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dc.rights.licenseopenen_US
dc.contributor.authorGILL, D.
dc.contributor.authorBREWER, C. F.
dc.contributor.authorMONORI, G.
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorTREGOUET, David-Alexandre
dc.contributor.authorFRANCESCHINI, N.
dc.contributor.authorGIAMBARTOLOMEI, C.
dc.contributor.authorTZOULAKI, I.
dc.contributor.authorDEHGHAN, A.
dc.date.accessioned2020-06-23T08:01:32Z
dc.date.available2020-06-23T08:01:32Z
dc.date.issued2019-08-06
dc.identifier.issn2047-9980en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/8089
dc.description.abstractEnBackground Systemic iron status has been implicated in atherosclerosis and thrombosis. The aim of this study was to investigate the effect of genetically determined iron status on carotid intima-media thickness, carotid plaque, and venous thromboembolism using Mendelian randomization. Methods and Results Genetic instrumental variables for iron status were selected from a genome-wide meta-analysis of 48 972 subjects. Genetic association estimates for carotid intima-media thickness and carotid plaque were obtained using data from 71 128 and 48 434 participants, respectively, and estimates for venous thromboembolism were obtained using data from a study incorporating 7507 cases and 52 632 controls. Conventional 2-sample summary data Mendelian randomization was performed for the main analysis. Higher genetically determined iron status was associated with increased risk of venous thromboembolism. Odds ratios per SD increase in biomarker levels were 1.37 (95% CI 1.14-1.66) for serum iron, 1.25 (1.09-1.43) for transferrin saturation, 1.92 (1.28-2.88) for ferritin, and 0.76 (0.63-0.92) for serum transferrin (with higher transferrin levels representing lower iron status). In contrast, higher iron status was associated with lower risk of carotid plaque. Corresponding odds ratios were 0.85 (0.73-0.99) for serum iron and 0.89 (0.80-1.00) for transferrin saturation, with concordant trends for serum transferrin and ferritin that did not reach statistical significance. There was no Mendelian randomization evidence of an effect of iron status on carotid intima-media thickness. Conclusions These findings support previous work to suggest that higher genetically determined iron status is protective against some forms of atherosclerotic disease but increases the risk of thrombosis related to stasis of blood.
dc.language.isoENen_US
dc.rightsAttribution-NonCommercial 3.0 United States
dc.rights.urihttps://creativecommons.org/licenses/by-nc/3.0/us/
dc.subject.enVINTAGE
dc.title.enEffects of Genetically Determined Iron Status on Risk of Venous Thromboembolism and Carotid Atherosclerotic Disease: A Mendelian Randomization Study
dc.title.alternativeJ Am Heart Assocen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1161/jaha.119.012994en_US
dc.subject.halSciences du Vivant [q-bio]/Santé publique et épidémiologieen_US
dc.identifier.pubmed31310728en_US
bordeaux.journalJournal of the American Heart Associationen_US
bordeaux.pagee012994en_US
bordeaux.volume8en_US
bordeaux.hal.laboratoriesBordeaux Population Health Research Center (BPH) - U1219en_US
bordeaux.issue15en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-03209509
hal.version1
hal.date.transferred2021-04-27T09:37:19Z
hal.exporttrue
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