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Insulin resistance and lower plasma adiponectin increase malignancy risk in nondiabetic continuous ambulatory peritoneal dialysis patients

DC Field Value Language
dc.contributor.author강신욱-
dc.contributor.author박정탁-
dc.contributor.author유태현-
dc.contributor.author이동형-
dc.contributor.author이정은-
dc.contributor.author이주현-
dc.contributor.author장태익-
dc.contributor.author한대석-
dc.date.accessioned2014-12-20T17:12:14Z-
dc.date.available2014-12-20T17:12:14Z-
dc.date.issued2011-
dc.identifier.issn0026-0495-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/94153-
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.-
dc.description.statementOfResponsibilityopen-
dc.format.extent121~126-
dc.relation.isPartOfMETABOLISM-CLINICAL AND EXPERIMENTAL-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdiponectin/blood*-
dc.subject.MESHAdult-
dc.subject.MESHAged-
dc.subject.MESHC-Reactive Protein/analysis-
dc.subject.MESHFemale-
dc.subject.MESHFollow-Up Studies-
dc.subject.MESHHumans-
dc.subject.MESHInsulinResistance*-
dc.subject.MESHKidney Failure, Chronic/complications*-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHNeoplasms/etiology*-
dc.subject.MESHPeritonealDialysis,ContinuousAmbulatory*-
dc.subject.MESHProspective Studies-
dc.titleInsulin resistance and lower plasma adiponectin increase malignancy risk in nondiabetic continuous ambulatory peritoneal dialysis patients-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorJung Tak Park-
dc.contributor.googleauthorTae-Hyun Yoo-
dc.contributor.googleauthorTae Ik Chang-
dc.contributor.googleauthorDong Hyung Lee-
dc.contributor.googleauthorJoo Hyun Lee-
dc.contributor.googleauthorJung Eun Lee-
dc.contributor.googleauthorHoon Young Choi-
dc.contributor.googleauthorShin-Wook Kang-
dc.contributor.googleauthorDae-Suk Han-
dc.contributor.googleauthorDong-Ryeol Ryu-
dc.identifier.doi10.1016/j.metabol.2010.02.006-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00053-
dc.contributor.localIdA01654-
dc.contributor.localIdA02526-
dc.contributor.localIdA02739-
dc.contributor.localIdA03486-
dc.contributor.localIdA04272-
dc.contributor.localIdA03119-
dc.contributor.localIdA03164-
dc.relation.journalcodeJ02223-
dc.identifier.eissn1532-8600-
dc.identifier.pmid20303125-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0026049510000600-
dc.contributor.alternativeNameKang, Shin Wook-
dc.contributor.alternativeNamePark, Jung Tak-
dc.contributor.alternativeNameYoo, Tae Hyun-
dc.contributor.alternativeNameLee, Dong Hyoung-
dc.contributor.alternativeNameLee, Jung Eun-
dc.contributor.alternativeNameLee, Joo Hyun-
dc.contributor.alternativeNameChang, Tae Ik-
dc.contributor.alternativeNameHan, Dae Suk-
dc.contributor.affiliatedAuthorKang, Shin Wook-
dc.contributor.affiliatedAuthorPark, Jung Tak-
dc.contributor.affiliatedAuthorYoo, Tae Hyun-
dc.contributor.affiliatedAuthorLee, Dong Hyoung-
dc.contributor.affiliatedAuthorChang, Tae Ik-
dc.contributor.affiliatedAuthorHan, Dae Suk-
dc.contributor.affiliatedAuthorLee, Jung Eun-
dc.contributor.affiliatedAuthorLee, Joo Hyun-
dc.rights.accessRightsnot free-
dc.citation.volume60-
dc.citation.number1-
dc.citation.startPage121-
dc.citation.endPage126-
dc.identifier.bibliographicCitationMETABOLISM-CLINICAL AND EXPERIMENTAL, Vol.60(1) : 121-126, 2011-
dc.identifier.rimsid27276-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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