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Serum Parathyroid Hormone and Risk of Coronary Artery Disease: Exploring Causality Using Mendelian Randomization
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical pharmacogenomics and osteoporosis.ORCID iD: 0000-0002-6857-5973
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.ORCID iD: 0000-0003-2815-1217
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Inst Environm Med, Unit Cardiovasc & Nutr Epidemiol, SE-17177 Stockholm, Sweden.ORCID iD: 0000-0003-0118-0341
2019 (English)In: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 104, no 11, p. 5595-5600Article in journal (Refereed) Published
Abstract [en]

Context: Elevated circulating parathyroid hormone concentrations have been associated with increased risk of cardiovascular disease in observational studies, but whether the association is causal is unknown.

Objective: We used the Mendelian randomization design to test whether genetically increased serum parathyroid hormone (S-PTH) concentrations are associated with coronary artery disease (CAD).

Design, Setting, and Participants: Five single-nucleotide polymorphisms robustly associated with S-PTH concentrations were used as instrumental variables to estimate the association of genetically higher S-PTH concentrations with CAD. Summary statistics data for CAD were obtained from a genetic consortium with data from 184,305 individuals (60,801 CAD cases and 123,504 noncases).

Main Outcome Measure: OR of CAD per genetically predicted one SD increase of S-PTH concentrations.

Results: Genetically higher S-PTH concentration was not associated with CAD as a whole or myocardial infarction specifically (similar to 70% of total cases). The ORs per genetically predicted one SD increase in S-PTH concentration were 1.01 (95% CI: 0.93 to 1.09; P = 0.88) for CAD and 1.02 (95% CI: 0.94 to 1.10; P = 0.64) for myocardial infarction. The lack of association remained in various sensitivity analyses.

Conclusion: Genetic predisposition to higher S-PTH concentrations does not appear to be an independent risk factor for CAD.

Place, publisher, year, edition, pages
ENDOCRINE SOC , 2019. Vol. 104, no 11, p. 5595-5600
National Category
Endocrinology and Diabetes
Identifiers
URN: urn:nbn:se:uu:diva-398419DOI: 10.1210/jc.2019-01063ISI: 000497979600074PubMedID: 31310319OAI: oai:DiVA.org:uu-398419DiVA, id: diva2:1377090
Funder
Forte, Swedish Research Council for Health, Working Life and Welfare, 2018-00123Swedish Research CouncilAvailable from: 2019-12-11 Created: 2019-12-11 Last updated: 2019-12-11Bibliographically approved

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Melhus, HåkanMichaëlsson, KarlLarsson, Susanna C.

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