File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Treatment of chronic hepatitis B

TitleTreatment of chronic hepatitis B
Authors
Issue Date2001
PublisherThe Lancet Publishing Group. The Journal's web site is located at http://www.elsevier.com/locate/j.lancetid
Citation
Lancet Infectious Diseases, 2001, v. 1 n. 4, p. 232-241 How to Cite?
AbstractThis review updates the treatment of chronic hepatitis B infection. Complete eradication of hepatitis B virus (HBV) is not possible, so the efficacy of treatment has to be assessed by whether it can limit long-term cirrhosis-related complications. We discuss two major groups of treatments - immunomodulators (interferon alfa, thymosin α1, therapeutic vaccines) and nucleoside analogues (lamivudine, adefovir, entecavir, emtricitabine, β-L-2′-deoxythymidine). To date, interferon alfa and lamivudine are the only two agents approved for chronic hepatitis B. Interferon alfa achieves a short-term outcome of around 20-30% loss of HBeAg. The efficacy is lower in Chinese patients, who are immunotolerant to HBV because of acquisition of the disease during early childhood, than in white patients. This difference is further confirmed on long-term follow-up. Interferon alfa does not affect the development of cirrhosis-related complications in Chinese patients, whereas in white patients, the frequency of long-term complications is reduced if interferon alfa is successful in inducing loss of HBeAg. Lamivudine profoundly suppresses viral replication and achieves an HBeAg seroconversion rate similar to that of interferon alfa. It is equally effective in Chinese and white patients because the main antiviral mechanism is through inhibition of reverse transcription of HBV during viral replication. However, long-term lamivudine therapy is associated with emergence of HBV variants, YMDD variants. Newer nucleoside analogues are being extensively investigated by studies in vivo and in vitro. Combination therapy with two or three nucleoside analogues or immunomodulators plus nucleoside analogues will be the future direction of treatment of chronic hepatitis B. © 2001 Elsevier Science Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/162537
ISSN
2015 Impact Factor: 21.372
2015 SCImago Journal Rankings: 11.233
References

 

DC FieldValueLanguage
dc.contributor.authorYuen, MFen_US
dc.contributor.authorLai, CLen_US
dc.date.accessioned2012-09-05T05:20:53Z-
dc.date.available2012-09-05T05:20:53Z-
dc.date.issued2001en_US
dc.identifier.citationLancet Infectious Diseases, 2001, v. 1 n. 4, p. 232-241en_US
dc.identifier.issn1473-3099en_US
dc.identifier.urihttp://hdl.handle.net/10722/162537-
dc.description.abstractThis review updates the treatment of chronic hepatitis B infection. Complete eradication of hepatitis B virus (HBV) is not possible, so the efficacy of treatment has to be assessed by whether it can limit long-term cirrhosis-related complications. We discuss two major groups of treatments - immunomodulators (interferon alfa, thymosin α1, therapeutic vaccines) and nucleoside analogues (lamivudine, adefovir, entecavir, emtricitabine, β-L-2′-deoxythymidine). To date, interferon alfa and lamivudine are the only two agents approved for chronic hepatitis B. Interferon alfa achieves a short-term outcome of around 20-30% loss of HBeAg. The efficacy is lower in Chinese patients, who are immunotolerant to HBV because of acquisition of the disease during early childhood, than in white patients. This difference is further confirmed on long-term follow-up. Interferon alfa does not affect the development of cirrhosis-related complications in Chinese patients, whereas in white patients, the frequency of long-term complications is reduced if interferon alfa is successful in inducing loss of HBeAg. Lamivudine profoundly suppresses viral replication and achieves an HBeAg seroconversion rate similar to that of interferon alfa. It is equally effective in Chinese and white patients because the main antiviral mechanism is through inhibition of reverse transcription of HBV during viral replication. However, long-term lamivudine therapy is associated with emergence of HBV variants, YMDD variants. Newer nucleoside analogues are being extensively investigated by studies in vivo and in vitro. Combination therapy with two or three nucleoside analogues or immunomodulators plus nucleoside analogues will be the future direction of treatment of chronic hepatitis B. © 2001 Elsevier Science Ltd.en_US
dc.languageengen_US
dc.publisherThe Lancet Publishing Group. The Journal's web site is located at http://www.elsevier.com/locate/j.lancetiden_US
dc.relation.ispartofLancet Infectious Diseasesen_US
dc.subject.meshAdjuvants, Immunologic - Pharmacology - Therapeutic Useen_US
dc.subject.meshAntiviral Agents - Pharmacology - Therapeutic Useen_US
dc.subject.meshDrug Therapy, Combinationen_US
dc.subject.meshFibrosis - Etiology - Prevention & Controlen_US
dc.subject.meshHepatitis B Antibodies - Blooden_US
dc.subject.meshHepatitis B Vaccines - Therapeutic Useen_US
dc.subject.meshHepatitis B E Antigens - Blood - Immunologyen_US
dc.subject.meshHepatitis B, Chronic - Complications - Drug Therapy - Ethnologyen_US
dc.subject.meshHumansen_US
dc.subject.meshInterferon-Alpha - Adverse Effects - Pharmacology - Therapeutic Useen_US
dc.subject.meshLamivudine - Pharmacology - Therapeutic Useen_US
dc.subject.meshNucleosides - Pharmacology - Therapeutic Useen_US
dc.subject.meshReverse Transcriptase Inhibitors - Pharmacology - Therapeutic Useen_US
dc.subject.meshTreatment Outcomeen_US
dc.titleTreatment of chronic hepatitis Ben_US
dc.typeArticleen_US
dc.identifier.emailYuen, MF:mfyuen@hkucc.hku.hken_US
dc.identifier.emailLai, CL:hrmelcl@hku.hken_US
dc.identifier.authorityYuen, MF=rp00479en_US
dc.identifier.authorityLai, CL=rp00314en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S1473-3099(01)00118-9en_US
dc.identifier.pmid11871510-
dc.identifier.scopuseid_2-s2.0-0035525235en_US
dc.identifier.hkuros66974-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035525235&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume1en_US
dc.identifier.issue4en_US
dc.identifier.spage232en_US
dc.identifier.epage241en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridYuen, MF=7102031955en_US
dc.identifier.scopusauthoridLai, CL=7403086396en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats