File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Hepatitis B reactivation in occult viral carriers undergoing hematopoietic stem cell transplantation: A prospective study

TitleHepatitis B reactivation in occult viral carriers undergoing hematopoietic stem cell transplantation: A prospective study
Authors
Issue Date2017
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
Hepatology, 2017, v. 65 n. 5, p. 1451-1461 How to Cite?
AbstractHepatitis B virus (HBV) reactivation in hepatitis B surface antigen (HBsAg)–negative, antibody to hepatitis B core antigen (anti‐HBc)–positive patients after allogeneic hematopoietic stem cell transplantation (HSCT) has not been prospectively studied. HBsAg‐negative, anti‐HBc–positive patients with undetectable HBV DNA undergoing allogeneic HSCT were prospectively monitored every 4 weeks. The primary endpoint was HBV reactivation, defined as detectable HBV DNA (≥10 IU/mL). Secondary endpoints included overall survival, HBsAg positivity, and changes in liver biochemistry and antibody to HBsAg levels. Among 297 allogeneic HSCT recipients, 85 (28.7%) were HBsAg‐negative, anti‐HBc–positive, of whom 62 were recruited and monitored for a median of 48 (4‐104) weeks. The 2‐year cumulative HBV DNA detectability rate was 40.8%, occurring at a median of 44 (8‐100) weeks. Multivariate analysis showed that age ≥50 years (P = 0.004, hazard ratio = 8.2) and chronic graft‐versus‐host disease (P = 0.010, hazard ratio = 5.3) were significantly associated with HBV reactivation. Other clinical parameters, including baseline antibody to HBsAg status, serial changes in antibody to HBsAg levels, and donor serology, were not associated with HBV reactivation. Patients <50 years old and without chronic graft‐versus‐host disease, compared with the remaining patient cohort, had a significantly lower 2‐year cumulative HBV reactivation rate (5.6% versus 65.0%, P = 0.004). Entecavir successfully suppressed HBV DNA to undetectable levels, with no cases developing biochemical hepatitis. Conclusion: HBsAg‐negative, anti‐HBc–positive patients had a high rate of HBV reactivation after allogeneic HSCT, with determinants of HBV reactivation including age ≥50 years and chronic graft‐versus‐host disease; treatment strategies based on these parameters may prevent HBV reactivation and subsequent complications. (ClinicalTrials.gov identifier NCT01481649.) (Hepatology 2017;65:1451‐1461).
Persistent Identifierhttp://hdl.handle.net/10722/237728
ISSN
2017 Impact Factor: 14.079
2015 SCImago Journal Rankings: 4.752
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSeto, WKW-
dc.contributor.authorChan, SYT-
dc.contributor.authorHwang, YYG-
dc.contributor.authorWong, DKH-
dc.contributor.authorFung, JYY-
dc.contributor.authorLiu, SHK-
dc.contributor.authorSingh, GHH-
dc.contributor.authorLam, YF-
dc.contributor.authorLau, EHY-
dc.contributor.authorCheung, KSM-
dc.contributor.authorLie, AKW-
dc.contributor.authorLai, CL-
dc.contributor.authorKwong, YL-
dc.contributor.authorYuen, RMF-
dc.date.accessioned2017-01-20T02:27:34Z-
dc.date.available2017-01-20T02:27:34Z-
dc.date.issued2017-
dc.identifier.citationHepatology, 2017, v. 65 n. 5, p. 1451-1461-
dc.identifier.issn0270-9139-
dc.identifier.urihttp://hdl.handle.net/10722/237728-
dc.description.abstractHepatitis B virus (HBV) reactivation in hepatitis B surface antigen (HBsAg)–negative, antibody to hepatitis B core antigen (anti‐HBc)–positive patients after allogeneic hematopoietic stem cell transplantation (HSCT) has not been prospectively studied. HBsAg‐negative, anti‐HBc–positive patients with undetectable HBV DNA undergoing allogeneic HSCT were prospectively monitored every 4 weeks. The primary endpoint was HBV reactivation, defined as detectable HBV DNA (≥10 IU/mL). Secondary endpoints included overall survival, HBsAg positivity, and changes in liver biochemistry and antibody to HBsAg levels. Among 297 allogeneic HSCT recipients, 85 (28.7%) were HBsAg‐negative, anti‐HBc–positive, of whom 62 were recruited and monitored for a median of 48 (4‐104) weeks. The 2‐year cumulative HBV DNA detectability rate was 40.8%, occurring at a median of 44 (8‐100) weeks. Multivariate analysis showed that age ≥50 years (P = 0.004, hazard ratio = 8.2) and chronic graft‐versus‐host disease (P = 0.010, hazard ratio = 5.3) were significantly associated with HBV reactivation. Other clinical parameters, including baseline antibody to HBsAg status, serial changes in antibody to HBsAg levels, and donor serology, were not associated with HBV reactivation. Patients <50 years old and without chronic graft‐versus‐host disease, compared with the remaining patient cohort, had a significantly lower 2‐year cumulative HBV reactivation rate (5.6% versus 65.0%, P = 0.004). Entecavir successfully suppressed HBV DNA to undetectable levels, with no cases developing biochemical hepatitis. Conclusion: HBsAg‐negative, anti‐HBc–positive patients had a high rate of HBV reactivation after allogeneic HSCT, with determinants of HBV reactivation including age ≥50 years and chronic graft‐versus‐host disease; treatment strategies based on these parameters may prevent HBV reactivation and subsequent complications. (ClinicalTrials.gov identifier NCT01481649.) (Hepatology 2017;65:1451‐1461).-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/-
dc.relation.ispartofHepatology-
dc.rightsThis is the peer reviewed version of the following article: Hepatology, 2017, v. 65 n. 5, p. 1451-1461, which has been published in final form at http://dx.doi.org/10.1002/hep.29022. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.-
dc.titleHepatitis B reactivation in occult viral carriers undergoing hematopoietic stem cell transplantation: A prospective study-
dc.typeArticle-
dc.identifier.emailSeto, WKW: wkseto2@hku.hk-
dc.identifier.emailChan, SYT: drtchan@hku.hk-
dc.identifier.emailHwang, YYG: yyhwang@hku.hk-
dc.identifier.emailWong, DKH: danywong@hku.hk-
dc.identifier.emailFung, JYY: jfung@hkucc.hku.hk-
dc.identifier.emailLiu, SHK: drkliu@hku.hk-
dc.identifier.emailSingh, GHH: gillhsh@hku.hk-
dc.identifier.emailLam, YF: fyflam@hku.hk-
dc.identifier.emailLau, EHY: ehylau@hku.hk-
dc.identifier.emailCheung, KSM: cks634@hku.hk-
dc.identifier.emailLie, AKW: akwlie@hkucc.hku.hk-
dc.identifier.emailLai, CL: hrmelcl@hku.hk-
dc.identifier.emailKwong, YL: ylkwong@hku.hk-
dc.identifier.emailYuen, RMF: mfyuen@hku.hk-
dc.identifier.authoritySeto, WKW=rp01659-
dc.identifier.authorityWong, DKH=rp00492-
dc.identifier.authorityFung, JYY=rp00518-
dc.identifier.authoritySingh, GHH=rp01914-
dc.identifier.authorityLau, EHY=rp01349-
dc.identifier.authorityCheung, KSM=rp02532-
dc.identifier.authorityLai, CL=rp00314-
dc.identifier.authorityKwong, YL=rp00358-
dc.identifier.authorityYuen, RMF=rp00479-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/hep.29022-
dc.identifier.pmid28027590-
dc.identifier.scopuseid_2-s2.0-85016436690-
dc.identifier.hkuros271015-
dc.identifier.volume65-
dc.identifier.issue5-
dc.identifier.spage1451-
dc.identifier.epage1461-
dc.identifier.isiWOS:000399459800004-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats