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dc.rights.licenseopenen_US
dc.contributor.authorLAOUALI, N.
dc.contributor.authorBRAILLY-TABARD, S.
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorHELMER, Catherine
dc.contributor.authorANCELIN, M. L.
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorTZOURIO, Christophe
IDREF: 69829209
dc.contributor.authorELBAZ, A.
dc.contributor.authorGUIOCHON-MANTEL, A.
dc.contributor.authorCANONICO, M.
dc.date.accessioned2020-11-23T15:52:36Z
dc.date.available2020-11-23T15:52:36Z
dc.date.issued2018-10
dc.identifier.issn1365-2265 (Electronic) 0300-0664 (Linking)en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/15587
dc.description.abstractEnCONTEXT: Although endogenous estradiol, generally considered as the female hormone, has been little investigated in men, it could play a role in men's health, mortality in particular. The influence of estrogen receptors (ER) genetic polymorphisms on this relationship has never been studied. DESIGN AND PARTICIPANTS: The Three-City cohort study included (1999-2001) 3650 men >/=65 years who were followed for mortality over 12 years. At baseline, total estradiol (tE2) was measured and ER genotyped in a random subsample of 472 men without hormonal treatment. Free estradiol (fE2) was estimated using Vermeulen and Sodergard algorithms. MAIN OUTCOME: Mortality data were obtained from death certificates. We used inverse probability weighted Cox models to examine the association of estradiol with all-cause and cause-specific mortality and its interaction with ER genetic polymorphisms. RESULTS: 183 men died over the follow-up (cardiovascular disease (CVD), n=44; cancer, n=57; other causes, n=82). After adjustment, there was a quadratic relationship of all-cause mortality with tE2 and fE2 (p-quadratic=0.04 and 0.05, respectively), with higher mortality for the top and bottom tertiles compared to the middle one. These associations were stronger for CVD mortality (p-quadratic=0.01 and 0.02 for tE2 and fE2, respectively) and disappeared for cancer mortality. There was no evidence of an interaction of estradiol with any ER polymorphisms on all-cause mortality. CONCLUSION: In elderly men, we showed a nonlinear association of tE2 and fE2 with all-cause mortality. These quadratic relationships were stronger for CVD mortality and did not exist for cancer mortality. ER genetic polymorphisms did not modify this association. This article is protected by copyright. All rights reserved.
dc.language.isoENen_US
dc.subject.enLEHA
dc.subject.enVINTAGE
dc.subject.en3C
dc.title.enOestradiol level, oestrogen receptors, and mortality in elderly men: The three-city cohort study
dc.title.alternativeClin Endocrinol (Oxf)en_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1111/cen.13797en_US
dc.subject.halSciences du Vivant [q-bio]/Santé publique et épidémiologieen_US
dc.identifier.pubmed29935032en_US
bordeaux.journalClinical Endocrinologyen_US
bordeaux.page514-525en_US
bordeaux.volume89en_US
bordeaux.hal.laboratoriesBordeaux Population Health Research Center (BPH) - U1219en_US
bordeaux.issue4en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.teamVINTAGEen_US
bordeaux.teamLEHA_BPH
bordeaux.team3Cen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-03193012
hal.version1
hal.date.transferred2021-04-08T13:08:48Z
hal.exporttrue
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