Recipient IL28B Polymorphism Is an Important Independent Predictor of Posttransplant Diabetes Mellitus in Liver Transplant Patients with Chronic Hepatitis C
IL28B polymorphisms are strongly associated with response to treatment for HCV infection. IL28B acts on interferon‐stimulated genes via the JAK‐STAT pathway, which has been implicated in development of insulin resistance. We investigated whether IL28B polymorphisms are associated with posttransplant...
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| Veröffentlicht in: | American journal of transplantation 2012-03, Vol.12 (3), p.737-744 |
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| creator | Veldt, B. J. Duarte‐Rojo, A. Thompson, A. J. Watt, K. D. Heimbach, J. K. Tillmann, H. L. Goldstein, D. D. McHutchison, J. G. Charlton, M. R. |
| description | IL28B polymorphisms are strongly associated with response to treatment for HCV infection. IL28B acts on interferon‐stimulated genes via the JAK‐STAT pathway, which has been implicated in development of insulin resistance. We investigated whether IL28B polymorphisms are associated with posttransplant diabetes mellitus (DM). Consecutive HCV patients who underwent liver transplantation between 1–1995 and 1–2011 were studied. Genotyping of the polymorphism rs12979860 was performed on DNA collected from donors and recipients. Posttransplant DM was screened for by fasting blood glucoses every 1–3 months. Of 221 included patients, 69 developed posttransplant DM (31%). Twenty‐two patients with recipient IL28B genotype TT (48%), 25 with IL28B genotype CT (25%) and 22 with IL28B genotype CC (29%) developed posttransplant DM. TT genotype was statistically significantly associated with posttransplant DM over time (log rank p = 0.012 for TT vs. CT and p = 0.045 for TT vs. CC). Multivariate Cox regression analysis correcting for donor age, body mass index, baseline serum glucose, baseline serum cholesterol, recipient age and treated rejection, showed that recipient IL28B genotype TT was independently associated with posttransplant DM (hazard ratio 2.51; 95% confidence interval 1.17–5.40; p = 0.011). We conclude that the risk of developing posttransplant DM is significantly increased in recipients carrying the TT polymorphism of the IL28B gene.
An analysis of liver transplant recipients with hepatitis C virus infection finds that the risk of developing posttransplant diabetes mellitus is significantly increased in recipients carrying the TT polymorphism of the IL28B gene. |
| doi_str_mv | 10.1111/j.1600-6143.2011.03843.x |
| format | Article |
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An analysis of liver transplant recipients with hepatitis C virus infection finds that the risk of developing posttransplant diabetes mellitus is significantly increased in recipients carrying the TT polymorphism of the IL28B gene.</description><identifier>ISSN: 1600-6135</identifier><identifier>EISSN: 1600-6143</identifier><identifier>DOI: 10.1111/j.1600-6143.2011.03843.x</identifier><identifier>PMID: 22300408</identifier><language>eng</language><publisher>Malden, USA: Blackwell Publishing Inc</publisher><subject>Adult ; Biological and medical sciences ; Diabetes mellitus ; Diabetes Mellitus - diagnosis ; Diabetes Mellitus - etiology ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Follow-Up Studies ; HCV ; Hepacivirus - pathogenicity ; Hepatitis C virus ; Hepatitis C, Chronic - complications ; Hepatitis C, Chronic - genetics ; Hepatitis C, Chronic - surgery ; Human viral diseases ; Humans ; Infectious diseases ; Interferon-gamma - metabolism ; Interferons ; Interleukins - genetics ; liver transplantation ; Liver Transplantation - adverse effects ; Liver, biliary tract, pancreas, portal circulation, spleen ; Male ; Medical sciences ; Middle Aged ; Polymorphism, Genetic - genetics ; Postoperative Complications ; Prognosis ; Prospective Studies ; RNA, Viral - genetics ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the digestive system ; Viral diseases ; Viral hepatitis</subject><ispartof>American journal of transplantation, 2012-03, Vol.12 (3), p.737-744</ispartof><rights>copyright 2012 The American Society of Transplantation and the American Society of Transplant Surgeons</rights><rights>2015 INIST-CNRS</rights><rights>copyright 2012 The American Society of Transplantation and the American Society of Transplant Surgeons.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4813-ce063df60ea9a40ec0f34044eb6d77704080c82649b1fcec826beb8ce976d53c3</citedby><cites>FETCH-LOGICAL-c4813-ce063df60ea9a40ec0f34044eb6d77704080c82649b1fcec826beb8ce976d53c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1600-6143.2011.03843.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1600-6143.2011.03843.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25720755$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22300408$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Veldt, B. J.</creatorcontrib><creatorcontrib>Duarte‐Rojo, A.</creatorcontrib><creatorcontrib>Thompson, A. J.</creatorcontrib><creatorcontrib>Watt, K. D.</creatorcontrib><creatorcontrib>Heimbach, J. K.</creatorcontrib><creatorcontrib>Tillmann, H. L.</creatorcontrib><creatorcontrib>Goldstein, D. D.</creatorcontrib><creatorcontrib>McHutchison, J. G.</creatorcontrib><creatorcontrib>Charlton, M. R.</creatorcontrib><title>Recipient IL28B Polymorphism Is an Important Independent Predictor of Posttransplant Diabetes Mellitus in Liver Transplant Patients with Chronic Hepatitis C</title><title>American journal of transplantation</title><addtitle>Am J Transplant</addtitle><description>IL28B polymorphisms are strongly associated with response to treatment for HCV infection. IL28B acts on interferon‐stimulated genes via the JAK‐STAT pathway, which has been implicated in development of insulin resistance. We investigated whether IL28B polymorphisms are associated with posttransplant diabetes mellitus (DM). Consecutive HCV patients who underwent liver transplantation between 1–1995 and 1–2011 were studied. Genotyping of the polymorphism rs12979860 was performed on DNA collected from donors and recipients. Posttransplant DM was screened for by fasting blood glucoses every 1–3 months. Of 221 included patients, 69 developed posttransplant DM (31%). Twenty‐two patients with recipient IL28B genotype TT (48%), 25 with IL28B genotype CT (25%) and 22 with IL28B genotype CC (29%) developed posttransplant DM. TT genotype was statistically significantly associated with posttransplant DM over time (log rank p = 0.012 for TT vs. CT and p = 0.045 for TT vs. CC). Multivariate Cox regression analysis correcting for donor age, body mass index, baseline serum glucose, baseline serum cholesterol, recipient age and treated rejection, showed that recipient IL28B genotype TT was independently associated with posttransplant DM (hazard ratio 2.51; 95% confidence interval 1.17–5.40; p = 0.011). We conclude that the risk of developing posttransplant DM is significantly increased in recipients carrying the TT polymorphism of the IL28B gene.
An analysis of liver transplant recipients with hepatitis C virus infection finds that the risk of developing posttransplant diabetes mellitus is significantly increased in recipients carrying the TT polymorphism of the IL28B gene.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus - diagnosis</subject><subject>Diabetes Mellitus - etiology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>HCV</subject><subject>Hepacivirus - pathogenicity</subject><subject>Hepatitis C virus</subject><subject>Hepatitis C, Chronic - complications</subject><subject>Hepatitis C, Chronic - genetics</subject><subject>Hepatitis C, Chronic - surgery</subject><subject>Human viral diseases</subject><subject>Humans</subject><subject>Infectious diseases</subject><subject>Interferon-gamma - metabolism</subject><subject>Interferons</subject><subject>Interleukins - genetics</subject><subject>liver transplantation</subject><subject>Liver Transplantation - adverse effects</subject><subject>Liver, biliary tract, pancreas, portal circulation, spleen</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Polymorphism, Genetic - genetics</subject><subject>Postoperative Complications</subject><subject>Prognosis</subject><subject>Prospective Studies</subject><subject>RNA, Viral - genetics</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Surgery of the digestive system</subject><subject>Viral diseases</subject><subject>Viral hepatitis</subject><issn>1600-6135</issn><issn>1600-6143</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU2PUyEUhonROOPoXzBsjG5aD3A_uAsXM_VjampsTF0TLvfclOZ-CdSZ_hd_rGBrZ2dkAW_geTkHXkIogzmL4-1uzgqAWcEyMefA2ByEjPL-Ebk8Hzw-a5FfkGfe7wBYySV_Si44FwAZyEvy6xsaO1kcAl2uuLyh67E79KObttb3dOmpHuiyn0YXdEKGBieMU9Rrh401YXR0bKPLh-D04Kcuce-trjGgp1-w62zYe2oHurI_0dHNA7XWIRX29M6GLV1s3ThYQ29xivvBerp4Tp60uvP44rReke8fP2wWt7PV10_LxfVqZjLJxMwgFKJpC0Bd6QzQQCsyyDKsi6Ysy_RQMJIXWVWz1mCSNdbSYFUWTS6MuCKvj_dObvyxRx9Ub72JresBx71XFc9LJqHgkXzzT5KB4FJWObCIyiNq3Oi9w1ZNzvbaHSKkUopqp1JAKoWlUorqT4rqPlpfnqrs6x6bs_FvbBF4dQK0N7pr458a6x-4vORQ5nnk3h25O9vh4b8bUNefN0mJ342rudo</recordid><startdate>201203</startdate><enddate>201203</enddate><creator>Veldt, B. J.</creator><creator>Duarte‐Rojo, A.</creator><creator>Thompson, A. J.</creator><creator>Watt, K. D.</creator><creator>Heimbach, J. K.</creator><creator>Tillmann, H. L.</creator><creator>Goldstein, D. D.</creator><creator>McHutchison, J. G.</creator><creator>Charlton, M. R.</creator><general>Blackwell Publishing Inc</general><general>Wiley</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>201203</creationdate><title>Recipient IL28B Polymorphism Is an Important Independent Predictor of Posttransplant Diabetes Mellitus in Liver Transplant Patients with Chronic Hepatitis C</title><author>Veldt, B. J. ; Duarte‐Rojo, A. ; Thompson, A. J. ; Watt, K. D. ; Heimbach, J. K. ; Tillmann, H. L. ; Goldstein, D. D. ; McHutchison, J. G. ; Charlton, M. 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Target tissue resistance</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>HCV</topic><topic>Hepacivirus - pathogenicity</topic><topic>Hepatitis C virus</topic><topic>Hepatitis C, Chronic - complications</topic><topic>Hepatitis C, Chronic - genetics</topic><topic>Hepatitis C, Chronic - surgery</topic><topic>Human viral diseases</topic><topic>Humans</topic><topic>Infectious diseases</topic><topic>Interferon-gamma - metabolism</topic><topic>Interferons</topic><topic>Interleukins - genetics</topic><topic>liver transplantation</topic><topic>Liver Transplantation - adverse effects</topic><topic>Liver, biliary tract, pancreas, portal circulation, spleen</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Polymorphism, Genetic - genetics</topic><topic>Postoperative Complications</topic><topic>Prognosis</topic><topic>Prospective Studies</topic><topic>RNA, Viral - genetics</topic><topic>Surgery (general aspects). 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R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Recipient IL28B Polymorphism Is an Important Independent Predictor of Posttransplant Diabetes Mellitus in Liver Transplant Patients with Chronic Hepatitis C</atitle><jtitle>American journal of transplantation</jtitle><addtitle>Am J Transplant</addtitle><date>2012-03</date><risdate>2012</risdate><volume>12</volume><issue>3</issue><spage>737</spage><epage>744</epage><pages>737-744</pages><issn>1600-6135</issn><eissn>1600-6143</eissn><abstract>IL28B polymorphisms are strongly associated with response to treatment for HCV infection. IL28B acts on interferon‐stimulated genes via the JAK‐STAT pathway, which has been implicated in development of insulin resistance. We investigated whether IL28B polymorphisms are associated with posttransplant diabetes mellitus (DM). Consecutive HCV patients who underwent liver transplantation between 1–1995 and 1–2011 were studied. Genotyping of the polymorphism rs12979860 was performed on DNA collected from donors and recipients. Posttransplant DM was screened for by fasting blood glucoses every 1–3 months. Of 221 included patients, 69 developed posttransplant DM (31%). Twenty‐two patients with recipient IL28B genotype TT (48%), 25 with IL28B genotype CT (25%) and 22 with IL28B genotype CC (29%) developed posttransplant DM. TT genotype was statistically significantly associated with posttransplant DM over time (log rank p = 0.012 for TT vs. CT and p = 0.045 for TT vs. CC). Multivariate Cox regression analysis correcting for donor age, body mass index, baseline serum glucose, baseline serum cholesterol, recipient age and treated rejection, showed that recipient IL28B genotype TT was independently associated with posttransplant DM (hazard ratio 2.51; 95% confidence interval 1.17–5.40; p = 0.011). We conclude that the risk of developing posttransplant DM is significantly increased in recipients carrying the TT polymorphism of the IL28B gene.
An analysis of liver transplant recipients with hepatitis C virus infection finds that the risk of developing posttransplant diabetes mellitus is significantly increased in recipients carrying the TT polymorphism of the IL28B gene.</abstract><cop>Malden, USA</cop><pub>Blackwell Publishing Inc</pub><pmid>22300408</pmid><doi>10.1111/j.1600-6143.2011.03843.x</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Biological and medical sciences Diabetes mellitus Diabetes Mellitus - diagnosis Diabetes Mellitus - etiology Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Follow-Up Studies HCV Hepacivirus - pathogenicity Hepatitis C virus Hepatitis C, Chronic - complications Hepatitis C, Chronic - genetics Hepatitis C, Chronic - surgery Human viral diseases Humans Infectious diseases Interferon-gamma - metabolism Interferons Interleukins - genetics liver transplantation Liver Transplantation - adverse effects Liver, biliary tract, pancreas, portal circulation, spleen Male Medical sciences Middle Aged Polymorphism, Genetic - genetics Postoperative Complications Prognosis Prospective Studies RNA, Viral - genetics Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the digestive system Viral diseases Viral hepatitis |
| title | Recipient IL28B Polymorphism Is an Important Independent Predictor of Posttransplant Diabetes Mellitus in Liver Transplant Patients with Chronic Hepatitis C |
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