 September 2013. In Journal of Gastroenterology and Hepatology, 2013, v. 28 n. Suppl. 3, p. 414, abstract no. P1035en_US
dc.identifier.issn0815-9319-
dc.identifier.urihttp://hdl.handle.net/10722/201273-
dc.descriptionPoster Presentation-
dc.description.abstractObjective: The role of hepatitis B surface antigen (HBsAg) and HBV DNA levels in predicting virologic kinetics after nucleoside analogue cessation has not been well-investigated. Methods: Following APASL guidelines, entecavir was stopped in HBeAg-negative patients treated for ≥2 years and undetectable HBV DNA levels on ≥3 separate occasions 6 months apart before treatment cessation. HBsAg and HBV DNA levels were monitored at every 6–12 weeks for 1 year. Entecavir was restarted if virologic relapse (defined HBV DNA >2,000 IU/mL) occurred. Results: 184 patients (mean age 53.9 years, 67.9% male) were recruited. The mean baseline HBsAg level was 2.86 (SD ± 0.56) log IU/mL. Mean duration of entecavir therapy before cessation was 3.06 (SD ± 0.63) years. At the time of writing, 168 (91.3%) and 119 (72.6%) patients have been followed up for 24 and 36 weeks respectively. Cumulative rates of virologic relapse, calculated using the Kaplan-Meier method, were 75.9% and 86.9% at weeks 24 and 36 respectively. Among patients with at least 24 weeks of follow-up, patients without virologic relapse (n = 25), when compared to patients with virologic relapse (n = 143), had a higher probability of undetectable viremia at week 12 off-treatment (64.0% and 18.2% respectively, p < 0.001). Mean HBsAg levels at entecavir commencement, entecavir cessation and the mean rate of HBsAg reduction during entecavir therapy had no association with virologic relapse (p = 0.738, 0.829 and 0.605 respectively). Off-treatment week-12 HBV DNA levels achieved an AUROC of 0.766 (p < 0.001, 95%CI 0.662–0.869) in predicting virologic relapse. Among patients with HBsAg <1,000 and <500 IU/mL at entecavir cessation, week-12 HBV DNA achieved an AUROC of 0.811 (p = 0.004, 95%CI 0.690–0.931) and 0.868 (p = 0.004, 95%CI 0.736–0.993) respectively. Conclusion: The combination of HBsAg levels at treatment cessation and off-treatment HBV DNA levels could predict virologic remission after entecavir cessation.-
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JGH-
dc.relation.ispartofJournal of Gastroenterology and Hepatologyen_US
dc.rightsThe definitive version is available at www3.interscience.wiley.com-
dc.subjecthepatitis B-
dc.subjectnucleoside analogue-
dc.subjecttreatment cessation-
dc.subjectHBsAg-
dc.titleViral Hepatitis (+Antiviral Therapy) HBsAg and HBV DNA levels guiding entecavir cessation in HBeAg-negative chronic hepatitis Ben_US
dc.typeConference_Paperen_US
dc.identifier.emailSeto, WKW: wkseto2@hku.hken_US
dc.identifier.emailLai, CL: hrmelcl@hku.hken_US
dc.identifier.emailYuen, RMF: mfyuen@hku.hken_US
dc.identifier.authoritySeto, WKW=rp01659en_US
dc.identifier.authorityLai, CL=rp00314en_US
dc.identifier.doi10.1111/jgh.12363_2en_US
dc.identifier.hkuros232991en_US
dc.identifier.hkuros232990-
dc.identifier.volume28en_US
dc.identifier.issueSuppl. 3en_US
dc.identifier.spage414, abstract no. P1035en_US
dc.identifier.epage414, abstract no. P1035en_US
dc.publisher.placeAustralia-

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