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Article: Treatment of chronic hepatitis B: Evolution over two decades
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TitleTreatment of chronic hepatitis B: Evolution over two decades
 
AuthorsYuen, MF1
Lai, CL1
 
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
 
CitationJournal Of Gastroenterology And Hepatology, 2011, v. 26 SUPPL. 1, p. 138-143 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1440-1746.2010.06545.x
 
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 Conventional interferon alpha (IFN-α), the only agent licensed in 1991, has been superseded by pegylated IFN-α.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.
 
ISSN0815-9319
2013 Impact Factor: 3.627
 
DOIhttp://dx.doi.org/10.1111/j.1440-1746.2010.06545.x
 
ISI Accession Number IDWOS:000285880400018
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.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorYuen, MF
 
dc.contributor.authorLai, CL
 
dc.date.accessioned2011-09-23T05:50:30Z
 
dc.date.available2011-09-23T05:50:30Z
 
dc.date.issued2011
 
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.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationJournal Of Gastroenterology And Hepatology, 2011, v. 26 SUPPL. 1, p. 138-143 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1440-1746.2010.06545.x
 
dc.identifier.doihttp://dx.doi.org/10.1111/j.1440-1746.2010.06545.x
 
dc.identifier.epage143
 
dc.identifier.hkuros195204
 
dc.identifier.hkuros189893
 
dc.identifier.isiWOS:000285880400018
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.

 
dc.identifier.issn0815-9319
2013 Impact Factor: 3.627
 
dc.identifier.issueSUPPL. 1
 
dc.identifier.pmid21199525
 
dc.identifier.scopuseid_2-s2.0-78650780786
 
dc.identifier.spage138
 
dc.identifier.urihttp://hdl.handle.net/10722/139477
 
dc.identifier.volume26
 
dc.languageeng
 
dc.publisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JGH
 
dc.publisher.placeAustralia
 
dc.relation.ispartofJournal of Gastroenterology and Hepatology
 
dc.relation.referencesReferences in Scopus
 
dc.rightsThe definitive version is available at www3.interscience.wiley.com
 
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.subjectAntiviral agents
 
dc.subjectChronic hepatitis B
 
dc.subjectHBV DNA
 
dc.subjectNucleoside analogs
 
dc.subjectTreatment
 
dc.titleTreatment of chronic hepatitis B: Evolution over two decades
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong