Viral clearance is associated with improved insulin resistance in genotype 1 chronic hepatitis C but not genotype 2/3
Identifieur interne : 001F21 ( Pmc/Corpus ); précédent : 001F20; suivant : 001F22Viral clearance is associated with improved insulin resistance in genotype 1 chronic hepatitis C but not genotype 2/3
Auteurs : Alexander J. Thompson ; Keyur Patel ; Wan-Long Chuang ; Eric J. Lawitz ; Maribel Rodriguez-Torres ; Vinod K. Rustgi ; Robert Flisiak ; Stephen Pianko ; Moises Diago ; Sanjeev Arora ; Graham R. Foster ; Michael Torbenson ; Yves Benhamou ; David R. Nelson ; Mark S. Sulkowski ; Stefan Zeuzem ; Erik Pulkstenis ; G Mani Subramanian ; John G. MchutchisonSource :
- Gut [ 0017-5749 ] ; 2011.
Abstract
Genotype-specific associations between hepatitis C virus (HCV) and insulin resistance (IR) have been described, but a causal relationship remains unclear. This study investigated the association between a sustained virological response (SVR) and IR after chronic HCV therapy.
2255 treatment-naive patients with chronic HCV genotype 1 or 2/3 were enrolled in two phase 3 trials of albinterferon alpha-2b versus pegylated interferon alpha-2a for 48 or 24 weeks, respectively. IR was measured before treatment and 12 weeks after treatment using homeostasis model assessment (HOMA)-IR.
Paired HOMA-IR measurements were available in 1038 non-diabetic patients (497 with genotype 1; 541 with genotype 2/3). At baseline the prevalence of HOMA-IR >3 was greater in patients with genotype 1 than 2/3 (33% vs 27%; p=0.048). There was a significant reduction in the prevalence of IR in patients with genotype 1 achieving SVR (δ 10%; p<0.001), but not in genotype 1 non-responders or those with genotype 2/3. Multivariate analysis indicated that SVR was associated with a significant reduction in mean HOMA-IR in patients with genotype 1 (p=0.004), but not in those with genotype 2/3, which was independent of body mass index, alanine transaminase, γ-glutamyl transpeptidase and lipid level changes.
SVR is associated with a reduction in HOMA-IR in patients with HCV genotype 1 but not in those with genotype 2/3. Genotype 1 may have a direct effect on the development of IR, independent of host metabolic factors, and may be partially reversed by viral eradication.
Url:
DOI: 10.1136/gut.2010.236158
PubMed: 21873466
PubMed Central: 3766841
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PMC:3766841Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Viral clearance is associated with improved insulin resistance in genotype 1 chronic hepatitis C but not genotype 2/3</title><author><name sortKey="Thompson, Alexander J" sort="Thompson, Alexander J" uniqKey="Thompson A" first="Alexander J" last="Thompson">Alexander J. Thompson</name><affiliation><nlm:aff id="A1">Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina, USA</nlm:aff></affiliation></author><author><name sortKey="Patel, Keyur" sort="Patel, Keyur" uniqKey="Patel K" first="Keyur" last="Patel">Keyur Patel</name><affiliation><nlm:aff id="A1">Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina, USA</nlm:aff></affiliation></author><author><name sortKey="Chuang, Wan Long" sort="Chuang, Wan Long" uniqKey="Chuang W" first="Wan-Long" last="Chuang">Wan-Long Chuang</name><affiliation><nlm:aff id="A2">Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan</nlm:aff></affiliation></author><author><name sortKey="Lawitz, Eric J" sort="Lawitz, Eric J" uniqKey="Lawitz E" first="Eric J" last="Lawitz">Eric J. Lawitz</name><affiliation><nlm:aff id="A3">Alamo Medical Research, San Antonio, Texas, USA</nlm:aff></affiliation></author><author><name sortKey="Rodriguez Torres, Maribel" sort="Rodriguez Torres, Maribel" uniqKey="Rodriguez Torres M" first="Maribel" last="Rodriguez-Torres">Maribel Rodriguez-Torres</name><affiliation><nlm:aff id="A4">Fundación de Investigación de Diego, Santurce, Puerto Rico, USA</nlm:aff></affiliation></author><author><name sortKey="Rustgi, Vinod K" sort="Rustgi, Vinod K" uniqKey="Rustgi V" first="Vinod K" last="Rustgi">Vinod K. Rustgi</name><affiliation><nlm:aff id="A5">Metropolitan Research, Fairfax, Virginia, USA</nlm:aff></affiliation></author><author><name sortKey="Flisiak, Robert" sort="Flisiak, Robert" uniqKey="Flisiak R" first="Robert" last="Flisiak">Robert Flisiak</name><affiliation><nlm:aff id="A6">Medical University of Bialystok, Bialystok, Poland</nlm:aff></affiliation></author><author><name sortKey="Pianko, Stephen" sort="Pianko, Stephen" uniqKey="Pianko S" first="Stephen" last="Pianko">Stephen Pianko</name><affiliation><nlm:aff id="A7">Monash Medical Centre, Clayton, Victoria, Australia</nlm:aff></affiliation></author><author><name sortKey="Diago, Moises" sort="Diago, Moises" uniqKey="Diago M" first="Moises" last="Diago">Moises Diago</name><affiliation><nlm:aff id="A8">Hospital Quiron de Valencia, Barcelona, Spain</nlm:aff></affiliation></author><author><name sortKey="Arora, Sanjeev" sort="Arora, Sanjeev" uniqKey="Arora S" first="Sanjeev" last="Arora">Sanjeev Arora</name><affiliation><nlm:aff id="A9">University of New Mexico, Albuquerque, USA</nlm:aff></affiliation></author><author><name sortKey="Foster, Graham R" sort="Foster, Graham R" uniqKey="Foster G" first="Graham R" last="Foster">Graham R. Foster</name><affiliation><nlm:aff id="A10">Queen Mary University of London, and Barts and The London NHS Trust, London, UK</nlm:aff></affiliation></author><author><name sortKey="Torbenson, Michael" sort="Torbenson, Michael" uniqKey="Torbenson M" first="Michael" last="Torbenson">Michael Torbenson</name><affiliation><nlm:aff id="A11">Johns Hopkins Center for Viral Hepatitis, Baltimore, Maryland, USA</nlm:aff></affiliation></author><author><name sortKey="Benhamou, Yves" sort="Benhamou, Yves" uniqKey="Benhamou Y" first="Yves" last="Benhamou">Yves Benhamou</name><affiliation><nlm:aff id="A12">Hôpital Pitié-Salpêtrière, Paris, France</nlm:aff></affiliation></author><author><name sortKey="Nelson, David R" sort="Nelson, David R" uniqKey="Nelson D" first="David R" last="Nelson">David R. Nelson</name><affiliation><nlm:aff id="A13">University of Florida, Gainesville, Florida, USA</nlm:aff></affiliation></author><author><name sortKey="Sulkowski, Mark S" sort="Sulkowski, Mark S" uniqKey="Sulkowski M" first="Mark S" last="Sulkowski">Mark S. Sulkowski</name><affiliation><nlm:aff id="A11">Johns Hopkins Center for Viral Hepatitis, Baltimore, Maryland, USA</nlm:aff></affiliation></author><author><name sortKey="Zeuzem, Stefan" sort="Zeuzem, Stefan" uniqKey="Zeuzem S" first="Stefan" last="Zeuzem">Stefan Zeuzem</name><affiliation><nlm:aff id="A14">J W Goethe University Hospital, Frankfurt, Germany</nlm:aff></affiliation></author><author><name sortKey="Pulkstenis, Erik" sort="Pulkstenis, Erik" uniqKey="Pulkstenis E" first="Erik" last="Pulkstenis">Erik Pulkstenis</name><affiliation><nlm:aff id="A15">Human Genome Sciences Inc, Rockville, Maryland, USA</nlm:aff></affiliation></author><author><name sortKey="Subramanian, G Mani" sort="Subramanian, G Mani" uniqKey="Subramanian G" first="G Mani" last="Subramanian">G Mani Subramanian</name><affiliation><nlm:aff id="A15">Human Genome Sciences Inc, Rockville, Maryland, USA</nlm:aff></affiliation></author><author><name sortKey="Mchutchison, John G" sort="Mchutchison, John G" uniqKey="Mchutchison J" first="John G" last="Mchutchison">John G. Mchutchison</name><affiliation><nlm:aff id="A1">Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina, USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">21873466</idno><idno type="pmc">3766841</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3766841</idno><idno type="RBID">PMC:3766841</idno><idno type="doi">10.1136/gut.2010.236158</idno><date when="2011">2011</date><idno type="wicri:Area/Pmc/Corpus">001F21</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">001F21</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Viral clearance is associated with improved insulin resistance in genotype 1 chronic hepatitis C but not genotype 2/3</title><author><name sortKey="Thompson, Alexander J" sort="Thompson, Alexander J" uniqKey="Thompson A" first="Alexander J" last="Thompson">Alexander J. Thompson</name><affiliation><nlm:aff id="A1">Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina, USA</nlm:aff></affiliation></author><author><name sortKey="Patel, Keyur" sort="Patel, Keyur" uniqKey="Patel K" first="Keyur" last="Patel">Keyur Patel</name><affiliation><nlm:aff id="A1">Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina, USA</nlm:aff></affiliation></author><author><name sortKey="Chuang, Wan Long" sort="Chuang, Wan Long" uniqKey="Chuang W" first="Wan-Long" last="Chuang">Wan-Long Chuang</name><affiliation><nlm:aff id="A2">Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan</nlm:aff></affiliation></author><author><name sortKey="Lawitz, Eric J" sort="Lawitz, Eric J" uniqKey="Lawitz E" first="Eric J" last="Lawitz">Eric J. Lawitz</name><affiliation><nlm:aff id="A3">Alamo Medical Research, San Antonio, Texas, USA</nlm:aff></affiliation></author><author><name sortKey="Rodriguez Torres, Maribel" sort="Rodriguez Torres, Maribel" uniqKey="Rodriguez Torres M" first="Maribel" last="Rodriguez-Torres">Maribel Rodriguez-Torres</name><affiliation><nlm:aff id="A4">Fundación de Investigación de Diego, Santurce, Puerto Rico, USA</nlm:aff></affiliation></author><author><name sortKey="Rustgi, Vinod K" sort="Rustgi, Vinod K" uniqKey="Rustgi V" first="Vinod K" last="Rustgi">Vinod K. Rustgi</name><affiliation><nlm:aff id="A5">Metropolitan Research, Fairfax, Virginia, USA</nlm:aff></affiliation></author><author><name sortKey="Flisiak, Robert" sort="Flisiak, Robert" uniqKey="Flisiak R" first="Robert" last="Flisiak">Robert Flisiak</name><affiliation><nlm:aff id="A6">Medical University of Bialystok, Bialystok, Poland</nlm:aff></affiliation></author><author><name sortKey="Pianko, Stephen" sort="Pianko, Stephen" uniqKey="Pianko S" first="Stephen" last="Pianko">Stephen Pianko</name><affiliation><nlm:aff id="A7">Monash Medical Centre, Clayton, Victoria, Australia</nlm:aff></affiliation></author><author><name sortKey="Diago, Moises" sort="Diago, Moises" uniqKey="Diago M" first="Moises" last="Diago">Moises Diago</name><affiliation><nlm:aff id="A8">Hospital Quiron de Valencia, Barcelona, Spain</nlm:aff></affiliation></author><author><name sortKey="Arora, Sanjeev" sort="Arora, Sanjeev" uniqKey="Arora S" first="Sanjeev" last="Arora">Sanjeev Arora</name><affiliation><nlm:aff id="A9">University of New Mexico, Albuquerque, USA</nlm:aff></affiliation></author><author><name sortKey="Foster, Graham R" sort="Foster, Graham R" uniqKey="Foster G" first="Graham R" last="Foster">Graham R. Foster</name><affiliation><nlm:aff id="A10">Queen Mary University of London, and Barts and The London NHS Trust, London, UK</nlm:aff></affiliation></author><author><name sortKey="Torbenson, Michael" sort="Torbenson, Michael" uniqKey="Torbenson M" first="Michael" last="Torbenson">Michael Torbenson</name><affiliation><nlm:aff id="A11">Johns Hopkins Center for Viral Hepatitis, Baltimore, Maryland, USA</nlm:aff></affiliation></author><author><name sortKey="Benhamou, Yves" sort="Benhamou, Yves" uniqKey="Benhamou Y" first="Yves" last="Benhamou">Yves Benhamou</name><affiliation><nlm:aff id="A12">Hôpital Pitié-Salpêtrière, Paris, France</nlm:aff></affiliation></author><author><name sortKey="Nelson, David R" sort="Nelson, David R" uniqKey="Nelson D" first="David R" last="Nelson">David R. Nelson</name><affiliation><nlm:aff id="A13">University of Florida, Gainesville, Florida, USA</nlm:aff></affiliation></author><author><name sortKey="Sulkowski, Mark S" sort="Sulkowski, Mark S" uniqKey="Sulkowski M" first="Mark S" last="Sulkowski">Mark S. Sulkowski</name><affiliation><nlm:aff id="A11">Johns Hopkins Center for Viral Hepatitis, Baltimore, Maryland, USA</nlm:aff></affiliation></author><author><name sortKey="Zeuzem, Stefan" sort="Zeuzem, Stefan" uniqKey="Zeuzem S" first="Stefan" last="Zeuzem">Stefan Zeuzem</name><affiliation><nlm:aff id="A14">J W Goethe University Hospital, Frankfurt, Germany</nlm:aff></affiliation></author><author><name sortKey="Pulkstenis, Erik" sort="Pulkstenis, Erik" uniqKey="Pulkstenis E" first="Erik" last="Pulkstenis">Erik Pulkstenis</name><affiliation><nlm:aff id="A15">Human Genome Sciences Inc, Rockville, Maryland, USA</nlm:aff></affiliation></author><author><name sortKey="Subramanian, G Mani" sort="Subramanian, G Mani" uniqKey="Subramanian G" first="G Mani" last="Subramanian">G Mani Subramanian</name><affiliation><nlm:aff id="A15">Human Genome Sciences Inc, Rockville, Maryland, USA</nlm:aff></affiliation></author><author><name sortKey="Mchutchison, John G" sort="Mchutchison, John G" uniqKey="Mchutchison J" first="John G" last="Mchutchison">John G. Mchutchison</name><affiliation><nlm:aff id="A1">Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina, USA</nlm:aff></affiliation></author></analytic><series><title level="j">Gut</title><idno type="ISSN">0017-5749</idno><idno type="eISSN">1468-3288</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>Objectives</title><p id="P1">Genotype-specific associations between hepatitis C virus (HCV) and insulin resistance (IR) have been described, but a causal relationship remains unclear. This study investigated the association between a sustained virological response (SVR) and IR after chronic HCV therapy.</p></sec><sec id="S2"><title>Methods</title><p id="P2">2255 treatment-naive patients with chronic HCV genotype 1 or 2/3 were enrolled in two phase 3 trials of albinterferon alpha-2b versus pegylated interferon alpha-2a for 48 or 24 weeks, respectively. IR was measured before treatment and 12 weeks after treatment using homeostasis model assessment (HOMA)-IR.</p></sec><sec id="S3"><title>Results</title><p id="P3">Paired HOMA-IR measurements were available in 1038 non-diabetic patients (497 with genotype 1; 541 with genotype 2/3). At baseline the prevalence of HOMA-IR >3 was greater in patients with genotype 1 than 2/3 (33% vs 27%; p=0.048). There was a significant reduction in the prevalence of IR in patients with genotype 1 achieving SVR (δ 10%; p<0.001), but not in genotype 1 non-responders or those with genotype 2/3. Multivariate analysis indicated that SVR was associated with a significant reduction in mean HOMA-IR in patients with genotype 1 (p=0.004), but not in those with genotype 2/3, which was independent of body mass index, alanine transaminase, γ-glutamyl transpeptidase and lipid level changes.</p></sec><sec id="S4"><title>Conclusions</title><p id="P4">SVR is associated with a reduction in HOMA-IR in patients with HCV genotype 1 but not in those with genotype 2/3. Genotype 1 may have a direct effect on the development of IR, independent of host metabolic factors, and may be partially reversed by viral eradication.</p></sec></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">2985108R</journal-id><journal-id journal-id-type="pubmed-jr-id">3923</journal-id><journal-id journal-id-type="nlm-ta">Gut</journal-id><journal-id journal-id-type="iso-abbrev">Gut</journal-id><journal-title-group><journal-title>Gut</journal-title></journal-title-group><issn pub-type="ppub">0017-5749</issn><issn pub-type="epub">1468-3288</issn></journal-meta><article-meta><article-id pub-id-type="pmid">21873466</article-id><article-id pub-id-type="pmc">3766841</article-id><article-id pub-id-type="doi">10.1136/gut.2010.236158</article-id><article-id pub-id-type="manuscript">NIHMS384213</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Viral clearance is associated with improved insulin resistance in genotype 1 chronic hepatitis C but not genotype 2/3</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Thompson</surname><given-names>Alexander J</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Patel</surname><given-names>Keyur</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Chuang</surname><given-names>Wan-Long</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Lawitz</surname><given-names>Eric J</given-names></name><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Rodriguez-Torres</surname><given-names>Maribel</given-names></name><xref ref-type="aff" rid="A4">4</xref></contrib><contrib contrib-type="author"><name><surname>Rustgi</surname><given-names>Vinod K</given-names></name><xref ref-type="aff" rid="A5">5</xref></contrib><contrib contrib-type="author"><name><surname>Flisiak</surname><given-names>Robert</given-names></name><xref ref-type="aff" rid="A6">6</xref></contrib><contrib contrib-type="author"><name><surname>Pianko</surname><given-names>Stephen</given-names></name><xref ref-type="aff" rid="A7">7</xref></contrib><contrib contrib-type="author"><name><surname>Diago</surname><given-names>Moises</given-names></name><xref ref-type="aff" rid="A8">8</xref></contrib><contrib contrib-type="author"><name><surname>Arora</surname><given-names>Sanjeev</given-names></name><xref ref-type="aff" rid="A9">9</xref></contrib><contrib contrib-type="author"><name><surname>Foster</surname><given-names>Graham R</given-names></name><xref ref-type="aff" rid="A10">10</xref></contrib><contrib contrib-type="author"><name><surname>Torbenson</surname><given-names>Michael</given-names></name><xref ref-type="aff" rid="A11">11</xref></contrib><contrib contrib-type="author"><name><surname>Benhamou</surname><given-names>Yves</given-names></name><xref ref-type="aff" rid="A12">12</xref></contrib><contrib contrib-type="author"><name><surname>Nelson</surname><given-names>David R</given-names></name><xref ref-type="aff" rid="A13">13</xref></contrib><contrib contrib-type="author"><name><surname>Sulkowski</surname><given-names>Mark S</given-names></name><xref ref-type="aff" rid="A11">11</xref></contrib><contrib contrib-type="author"><name><surname>Zeuzem</surname><given-names>Stefan</given-names></name><xref ref-type="aff" rid="A14">14</xref></contrib><contrib contrib-type="author"><name><surname>Pulkstenis</surname><given-names>Erik</given-names></name><xref ref-type="aff" rid="A15">15</xref></contrib><contrib contrib-type="author"><name><surname>Subramanian</surname><given-names>G Mani</given-names></name><xref ref-type="aff" rid="A15">15</xref></contrib><contrib contrib-type="author"><name><surname>McHutchison</surname><given-names>John G</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><on-behalf-of>for the ACHIEVE-1 and ACHIEVE-2/3 Study Teams</on-behalf-of><xref rid="FN2" ref-type="author-notes">*</xref></contrib-group><aff id="A1"><label>1</label>Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina, USA</aff><aff id="A2"><label>2</label>Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan</aff><aff id="A3"><label>3</label>Alamo Medical Research, San Antonio, Texas, USA</aff><aff id="A4"><label>4</label>Fundación de Investigación de Diego, Santurce, Puerto Rico, USA</aff><aff id="A5"><label>5</label>Metropolitan Research, Fairfax, Virginia, USA</aff><aff id="A6"><label>6</label>Medical University of Bialystok, Bialystok, Poland</aff><aff id="A7"><label>7</label>Monash Medical Centre, Clayton, Victoria, Australia</aff><aff id="A8"><label>8</label>Hospital Quiron de Valencia, Barcelona, Spain</aff><aff id="A9"><label>9</label>University of New Mexico, Albuquerque, USA</aff><aff id="A10"><label>10</label>Queen Mary University of London, and Barts and The London NHS Trust, London, UK</aff><aff id="A11"><label>11</label>Johns Hopkins Center for Viral Hepatitis, Baltimore, Maryland, USA</aff><aff id="A12"><label>12</label>Hôpital Pitié-Salpêtrière, Paris, France</aff><aff id="A13"><label>13</label>University of Florida, Gainesville, Florida, USA</aff><aff id="A14"><label>14</label>J W Goethe University Hospital, Frankfurt, Germany</aff><aff id="A15"><label>15</label>Human Genome Sciences Inc, Rockville, Maryland, USA</aff><author-notes><corresp id="FN1">Correspondence to Alexander J Thompson, Duke Clinical Research Institute, Duke University Medical Center, P O Box 17969, Durham, NC 27715, USA; <email>alexander.thompson@svhm.org.au</email></corresp><fn id="FN2" fn-type="other"><label>*</label><p>A complete list of the ACHIEVE-1 and -2/3 investigators appears in online appendix 1</p></fn></author-notes><pub-date pub-type="nihms-submitted"><day>10</day><month>7</month><year>2013</year></pub-date><pub-date pub-type="epub"><day>26</day><month>8</month><year>2011</year></pub-date><pub-date pub-type="ppub"><month>1</month><year>2012</year></pub-date><pub-date pub-type="pmc-release"><day>09</day><month>9</month><year>2013</year></pub-date><volume>61</volume><issue>1</issue><fpage>128</fpage><lpage>134</lpage><abstract><sec id="S1"><title>Objectives</title><p id="P1">Genotype-specific associations between hepatitis C virus (HCV) and insulin resistance (IR) have been described, but a causal relationship remains unclear. This study investigated the association between a sustained virological response (SVR) and IR after chronic HCV therapy.</p></sec><sec id="S2"><title>Methods</title><p id="P2">2255 treatment-naive patients with chronic HCV genotype 1 or 2/3 were enrolled in two phase 3 trials of albinterferon alpha-2b versus pegylated interferon alpha-2a for 48 or 24 weeks, respectively. IR was measured before treatment and 12 weeks after treatment using homeostasis model assessment (HOMA)-IR.</p></sec><sec id="S3"><title>Results</title><p id="P3">Paired HOMA-IR measurements were available in 1038 non-diabetic patients (497 with genotype 1; 541 with genotype 2/3). At baseline the prevalence of HOMA-IR >3 was greater in patients with genotype 1 than 2/3 (33% vs 27%; p=0.048). There was a significant reduction in the prevalence of IR in patients with genotype 1 achieving SVR (δ 10%; p<0.001), but not in genotype 1 non-responders or those with genotype 2/3. Multivariate analysis indicated that SVR was associated with a significant reduction in mean HOMA-IR in patients with genotype 1 (p=0.004), but not in those with genotype 2/3, which was independent of body mass index, alanine transaminase, γ-glutamyl transpeptidase and lipid level changes.</p></sec><sec id="S4"><title>Conclusions</title><p id="P4">SVR is associated with a reduction in HOMA-IR in patients with HCV genotype 1 but not in those with genotype 2/3. Genotype 1 may have a direct effect on the development of IR, independent of host metabolic factors, and may be partially reversed by viral eradication.</p></sec></abstract><funding-group><award-group><funding-source country="United States">National Cancer Institute : NCI</funding-source><award-id>K24 CA139570 || CA</award-id></award-group></funding-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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