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Lack of association between RETN rs1862513 polymorphism and cardiovascular disease in rheumatoid arthritis patients


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CER3933
2011 Vol.29, N°1
PI 0019, PF 0025
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PMID: 21345288 [PubMed]

Received: 14/06/2010
Accepted : 05/10/2010
In Press: 23/02/2011
Published: 23/02/2011

Abstract

OBJECTIVES:
To assess the influence of the RETN rs1862513 polymorphism in the risk of cardiovascular (CV) disease and subclinical atherosclerosis in patients with rheumatoid arthritis (RA).
METHODS:
Six hundred and sixty-eight patients fulfilling the 1987 American College of Rheumatology classification criteria for RA, seen at the rheumatology outpatient clinics of Hospital Xeral-Calde, Lugo, and Hospital San Carlos, Madrid, Spain, were studied. Patients were genotyped for the RETN rs1862513 polymorphism using predesigned TaqMan single nucleotide polymorphism genotyping assay. Also, HLA-DRB1 genotyping was performed using molecular based methods. Carotid intima-media thickness (IMT), flow-mediated endothelium-dependent and endothelium independent vasodilatation, used as surrogate markers of subclinical atherosclerosis, were measured in a subgroup of patients.
RESULTS:
No significant differences in the genotypic or in the allelic distribution between RA patients with or without CV disease were found. In this regard, we only observed a slight increased frequency of homozygous and heterozygous for the minor allele G (CG+GG genotypes) among patients who experienced CV events compared to those without CV events (53.04% vs. 52.62%, p=0.94). A higher frequency of classic CV risk factors was observed among the carriers of the minor allele G. However, in the adjusted logistic regression model no association between the RETN variant and CV disease was found (p=0.50). Also, when surrogate markers of subclinical atherosclerosis were assessed, in the adjusted ANCOVA model only a trend towards a higher carotid IMT was found among allele G carriers (p=0.06).
CONCLUSIONS:
RETN rs1862513 polymorphism does not seem to be a genetic risk factor for both clinically evident CV disease and subclinical atherosclerosis in patients with RA.

Rheumatology Article