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Article: Treatment of chronic hepatitis B: Evolution over two decades

TitleTreatment of chronic hepatitis B: Evolution over two decades
Authors
KeywordsAntiviral agents
Chronic hepatitis B
HBV DNA
Nucleoside analogs
Treatment
Issue Date2011
PublisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JGH
Citation
Journal Of Gastroenterology And Hepatology, 2011, v. 26 SUPPL. 1, p. 138-143 How to Cite?
Abstract
There has been a recent paradigm shift in the indications and endpoints of treatment for chronic hepatitis B (CHB). Hepatitis B e antigen (HBeAg)-negative disease is being increasingly recognized. Antiviral treatment for both HBeAg-positive and HBeAg-negative patients should aim at long-term suppression of HBV DNA, with the ultimate ideal endpoint of hepatitis B surface antigen (HBsAg) seroconversion. Conventional interferon alpha (IFN-α), the only agent licensed in 1991, has been superseded by pegylated IFN-α. HBeAg seroconversion using pegylated IFN-α is 33%, with only 25% of HBeAg-positive patients achieving undetectable HBV DNA by polymerase chain reaction (PCR) assay. Five nucleoside/nucleotide analogues have been licensed since 1998. Lamivudine, an L-nucleoside, is limited by the development of resistance in 76% of patients after 5 years of therapy. Telbivudine, another L-nucleoside, is more potent than lamivudine but resistance still develops in 25% of HBeAg-positive and 11% HBeAg-negative patients after 2 years. Adefovir, an acyclic phosphonate, is relatively weak, but is effective against lamivudine- and telbivudine- resistant mutations, for which it should be used in combination (add-on therapy) rather than substituted. Resistance to adefovir develops slowly, rising to 29% for HBeAg-negative patients by year 5, but more rapidly when used alone for lamivudine-resistant HBV. Currently the two first line nucleoside/nucleotides are entecavir and tenofovir. Entecavir, a cyclopentane (D-nucleoside), is very potent, with 94% of patients having undetectable HBV DNA after 5 years. Resistance develops in only 1.2% of treatment-naïve patients. Tenofovir, another acyclic nucleotide, is more potent with less renal toxicity compared to adefovir. It is effective against lamivudine-resistant mutations when used alone. No resistance to tenofovir has been described after its use for 3 years or longer, often for patients with human immunodeficiency virus/HBV co-infection. With these current, potent antiviral agents associated with very low rates of resistance, long-term HBV DNA suppression and possibly even reversal of cirrhosis can now be achieved in a proportion of patients. In addition, long-term treatment with these antiviral agents is associated with a reduced risk of development of hepatocellular carcinoma. © 2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/139477
ISSN
2013 Impact Factor: 3.627
ISI Accession Number ID
Funding AgencyGrant Number
Glaxo Smith Kline
Gristol Myers Squibb
Novertis
Funding Information:

MF Yuen acted as consultant and received research grants from Glaxo Smith Kline, Gristol Myers Squibb and Novertis. CL Lai has acted as consultant for Bristol Myers Squibb and Gilead Sciences.

References

 

DC FieldValueLanguage
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorLai, CLen_HK
dc.date.accessioned2011-09-23T05:50:30Z-
dc.date.available2011-09-23T05:50:30Z-
dc.date.issued2011en_HK
dc.identifier.citationJournal Of Gastroenterology And Hepatology, 2011, v. 26 SUPPL. 1, p. 138-143en_HK
dc.identifier.issn0815-9319en_HK
dc.identifier.urihttp://hdl.handle.net/10722/139477-
dc.description.abstractThere has been a recent paradigm shift in the indications and endpoints of treatment for chronic hepatitis B (CHB). Hepatitis B e antigen (HBeAg)-negative disease is being increasingly recognized. Antiviral treatment for both HBeAg-positive and HBeAg-negative patients should aim at long-term suppression of HBV DNA, with the ultimate ideal endpoint of hepatitis B surface antigen (HBsAg) seroconversion. Conventional interferon alpha (IFN-α), the only agent licensed in 1991, has been superseded by pegylated IFN-α. HBeAg seroconversion using pegylated IFN-α is 33%, with only 25% of HBeAg-positive patients achieving undetectable HBV DNA by polymerase chain reaction (PCR) assay. Five nucleoside/nucleotide analogues have been licensed since 1998. Lamivudine, an L-nucleoside, is limited by the development of resistance in 76% of patients after 5 years of therapy. Telbivudine, another L-nucleoside, is more potent than lamivudine but resistance still develops in 25% of HBeAg-positive and 11% HBeAg-negative patients after 2 years. Adefovir, an acyclic phosphonate, is relatively weak, but is effective against lamivudine- and telbivudine- resistant mutations, for which it should be used in combination (add-on therapy) rather than substituted. Resistance to adefovir develops slowly, rising to 29% for HBeAg-negative patients by year 5, but more rapidly when used alone for lamivudine-resistant HBV. Currently the two first line nucleoside/nucleotides are entecavir and tenofovir. Entecavir, a cyclopentane (D-nucleoside), is very potent, with 94% of patients having undetectable HBV DNA after 5 years. Resistance develops in only 1.2% of treatment-naïve patients. Tenofovir, another acyclic nucleotide, is more potent with less renal toxicity compared to adefovir. It is effective against lamivudine-resistant mutations when used alone. No resistance to tenofovir has been described after its use for 3 years or longer, often for patients with human immunodeficiency virus/HBV co-infection. With these current, potent antiviral agents associated with very low rates of resistance, long-term HBV DNA suppression and possibly even reversal of cirrhosis can now be achieved in a proportion of patients. In addition, long-term treatment with these antiviral agents is associated with a reduced risk of development of hepatocellular carcinoma. © 2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd.en_HK
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JGHen_HK
dc.relation.ispartofJournal of Gastroenterology and Hepatologyen_HK
dc.rightsThe definitive version is available at www3.interscience.wiley.com-
dc.subjectAntiviral agentsen_HK
dc.subjectChronic hepatitis Ben_HK
dc.subjectHBV DNAen_HK
dc.subjectNucleoside analogsen_HK
dc.subjectTreatmenten_HK
dc.subject.meshAntiviral Agents - therapeutic use-
dc.subject.meshCarcinoma, Hepatocellular - prevention and control - virology-
dc.subject.meshHepatitis B virus - genetics - immunology - pathogenicity-
dc.subject.meshHepatitis B, Chronic - complications - diagnosis - drug therapy-
dc.subject.meshLiver Neoplasms - prevention and control - virology-
dc.titleTreatment of chronic hepatitis B: Evolution over two decadesen_HK
dc.typeArticleen_HK
dc.identifier.emailYuen, MF:mfyuen@hkucc.hku.hken_HK
dc.identifier.emailLai, CL:hrmelcl@hku.hken_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.identifier.authorityLai, CL=rp00314en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1111/j.1440-1746.2010.06545.xen_HK
dc.identifier.pmid21199525en_HK
dc.identifier.scopuseid_2-s2.0-78650780786en_HK
dc.identifier.hkuros195204en_US
dc.identifier.hkuros189893-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78650780786&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume26en_HK
dc.identifier.issueSUPPL. 1en_HK
dc.identifier.spage138en_HK
dc.identifier.epage143en_HK
dc.identifier.isiWOS:000285880400018-
dc.publisher.placeAustraliaen_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK
dc.identifier.scopusauthoridLai, CL=7403086396en_HK

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