Effect of treatment with interferon α‐2b and ribavirin in patients infected with genotype 2 hepatitis C virus
Identifieur interne : 000F08 ( Istex/Corpus ); précédent : 000F07; suivant : 000F09Effect of treatment with interferon α‐2b and ribavirin in patients infected with genotype 2 hepatitis C virus
Auteurs : Yoshihiko Nagase ; Hiroshi Yotsuyanagi ; Chiaki Okuse ; Kiyomi Yasuda ; Tomohiro Kato ; Kazuhiko Koike ; Michihiro Suzuki ; Kusuki Nishioka ; Shiro Iino ; Fumio ItohSource :
- Hepatology Research [ 1386-6346 ] ; 2008-03.
Abstract
Aim: Nearly 20% of chronic hepatitis C (CHC) patients with genotype 2 hepatitis C virus (HCV) infection are not curable, even by interferon (IFN)–ribavirin combination therapy. The aim of this study is to investigate the factors that determine the efficacy of combination therapy in patients with genotype 2 HCV infection. Methods: Fifty patients with CHC who underwent a treatment of 6 MU IFN α‐2b with ribavirin for 24 weeks were retrospectively analyzed. Results: All the patients showed no serum HCV‐RNA within 12 weeks after starting the therapy. Forty‐one of the 50 patients (82%) achieved a sustained virological response (SVR). The age, sex, genotype (2a vs. 2b) and grade/stage of the liver by histopathology and pretreatment viral load werenot different between the sustained responders and relapsers. Univariate analysis showed that an earlier viral clearance from blood and a larger number of amino acid substitutions in the interferon sensitivity determining region (ISDR) were predictors of SVR. Multivariate analysis showed that a large number of amino acid substitutions in the ISDR was a predictor of SVR. Conclusion: The characterization of the amino acid sequences of ISDR may be helpful for predicting a relapse after combination therapy in patients with genotype 2 HCV infection.
Url:
DOI: 10.1111/j.1872-034X.2007.00257.x
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ISTEX:EA9D57EE4C2ECF4738DAD43376684DF921B2EAA1Le document en format XML
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α‐2b and ribavirin in patients infected with genotype 2 hepatitis C virus</title><author><name sortKey="Nagase, Yoshihiko" sort="Nagase, Yoshihiko" uniqKey="Nagase Y" first="Yoshihiko" last="Nagase">Yoshihiko Nagase</name><affiliation><mods:affiliation>Department of Internal Medicine, Division of Gastroenterology and Hepatology and</mods:affiliation></affiliation></author><author><name sortKey="Yotsuyanagi, Hiroshi" sort="Yotsuyanagi, Hiroshi" uniqKey="Yotsuyanagi H" first="Hiroshi" last="Yotsuyanagi">Hiroshi Yotsuyanagi</name><affiliation><mods:affiliation>Department of Internal Medicine, Division of Gastroenterology and Hepatology and</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Infectious Diseases, Internal Medicine, Graduate School of Medicine, University of Tokyo and</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: hyotsu‐tky@umin.ac.jp</mods:affiliation></affiliation></author><author><name sortKey="Okuse, Chiaki" sort="Okuse, 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xml:lang="en">Aim: Nearly 20% of chronic hepatitis C (CHC) patients with genotype 2 hepatitis C virus (HCV) infection are not curable, even by interferon (IFN)–ribavirin combination therapy. 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The aim of this study is to investigate the factors that determine the efficacy of combination therapy in patients with genotype 2 HCV infection. Methods: Fifty patients with CHC who underwent a treatment of 6 MU IFN α‐2b with ribavirin for 24 weeks were retrospectively analyzed. Results: All the patients showed no serum HCV‐RNA within 12 weeks after starting the therapy. Forty‐one of the 50 patients (82%) achieved a sustained virological response (SVR). The age, sex, genotype (2a vs. 2b) and grade/stage of the liver by histopathology and pretreatment viral load werenot different between the sustained responders and relapsers. Univariate analysis showed that an earlier viral clearance from blood and a larger number of amino acid substitutions in the interferon sensitivity determining region (ISDR) were predictors of SVR. Multivariate analysis showed that a large number of amino acid substitutions in the ISDR was a predictor of SVR. 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<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract xml:lang="en" style="main"><p><hi rend="bold">Aim: </hi> Nearly 20% of chronic hepatitis C (CHC) patients with genotype 2 hepatitis C virus (HCV) infection are not curable, even by interferon (IFN)–ribavirin combination therapy. The aim of this study is to investigate the factors that determine the efficacy of combination therapy in patients with genotype 2 HCV infection.</p><p><hi rend="bold">Methods: </hi> Fifty patients with CHC who underwent a treatment of 6 MU IFN α‐2b with ribavirin for 24 weeks were retrospectively analyzed.</p><p><hi rend="bold">Results: </hi> All the patients showed no serum HCV‐RNA within 12 weeks after starting the therapy. Forty‐one of the 50 patients (82%) achieved a sustained virological response (SVR). The age, sex, genotype (2a vs. 2b) and grade/stage of the liver by histopathology and pretreatment viral load werenot different between the sustained responders and relapsers. Univariate analysis showed that an earlier viral clearance from blood and a larger number of amino acid substitutions in the interferon sensitivity determining region (ISDR) were predictors of SVR. Multivariate analysis showed that a large number of amino acid substitutions in the ISDR was a predictor of SVR.</p><p><hi rend="bold">Conclusion: </hi> The characterization of the amino acid sequences of ISDR may be helpful for predicting a relapse after combination therapy in patients with genotype 2 HCV infection.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">genotype</term><term xml:id="k2">hepatitis C virus</term><term xml:id="k3">interferon</term><term xml:id="k4">ISDR</term><term xml:id="k5">ribavirin</term></keywords><keywords rend="tocHeading1"><term>Original Articles</term></keywords><keywords rend="tocHeading2"><term>Clinical hepatology</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-1L21T0WS-3/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Asia</publisherName><publisherLoc>Melbourne, Australia</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1872-034X</doi><issn type="print">1386-6346</issn><issn type="electronic">1872-034X</issn><idGroup><id type="product" value="HEPR"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="HEPATOLOGY RESEARCH">Hepatology Research</title></titleGroup></publicationMeta><publicationMeta level="part" position="03003"><doi origin="wiley">10.1111/hep.2008.38.issue-3</doi><numberingGroup><numbering type="journalVolume" number="38">38</numbering><numbering type="journalIssue" number="3">3</numbering></numberingGroup><coverDate startDate="2008-03">March 2008</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="5" status="forIssue"><doi origin="wiley">10.1111/j.1872-034X.2007.00257.x</doi><idGroup><id type="unit" value="HEPR257"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title><title type="tocHeading2">Clinical hepatology</title></titleGroup><eventGroup><event type="firstOnline" date="2007-09-06"></event><event type="publishedOnlineFinalForm" date="2007-09-06"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-06"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-26"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-23"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="252">252</numbering><numbering type="pageLast" number="258">258</numbering></numberingGroup><correspondenceTo>Dr Hiroshi Yotsuyanagi, Department of Infectious Diseases, Internal Medicine, Graduate School of Medicine, University of Tokyo, 7‐3‐1 Hongo, Bunkyo‐ku, Tokyo 113‐8655, Japan. Email: <email normalForm="hyotsu-tky@umin.ac.jp">hyotsu‐tky@umin.ac.jp</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:HEPR.HEPR257.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 7 September 2006; revision 28 June 2007; accepted 16 July 2007.</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="3"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="39"></count><count type="wordTotal" number="2483"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Effect of treatment with interferon α‐2b and ribavirin in patients infected with genotype 2 hepatitis C virus</title><title type="shortAuthors">Y. Nagase <i>et al</i>.</title><title type="short">Combination therapy for genotype 2 HCV infection</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Yoshihiko</givenNames><familyName>Nagase</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1 #a2" corresponding="yes"><personName><givenNames>Hiroshi</givenNames><familyName>Yotsuyanagi</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Chiaki</givenNames><familyName>Okuse</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a3"><personName><givenNames>Kiyomi</givenNames><familyName>Yasuda</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a4"><personName><givenNames>Tomohiro</givenNames><familyName>Kato</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a2"><personName><givenNames>Kazuhiko</givenNames><familyName>Koike</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1"><personName><givenNames>Michihiro</givenNames><familyName>Suzuki</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a4"><personName><givenNames>Kusuki</givenNames><familyName>Nishioka</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a3"><personName><givenNames>Shiro</givenNames><familyName>Iino</familyName></personName></creator><creator creatorRole="author" xml:id="cr10" affiliationRef="#a1"><personName><givenNames>Fumio</givenNames><familyName>Itoh</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Department of Internal Medicine, Division of Gastroenterology and Hepatology and</unparsedAffiliation></affiliation><affiliation xml:id="a4"><unparsedAffiliation>Department of Bioregulation and Proteomics, St. Marianna University, Kawasaki,</unparsedAffiliation></affiliation><affiliation xml:id="a2"><unparsedAffiliation>Department of Infectious Diseases, Internal Medicine, Graduate School of Medicine, University of Tokyo and</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="JP"><unparsedAffiliation>Center for Liver Diseases, Kiyokawa Hospital, Tokyo, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">genotype</keyword><keyword xml:id="k2">hepatitis C virus</keyword><keyword xml:id="k3">interferon</keyword><keyword xml:id="k4">ISDR</keyword><keyword xml:id="k5">ribavirin</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>Aim: </b> Nearly 20% of chronic hepatitis C (CHC) patients with genotype 2 hepatitis C virus (HCV) infection are not curable, even by interferon (IFN)–ribavirin combination therapy. The aim of this study is to investigate the factors that determine the efficacy of combination therapy in patients with genotype 2 HCV infection.</p><p><b>Methods: </b> Fifty patients with CHC who underwent a treatment of 6 MU IFN α‐2b with ribavirin for 24 weeks were retrospectively analyzed.</p><p><b>Results: </b> All the patients showed no serum HCV‐RNA within 12 weeks after starting the therapy. Forty‐one of the 50 patients (82%) achieved a sustained virological response (SVR). The age, sex, genotype (2a vs. 2b) and grade/stage of the liver by histopathology and pretreatment viral load werenot different between the sustained responders and relapsers. Univariate analysis showed that an earlier viral clearance from blood and a larger number of amino acid substitutions in the interferon sensitivity determining region (ISDR) were predictors of SVR. Multivariate analysis showed that a large number of amino acid substitutions in the ISDR was a predictor of SVR.</p><p><b>Conclusion: </b> The characterization of the amino acid sequences of ISDR may be helpful for predicting a relapse after combination therapy in patients with genotype 2 HCV infection.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1" numbered="no"><p>Grant sponsor: Japanese Ministry of Health, Labor and Welfare.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Effect of treatment with interferon α‐2b and ribavirin in patients infected with genotype 2 hepatitis C virus</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Combination therapy for genotype 2 HCV infection</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Effect of treatment with interferon α‐2b and ribavirin in patients infected with genotype 2 hepatitis C virus</title></titleInfo><name type="personal"><namePart type="given">Yoshihiko</namePart><namePart type="family">Nagase</namePart><affiliation>Department of Internal Medicine, Division of Gastroenterology and Hepatology and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hiroshi</namePart><namePart type="family">Yotsuyanagi</namePart><affiliation>Department of Internal Medicine, Division of Gastroenterology and Hepatology and</affiliation><affiliation>Department of Infectious Diseases, Internal Medicine, Graduate School of Medicine, University of Tokyo and</affiliation><affiliation>E-mail: hyotsu‐tky@umin.ac.jp</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chiaki</namePart><namePart type="family">Okuse</namePart><affiliation>Department of Internal Medicine, Division of Gastroenterology and Hepatology and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kiyomi</namePart><namePart type="family">Yasuda</namePart><affiliation>Center for Liver Diseases, Kiyokawa Hospital, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tomohiro</namePart><namePart type="family">Kato</namePart><affiliation>Department of Bioregulation and Proteomics, St. Marianna University, Kawasaki,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kazuhiko</namePart><namePart type="family">Koike</namePart><affiliation>Department of Infectious Diseases, Internal Medicine, Graduate School of Medicine, University of Tokyo and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michihiro</namePart><namePart type="family">Suzuki</namePart><affiliation>Department of Internal Medicine, Division of Gastroenterology and Hepatology and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kusuki</namePart><namePart type="family">Nishioka</namePart><affiliation>Department of Bioregulation and Proteomics, St. Marianna University, Kawasaki,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shiro</namePart><namePart type="family">Iino</namePart><affiliation>Center for Liver Diseases, Kiyokawa Hospital, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Fumio</namePart><namePart type="family">Itoh</namePart><affiliation>Department of Internal Medicine, Division of Gastroenterology and Hepatology and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Asia</publisher><place><placeTerm type="text">Melbourne, Australia</placeTerm></place><dateIssued encoding="w3cdtf">2008-03</dateIssued><edition>Received 7 September 2006; revision 28 June 2007; accepted 16 July 2007.</edition><copyrightDate encoding="w3cdtf">2008</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">1</extent><extent unit="tables">3</extent><extent unit="formulas">0</extent><extent unit="references">39</extent><extent unit="linksCrossRef">0</extent><extent unit="words">2483</extent></physicalDescription><abstract lang="en">Aim: Nearly 20% of chronic hepatitis C (CHC) patients with genotype 2 hepatitis C virus (HCV) infection are not curable, even by interferon (IFN)–ribavirin combination therapy. The aim of this study is to investigate the factors that determine the efficacy of combination therapy in patients with genotype 2 HCV infection. Methods: Fifty patients with CHC who underwent a treatment of 6 MU IFN α‐2b with ribavirin for 24 weeks were retrospectively analyzed. Results: All the patients showed no serum HCV‐RNA within 12 weeks after starting the therapy. Forty‐one of the 50 patients (82%) achieved a sustained virological response (SVR). The age, sex, genotype (2a vs. 2b) and grade/stage of the liver by histopathology and pretreatment viral load werenot different between the sustained responders and relapsers. Univariate analysis showed that an earlier viral clearance from blood and a larger number of amino acid substitutions in the interferon sensitivity determining region (ISDR) were predictors of SVR. Multivariate analysis showed that a large number of amino acid substitutions in the ISDR was a predictor of SVR. 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