Viral clearance is associated with improved insulin resistance in genotype 1 chronic hepatitis C but not genotype 2/3
Identifieur interne : 006254 ( Main/Exploration ); précédent : 006253; suivant : 006255Viral clearance is associated with improved insulin resistance in genotype 1 chronic hepatitis C but not genotype 2/3
Auteurs : Alexander J. Thompson [États-Unis, Australie] ; Keyur Patel [États-Unis] ; Wan-Long Chuang [Taïwan] ; Eric J. Lawitz [États-Unis] ; Maribel Rodriguez-Torres [États-Unis] ; Vinod K. Rustgi [États-Unis] ; Robert Flisiak [Pologne] ; Stephen Pianko [Australie] ; Moises Diago [Espagne] ; Sanjeev Arora [États-Unis] ; Graham R. Foster [Royaume-Uni] ; Michael Torbenson [États-Unis] ; Yves Benhamou [France] ; David R. Nelson [États-Unis] ; Mark S. Sulkowski [États-Unis] ; Stefan Zeuzem [Allemagne] ; Erik Pulkstenis [États-Unis] ; G Mani Subramanian [États-Unis] ; John G. Mchutchison [États-Unis]Source :
- Gut [ 0017-5749 ] ; 2012-01.
Descripteurs français
English descriptors
- KwdEn :
- Alanine transaminase, Antiviral therapy, Baseline, Body mass index, Brosis, Caucasian, Causal relationship, Centile, Cholesterol levels, Chronic hepatitis, Cohort, Continuous variables, Data acquisition, Data analysis, Diabetes, Diabetes mellitus, Fasting, Gastroenterology, Genotype, Glucose, Hepatic, Hepatic steatosis, Hepatitis, Hepatocellular, Hepatocellular carcinoma, Hepatol, Hepatology, Homeostasis, Human genome sciences, Insulin, Insulin resistance, Insulin sensitivity, Lipid, Liver histology, Manuscript revision, Median, Mellitus, Metavir, Metavir activity, Metavir stage, Multivariable, Novartis, Research grants, Research institute, Roche, Steatosis, Study conception, Total cholesterol, Triglyceride, Triglyceride levels, Univariable analysis, Viral, Viral clearance, Virological, Virological response, Virus infection.
- Teeft :
- Alanine transaminase, Antiviral therapy, Baseline, Body mass index, Brosis, Caucasian, Causal relationship, Centile, Cholesterol levels, Chronic hepatitis, Cohort, Continuous variables, Data acquisition, Data analysis, Diabetes, Diabetes mellitus, Fasting, Gastroenterology, Genotype, Glucose, Hepatic, Hepatic steatosis, Hepatitis, Hepatocellular, Hepatocellular carcinoma, Hepatol, Hepatology, Homeostasis, Human genome sciences, Insulin, Insulin resistance, Insulin sensitivity, Lipid, Liver histology, Manuscript revision, Median, Mellitus, Metavir, Metavir activity, Metavir stage, Multivariable, Novartis, Research grants, Research institute, Roche, Steatosis, Study conception, Total cholesterol, Triglyceride, Triglyceride levels, Univariable analysis, Viral, Viral clearance, Virological, Virological response, Virus infection.
Abstract
Objectives 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. Methods 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. Results 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. Conclusions 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:
- https://api.istex.fr/document/F6C90B151A67E2DC25F6E362634A1449E41036EB/fulltext/pdf
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3766841
DOI: 10.1136/gut.2010.236158
Affiliations:
- Allemagne, Australie, Espagne, France, Pologne, Royaume-Uni, Taïwan, États-Unis
- Angleterre, Caroline du Nord, Catalogne, District de Darmstadt, Floride, Grand Londres, Hesse (Land), Maryland, Texas, Virginie, Île-de-France
- Barcelone, Francfort-sur-le-Main, Londres, Paris
- Université de Londres
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Mchutchison</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina</wicri:regionArea><placeName><region type="state">Caroline du Nord</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Gut</title><title level="j" type="abbrev">Gut</title><idno type="ISSN">0017-5749</idno><idno type="eISSN">1468-3288</idno><imprint><publisher>BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><date type="published" when="2012-01">2012-01</date><biblScope unit="volume">61</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="128">128</biblScope></imprint><idno type="ISSN">0017-5749</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0017-5749</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alanine transaminase</term><term>Antiviral therapy</term><term>Baseline</term><term>Body mass index</term><term>Brosis</term><term>Caucasian</term><term>Causal relationship</term><term>Centile</term><term>Cholesterol levels</term><term>Chronic hepatitis</term><term>Cohort</term><term>Continuous variables</term><term>Data acquisition</term><term>Data analysis</term><term>Diabetes</term><term>Diabetes mellitus</term><term>Fasting</term><term>Gastroenterology</term><term>Genotype</term><term>Glucose</term><term>Hepatic</term><term>Hepatic steatosis</term><term>Hepatitis</term><term>Hepatocellular</term><term>Hepatocellular carcinoma</term><term>Hepatol</term><term>Hepatology</term><term>Homeostasis</term><term>Human genome sciences</term><term>Insulin</term><term>Insulin resistance</term><term>Insulin sensitivity</term><term>Lipid</term><term>Liver histology</term><term>Manuscript revision</term><term>Median</term><term>Mellitus</term><term>Metavir</term><term>Metavir activity</term><term>Metavir stage</term><term>Multivariable</term><term>Novartis</term><term>Research grants</term><term>Research institute</term><term>Roche</term><term>Steatosis</term><term>Study conception</term><term>Total cholesterol</term><term>Triglyceride</term><term>Triglyceride levels</term><term>Univariable analysis</term><term>Viral</term><term>Viral clearance</term><term>Virological</term><term>Virological response</term><term>Virus infection</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Alanine transaminase</term><term>Antiviral therapy</term><term>Baseline</term><term>Body mass index</term><term>Brosis</term><term>Caucasian</term><term>Causal relationship</term><term>Centile</term><term>Cholesterol levels</term><term>Chronic hepatitis</term><term>Cohort</term><term>Continuous variables</term><term>Data acquisition</term><term>Data analysis</term><term>Diabetes</term><term>Diabetes mellitus</term><term>Fasting</term><term>Gastroenterology</term><term>Genotype</term><term>Glucose</term><term>Hepatic</term><term>Hepatic steatosis</term><term>Hepatitis</term><term>Hepatocellular</term><term>Hepatocellular carcinoma</term><term>Hepatol</term><term>Hepatology</term><term>Homeostasis</term><term>Human genome sciences</term><term>Insulin</term><term>Insulin resistance</term><term>Insulin sensitivity</term><term>Lipid</term><term>Liver histology</term><term>Manuscript revision</term><term>Median</term><term>Mellitus</term><term>Metavir</term><term>Metavir activity</term><term>Metavir stage</term><term>Multivariable</term><term>Novartis</term><term>Research grants</term><term>Research institute</term><term>Roche</term><term>Steatosis</term><term>Study conception</term><term>Total cholesterol</term><term>Triglyceride</term><term>Triglyceride levels</term><term>Univariable analysis</term><term>Viral</term><term>Viral clearance</term><term>Virological</term><term>Virological response</term><term>Virus infection</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Diabète</term><term>Glucose</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Objectives 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. Methods 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. Results 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. Conclusions 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.</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Australie</li><li>Espagne</li><li>France</li><li>Pologne</li><li>Royaume-Uni</li><li>Taïwan</li><li>États-Unis</li></country><region><li>Angleterre</li><li>Caroline du Nord</li><li>Catalogne</li><li>District de Darmstadt</li><li>Floride</li><li>Grand Londres</li><li>Hesse (Land)</li><li>Maryland</li><li>Texas</li><li>Virginie</li><li>Île-de-France</li></region><settlement><li>Barcelone</li><li>Francfort-sur-le-Main</li><li>Londres</li><li>Paris</li></settlement><orgName><li>Université de Londres</li></orgName></list><tree><country name="États-Unis"><region name="Caroline du Nord"><name sortKey="Thompson, Alexander J" sort="Thompson, Alexander J" uniqKey="Thompson A" first="Alexander J" last="Thompson">Alexander J. Thompson</name></region><name sortKey="Arora, Sanjeev" sort="Arora, Sanjeev" uniqKey="Arora S" first="Sanjeev" last="Arora">Sanjeev Arora</name><name sortKey="Lawitz, Eric J" sort="Lawitz, Eric J" uniqKey="Lawitz E" first="Eric J" last="Lawitz">Eric J. Lawitz</name><name sortKey="Mchutchison, John G" sort="Mchutchison, John G" uniqKey="Mchutchison J" first="John G" last="Mchutchison">John G. Mchutchison</name><name sortKey="Nelson, David R" sort="Nelson, David R" uniqKey="Nelson D" first="David R" last="Nelson">David R. Nelson</name><name sortKey="Patel, Keyur" sort="Patel, Keyur" uniqKey="Patel K" first="Keyur" last="Patel">Keyur Patel</name><name sortKey="Pulkstenis, Erik" sort="Pulkstenis, Erik" uniqKey="Pulkstenis E" first="Erik" last="Pulkstenis">Erik Pulkstenis</name><name sortKey="Rodriguez Torres, Maribel" sort="Rodriguez Torres, Maribel" uniqKey="Rodriguez Torres M" first="Maribel" last="Rodriguez-Torres">Maribel Rodriguez-Torres</name><name sortKey="Rustgi, Vinod K" sort="Rustgi, Vinod K" uniqKey="Rustgi V" first="Vinod K" last="Rustgi">Vinod K. Rustgi</name><name sortKey="Subramanian, G Mani" sort="Subramanian, G Mani" uniqKey="Subramanian G" first="G Mani" last="Subramanian">G Mani Subramanian</name><name sortKey="Sulkowski, Mark S" sort="Sulkowski, Mark S" uniqKey="Sulkowski M" first="Mark S" last="Sulkowski">Mark S. Sulkowski</name><name sortKey="Torbenson, Michael" sort="Torbenson, Michael" uniqKey="Torbenson M" first="Michael" last="Torbenson">Michael Torbenson</name></country><country name="Australie"><noRegion><name sortKey="Thompson, Alexander J" sort="Thompson, Alexander J" uniqKey="Thompson A" first="Alexander J" last="Thompson">Alexander J. Thompson</name></noRegion><name sortKey="Pianko, Stephen" sort="Pianko, Stephen" uniqKey="Pianko S" first="Stephen" last="Pianko">Stephen Pianko</name></country><country name="Taïwan"><noRegion><name sortKey="Chuang, Wan Long" sort="Chuang, Wan Long" uniqKey="Chuang W" first="Wan-Long" last="Chuang">Wan-Long Chuang</name></noRegion></country><country name="Pologne"><noRegion><name sortKey="Flisiak, Robert" sort="Flisiak, Robert" uniqKey="Flisiak R" first="Robert" last="Flisiak">Robert Flisiak</name></noRegion></country><country name="Espagne"><region name="Catalogne"><name sortKey="Diago, Moises" sort="Diago, Moises" uniqKey="Diago M" first="Moises" last="Diago">Moises Diago</name></region></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Foster, Graham R" sort="Foster, Graham R" uniqKey="Foster G" first="Graham R" last="Foster">Graham R. Foster</name></region></country><country name="France"><region name="Île-de-France"><name sortKey="Benhamou, Yves" sort="Benhamou, Yves" uniqKey="Benhamou Y" first="Yves" last="Benhamou">Yves Benhamou</name></region></country><country name="Allemagne"><region name="Hesse (Land)"><name sortKey="Zeuzem, Stefan" sort="Zeuzem, Stefan" uniqKey="Zeuzem S" first="Stefan" last="Zeuzem">Stefan Zeuzem</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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