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dc.contributor.authorLópez Mejías, Raquel
dc.contributor.authorGonzález Juanatey, Carlos
dc.contributor.authorGarcía Bermúdez, Mercedes
dc.contributor.authorCastañeda Sanz, Santos
dc.contributor.authorMiranda Filloy, José Alberto
dc.contributor.authorBlanco Alonso, Ricardo 
dc.contributor.authorLlorca Díaz, Javier
dc.contributor.authorMartín Ibáñez, Javier
dc.contributor.authorGonzález-Gay Mantecón, Miguel Ángel 
dc.contributor.otherUniversidad de Cantabriaes_ES
dc.date.accessioned2012-05-09T15:54:22Z
dc.date.available2012-05-09T15:54:22Z
dc.date.issued2012-03-01
dc.identifier.issn1478-6354
dc.identifier.urihttp://hdl.handle.net/10902/531
dc.description.abstractIntroduction: Rheumatoid arthritis (RA) is an inflammatory disease associated with accelerated atherosclerosis and high risk of cardiovascular (CV) disease. Since genome-wide association studies demonstrated association between rs599839 polymorphism and coronary artery disease, in the present study we assessed the potential association of this polymorphism with endothelial dysfunction, an early step in atherogenesis. Methods: A total of 128 RA patients without history of CV events were genotyped for rs599839 A/G polymorphism. The presence of endothelial dysfunction was assessed by brachial ultrasonography (brachial flow-mediated endothelium-dependent (FMD)). Results: Patients carrying the allele G exhibited more severe endothelial dysfunction (FMD%: 4.61 ± 3.94%) than those carrying the wild allele A (FMD%: 6.01 ± 5.15%) (P = 0.08). Adjustment for gender, age at the time of study, follow-up time and classic CV risk factors disclosed a significant association between the rs599839 polymorphism and FMD (G vs. A: P = 0.0062). Conclusions: Our results confirm an association of the rs599839 polymorphism with endothelial dysfunction in RA.es_ES
dc.description.sponsorshipAcknowledgements: We thank Rodrigo Ochoa, Sofía Vargas, M. Luisa López, M. Jesús Ibañez and Sara Olavarria for their technical assistance. This study was supported by two grants from “Fondo de Investigaciones Sanitarias” PI06-0024 and PI09/007/48 (Spain). This work was partially supported by RETICS Program, RD08/0075 (RIER) from “Instituto de Salud Carlos III” (ISCIII). MGB is a beneficiary of a grant from Fundación Española de Reumatología (FER).
dc.format.extent4 p.es_ES
dc.language.isoenges_ES
dc.publisherBioMed Centrales_ES
dc.rightsAttribution 4.0 International. © 2012 López Mejías et al.; licensee BioMed Central Ltd.es_ES
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/
dc.sourceArthritis Research and Therapy, 2012, 14(42), 1-4es_ES
dc.subject.otherAtherosclerosises_ES
dc.subject.otherCardiovascular diseasees_ES
dc.subject.otherEndothelial dysfunctiones_ES
dc.subject.otherrs599839es_ES
dc.subject.otherRheumatoid arthritises_ES
dc.titleThe lp13.3 genomic region -rs599839- is associated with endothelial dysfunction in patients with rheumatoid arthritises_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.accessRightsopenAccesses_ES
dc.identifier.DOI10.1186/ar3755
dc.type.versionpublishedVersiones_ES


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Attribution 4.0 International. © 2012 López Mejías et al.; licensee BioMed Central Ltd.Excepto si se señala otra cosa, la licencia del ítem se describe como Attribution 4.0 International. © 2012 López Mejías et al.; licensee BioMed Central Ltd.