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Article: Hepatitis B virus (HBV) reactivation after cytotoxic or immunosuppressive therapy - Pathogenesis and management

TitleHepatitis B virus (HBV) reactivation after cytotoxic or immunosuppressive therapy - Pathogenesis and management
Authors
Issue Date2001
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/5616
Citation
Reviews In Medical Virology, 2001, v. 11 n. 5, p. 287-299 How to Cite?
AbstractIn an endemic area for chronic hepatitis B infection, reactivation of this virus is a serious cause of morbidity and mortality in patients undergoing cytotoxic or immunosuppressive therapy. Careful prospective serological testing has shown that hepatitis B virus reactivation is a two-staged process. The initial stage occurs during intense cytotoxic or immunosuppressive therapy and is characterised by enhanced viral replication, as reflected by increases in the serum levels of hepatitis B virus DNA, hepatitis B e antigen, hepatitis B virus DNA polymerase and infection of naïve hepatocytes with hepatitis B virus. The second stage is related to restoration of immune function following withdrawal of cytotoxic or immunosuppressive therapy, which causes rapid immune-mediated destruction of infected hepatocytes. Clinically, this can lead to hepatitis, hepatic failure and even death. The occurrence and severity of hepatitis B virus reactivation after various cytotoxic or immunosuppressive therapy is unpredictable and treatment has been disappointing, largely due to the late administration of therapy. Recently, pre-emptive treatment of chronic hepatitis B patients undergoing cytotoxic or immunosuppressive therapy, with potent nucleoside analogues has shown some promising results. Further controlled studies are needed to define the incidence and risk factors of hepatitis B reactivation so that pre-emptive treatment with nucleoside analogues could be administered to those patients at high risk of disease. Copyright © 2001 John Wiley & Sons, Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/162464
ISSN
2015 Impact Factor: 4.308
2015 SCImago Journal Rankings: 2.208
References

 

DC FieldValueLanguage
dc.contributor.authorLuo, Xen_US
dc.contributor.authorAu, WYen_US
dc.contributor.authorLiang, Ren_US
dc.contributor.authorLau, GKKen_US
dc.date.accessioned2012-09-05T05:20:12Z-
dc.date.available2012-09-05T05:20:12Z-
dc.date.issued2001en_US
dc.identifier.citationReviews In Medical Virology, 2001, v. 11 n. 5, p. 287-299en_US
dc.identifier.issn1052-9276en_US
dc.identifier.urihttp://hdl.handle.net/10722/162464-
dc.description.abstractIn an endemic area for chronic hepatitis B infection, reactivation of this virus is a serious cause of morbidity and mortality in patients undergoing cytotoxic or immunosuppressive therapy. Careful prospective serological testing has shown that hepatitis B virus reactivation is a two-staged process. The initial stage occurs during intense cytotoxic or immunosuppressive therapy and is characterised by enhanced viral replication, as reflected by increases in the serum levels of hepatitis B virus DNA, hepatitis B e antigen, hepatitis B virus DNA polymerase and infection of naïve hepatocytes with hepatitis B virus. The second stage is related to restoration of immune function following withdrawal of cytotoxic or immunosuppressive therapy, which causes rapid immune-mediated destruction of infected hepatocytes. Clinically, this can lead to hepatitis, hepatic failure and even death. The occurrence and severity of hepatitis B virus reactivation after various cytotoxic or immunosuppressive therapy is unpredictable and treatment has been disappointing, largely due to the late administration of therapy. Recently, pre-emptive treatment of chronic hepatitis B patients undergoing cytotoxic or immunosuppressive therapy, with potent nucleoside analogues has shown some promising results. Further controlled studies are needed to define the incidence and risk factors of hepatitis B reactivation so that pre-emptive treatment with nucleoside analogues could be administered to those patients at high risk of disease. Copyright © 2001 John Wiley & Sons, Ltd.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/5616en_US
dc.relation.ispartofReviews in Medical Virologyen_US
dc.rightsReviews in Medical Virology. Copyright © John Wiley & Sons Ltd.-
dc.subject.meshAntineoplastic Agents - Adverse Effectsen_US
dc.subject.meshAntiviral Agents - Therapeutic Useen_US
dc.subject.meshDna Polymerase Iii - Blooden_US
dc.subject.meshDna, Viral - Blooden_US
dc.subject.meshHepatitis B E Antigens - Blooden_US
dc.subject.meshHepatitis B Virus - Drug Effects - Growth & Developmenten_US
dc.subject.meshHepatitis B, Chronic - Drug Therapy - Virologyen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunosuppressive Agents - Adverse Effectsen_US
dc.subject.meshRecurrenceen_US
dc.subject.meshVirus Activation - Drug Effectsen_US
dc.titleHepatitis B virus (HBV) reactivation after cytotoxic or immunosuppressive therapy - Pathogenesis and managementen_US
dc.typeArticleen_US
dc.identifier.emailLiang, R:rliang@hku.hken_US
dc.identifier.authorityLiang, R=rp00345en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/rmv.322en_US
dc.identifier.pmid11590667en_US
dc.identifier.scopuseid_2-s2.0-0034776221en_US
dc.identifier.hkuros64631-
dc.identifier.hkuros68055-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034776221&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume11en_US
dc.identifier.issue5en_US
dc.identifier.spage287en_US
dc.identifier.epage299en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridXunrong, L=23108126000en_US
dc.identifier.scopusauthoridYan, AW=23108130600en_US
dc.identifier.scopusauthoridLiang, R=26643224900en_US
dc.identifier.scopusauthoridLau, GKK=7102301257en_US
dc.customcontrol.immutablejt 130726-

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