AB0455 DRUGS, AUTOANTIBODIES AND GENES CONTRIBUTE TO THE DEVELOPMENT OF CHRONIC DAMAGE IN PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS

Background Genetic contribution to development of chronic damage have been scarcely investigated in systemic lupus erythematosus (SLE). In fact, whereas most studies looked for an association between genetic variants and SLE susceptibility or disease phenotypes, only few focused on the relationship these biomarkers development. Objectives Moving from premises, we firstly analyzed distribution organ a cohort patients secondly evaluate role clinical factors determining damage. Methods Caucasian patients, diagnosed according with 1997 ACR criteria, were enrolled, laboratory data collected. Based literature data, selected panel 17 SNPs following genes STAT4, IL10, IRAK1, HCP5, MIR146a, ATG16L1, IRGM, ATG5, MIR124, MIR1279, TNFSF4, CD40. Genotyping was performed by allelic discrimination assays. A phenotype-genotype correlation analysis evaluating specific domains SLICC Damage Index (SDI). Results Among 175 105 (60%) exhibited (SDI ≥1) median value 1.0 (IQR 3.0). The musculoskeletal (26.2%), neuropsychiatric (24.6%) ocular (20.6%) involved frequently. presence associated higher age, longer duration, (NP) manifestations, anti-phospholipid syndrome positivity anti-dsDNA antibodies. Concerning therapies cyclophosphamide, mycophenolate mofetil glucocorticoids resulted genotype/phenotype showed renal damage, identified 6.9% rs2205960 TNFSF4 (p=0.001; OR 17.0). This SNP significantly end-stage (p= 0.018, 9.68) estimated GFR<50% (p=0.025, 1.06, Figure 1). rs1463335 MIR1279 gene NP (p=0.029; 2.783). multivariate logistic regression confirmed associations (p=0.020, r=2.53) (p=0.013, r=1.26)]. 1. Association (p=0.001). addition, this two items SDI domain: glomerular filtration rate (GFR) <50% (ESRD) p=0.018 respectively). Conclusion We drugs, autoantibody profile Our suggest possible background as demonstrated polymorphisms TFNSF4 respectively. These results agree previous suggesting involvement Lupus nephritis microRNA neuroinflammation. Disclosure Interests None declared