AB0006 GENETIC RISK PROFILE FOR PSORIATIC ARTHRITIS PREDISPOSITION IN ITALIAN PATIENTS

Background: Psoriatic arthritis (PsA) is a chronic inflammatory joint disease typically associated with psoriasis and classified in the group of spondyloarthritis (1). The pathogenesis based on an interplay different genes interacting several environmental factors including stress, trauma, infections, triggering response related to activation innate acquired immunity tissues organs (2). However, risk for development PsA not clearly understood. Objectives: aim this study was evaluate, cohort Italian out-patients Rheumatology Unit University Rome Tor Vergata, association genetic variants candidate PSA susceptibility their possible contribute modulation clinical laboratory features. Methods: were selected according previous studies describing these as involved rheumatoid (RA) (3), since common background can be shared between diseases. Nine SNPs (single nucleotide polymorphism) eight analysed: STAT4 (rs7574865), TRAF3IP2 (rs33980500), TNFAIP3 (rs6920220 rs2230926), MIR146A (rs2910164), PSORS1C1 (rs2233945), IL-10 (rs1800872), HCP5 (rs3099844) ERAP1 (rs27524). Polymorphisms analysed 163 consecutive 198 healthy controls (HC). Genotyping performed by allelic discrimination TaqMan assay. Alleles frequencies differences cases or phenotypic groups compared using Pearson’s χ 2 test. Results: We have observed variant alleles [OR= 1.60 (1.15-2.21), P= 0.005], 1.65 (1.01-2.65), 0.04], 1.40 (1.05-1.85), 0.02] (rs6920220) 1.75 (1.19-2.57), 0.004]. On contrary, allele polymorphism seems play protective role 0.74 0.05]. Moreover, order define profile, we counted total number each subject, considering rs7574865 (STAT4), rs33980500 (TRAF3IP2), rs6920220 (TNFAIP3) rs27524 (ERAP1) SNPs. Then, distribution patients HC (Fig.1). Classes 3 more are significantly represented than (OR= 2.03, P=0.004). develop increases subjects at least four 2.96, P=0.002). Figure 1. Number controls: Conclusion: confirm associations five SNPs, already studied RA, susceptibility, suggesting pathway rheumatological show how genotyping only few could help profile development. References: [1]Calabresi E, et al. One year review 2019: psoriatic arthritis. Clin Exp Rheumatol. 2020;38:1046-55. [2]Chimenti MS, Triggianese P, De Martino Conigliaro Fonti GL, Sunzini F, Caso Perricone C, Costa L, R. An update potential therapeutic targets. Expert Rev Immunol. 2019 Aug;15(8):823-836. [3]Ciccacci STAT-4, IL-10, PSORS1C1, PTPN2 differently prognostic affected 2016;186:157-63. Disclosure Interests: None declared