@article{10902/531,
year = {2012},
month = {3},
url = {http://hdl.handle.net/10902/531},
abstract = {Introduction: 
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.},
organization = {Acknowledgements: 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).},
publisher = {BioMed Central},
publisher = {Arthritis Research and Therapy, 2012, 14(42), 1-4},
title = {The lp13.3 genomic region -rs599839- is associated with endothelial dysfunction in patients with rheumatoid arthritis},
author = {López Mejías, Raquel and González Juanatey, Carlos and García Bermúdez, Mercedes and Castañeda Sanz, Santos and Miranda Filloy, José Alberto and Blanco Alonso, Ricardo and Llorca Díaz, Javier and Martín Ibáñez, Javier and González-Gay Mantecón, Miguel Ángel},
}