SAT0016 Role of PCR, GCKR, HNF1A, LEPR, ASCL1 and NLRP3 in Atherosclerosis in Patients with Rheumatoid Arthritis

Abstract

BackgroundRheumatoid 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].ObjectivesWe aimed to determine the potential role of these genes in the development of CV disease and subclinical atherosclerosis in patients with RA.MethodsGenotyping was performed in 2,384 Spanish RA patients by TaqMan assays. Subclinical atherosclerosis was determined by carotid ultrasonography (US) in 1,193 patients.ResultsNo 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.ConclusionsOur results do not confirm an association between these genes and the development of CV disease and subclinical atherosclerosis in patients with RA.ReferencesDanesh 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.AcknowledgementThis 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 InterestNone declared

SAT0014 Association of Hla Genes in Systemic Sclerosis with Interstitial Lung Disease: Table 1.

“…Methods: The sample set consisted of 128 (70.3% female) Caucasian JIA patients and 221 (28.1% female) healthy controls from Northern Greece. Genotyping for the PTPN22 rs2476601 (XcmI) was performed by restriction fragment length polymorphism (RFLP) analysis [3]. Logistic regression or the Gart (Woolf) method were used to estimate ORs and 95% CIs.…”

“…Background: Polyautoimmunity (i.e., the presence of two or more autoimmune diseases in a single patient) and familial autoimmunity (i.e., diverse autoimmune diseases in a nuclear family) represent extreme phenotypes ideal for identifying major genomic variants contributing to autoimmunity (1)(2)(3). Whole Exome Sequencing (WES) and linkage analysis are well suited for this purpose due to its strong resolution upon familial segregation patterns of functional protein coding and splice variants (3). Objectives: The primary objective of this study was to identify potentially autoimmune causative variants using WES data from extreme pedigrees segregating polyautoimmunity phenotypes.…”