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dc.contributor.author류동열*
dc.date.accessioned2016-08-28T12:08:00Z-
dc.date.available2016-08-28T12:08:00Z-
dc.date.issued2011*
dc.identifier.issn0026-0495*
dc.identifier.otherOAK-7152*
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/221243-
dc.description.abstractEnd-stage renal disease patients have a higher risk for developing cancer. Although several causes for this increased risk have been proposed, the risk factors for cancer development in this population have not been elucidated. The aim of this study was to determine whether metabolic derangements, including insulin resistance and altered adipokines, increase the risk of developing malignancies in peritoneal dialysis (PD) patients, who are vulnerable to metabolic disorders because of excessive glucose absorbed from the dialysate. Study subjects comprised 106 nondiabetic PD patients who had been on PD for a minimum of 3 months with no overt malignancy. Baseline anthropometry, fasting glucose, insulin, and adiponectin were measured. The development of malignancy was evaluated during the follow-up period. During the mean follow-up of 47.0 ± 23.7 months, malignancy occurred in 15 patients (14.2%). The most common site of cancer was the kidney (26.7%), followed by thyroid (13.3%) and stomach (13.3%). Baseline insulin levels and homeostasis model assessment of insulin resistance were significantly higher, whereas plasma adiponectin levels were significantly lower, in patients who developed malignancy. Cox proportional hazards analysis revealed that insulin levels, homeostasis model assessment of insulin resistance, and lower adiponectin were independent predictors of malignancy. These findings demonstrate that insulin resistance and lower adiponectin levels could be risk factors for malignancy in nondiabetic PD patients. © 2011 Elsevier Inc. All rights reserved.*
dc.languageEnglish*
dc.titleInsulin resistance and lower plasma adiponectin increase malignancy risk in nondiabetic continuous ambulatory peritoneal dialysis patients*
dc.typeArticle*
dc.relation.issue1*
dc.relation.volume60*
dc.relation.indexSCI*
dc.relation.indexSCIE*
dc.relation.indexSCOPUS*
dc.relation.startpage121*
dc.relation.lastpage126*
dc.relation.journaltitleMetabolism: Clinical and Experimental*
dc.identifier.doi10.1016/j.metabol.2010.02.006*
dc.identifier.wosidWOS:000285441300015*
dc.identifier.scopusid2-s2.0-78649952873*
dc.author.googlePark J.T.*
dc.author.googleYoo T.-H.*
dc.author.googleChang T.I.*
dc.author.googleLee D.H.*
dc.author.googleLee J.H.*
dc.author.googleLee J.E.*
dc.author.googleChoi H.Y.*
dc.author.googleKang S.-W.*
dc.author.googleHan D.-S.*
dc.author.googleRyu D.-R.*
dc.contributor.scopusid류동열(7103144218;56997547400;56669926200)*
dc.date.modifydate20240123102517*
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의과대학 > 의학과 > Journal papers
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