SAT0016 Role of PCR, GCKR, HNF1A, LEPR, ASCL1 and NLRP3 in Atherosclerosis in Patients with Rheumatoid Arthritis. (15th July 2016)

• Record Type: Journal Article
• Authors: Lopez-Mejías, R.; Genre, F.; Remuzgo-Martínez, S.; Robustillo-Villarino, M.; Ubilla, B.; Llorca, J.; Mijares, V.; Corrales, A.; González-Juanatey, C.; Miranda-Filloy, J.A.; Pina, T.; Blanco, R.; Vicente, E.; Alegre-Sancho, J.J.; Magro, C.; Raya, E.; Tejera-Segura, B.; Ramírez Huaranga, M.A.; Gόmez-Vaquero, C.; Balsa, A.; Pascual-Salcedo, D.; Lόpez-Longo, F.J.; Carreira, P.; González-Άlvaro, I.; Rodríguez-Rodríguez, L.; Fernández-Gutiérrez, B.; Ferraz-Amaro, I.; Castañeda, S.; Martín, J.; González-Gay, M.A.
• Is Part Of: Annals of the rheumatic diseases. Volume 75(2016)Supplement 2
• Page Start: 669
• Page End: 669
• Publication Date: 2016-07-15
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2016-eular.2654
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: Rheumatoid arthritis (RA) is an autoimmune inflammatory disease associated with accelerated atherosclerosis and increased cardiovascular (CV) disease. Elevated levels of the C-reactive protein (CRP) are related to an increase risk of coronary artery disease [1] and stroke [2]. Recently, PCR, GCKR, HNF1A, LEPR, ASCL1 and NLRP3 have been associated with CRP levels in non-rheumatic population [2]. Objectives: We aimed to determine the potential role of these genes in the development of CV disease and subclinical atherosclerosis in patients with RA. Methods: Genotyping was performed in 2, 384 Spanish RA patients by TaqMan assays. Subclinical atherosclerosis was determined by carotid ultrasonography (US) in 1, 193 patients. Results: No statistically significant differences were found when PCR, GCKR, HNF1A, LEPR, ASCL1 and NLRP3 were assessed according to the presence/absence of CV disease. It was also the case when patients were stratified according the presence/absence of subclinical atherosclerosis. Conclusions: Our results do not confirm an association between these genes and the development of CV disease and subclinical atherosclerosis in patients with RA. References: Danesh et al. N Engl J Med 2004, 350(14):1387–1397; Ridker et al. N Engl J Med 1997, 336(14):973–979; Dehghan A et al. Circulation, 123(7):731–738. Acknowledgement: This study was supported by European Union FEDER funds and "Fondo de Investigaciόn Sanitaria" (grants PI12/00060 and PI15/00525) from `Instituto de Salud Carlos III" (ISCIII, Health Ministry, Spain). It was also partially supported by RETICS Programs RD12/0009 (RIER) from "Instituto de Salud Carlos III" (ISCIII, Health Ministry, Spain), and in part by grants from the European IMI BTCure Program. RL-M and BU is supported by funds from the RETICS Program (RIER) (RD12/0009/0013). FG is a recipient of a Sara Borrell postdoctoral fellowship from the "Instituto Carlos III de Salud" at the Spanish Ministry of Health (Spain) (CD15/00095). Disclosure of Interest: None declared