AB0087 THE SYNOVIAL EXPRESSION OF PSTAT1-3-5 IN PATIENTS WITH KNEE TREATMENT-RESISTANT MONOARTHRITIS IN THE COURSE OF RHEUMATOID AND PSORIATIC ARTHRITIS

Background Rheumatoid and Psoriatic Arthritis are both chronic inflammatory diseases of the joints characterized by synovial proliferation [1]. The JAK/STAT signalling pathway is critical in pathogenesis diseases, among them STAT3 activated numerous cytokines, growth factors, interferons Hypoxia also an important stimulus for activation consequent production accumulation HIF-1α, leading to neovascularization [2]. Objectives aim present study was analyse phosphorylation pattern pSTAT1, pSTAT3 pSTAT5 score tissue from RA PsA patients with knee treatment resistant monoarthritis. Methods diagnosis based on 2010 American College Rheumatology/European League Against Rheumatism [3] Classification Criteria [4], respectively. All presented treatment-resistant monoarthritis underwent In Office Needle Arthroscopy (IONA) a maximum 3 samples taken during each procedure. Synovial specimens were examined histologically using Krenn scoring system [5]; immunohistochemistry (IHC) used assess STAT1, STAT5 expression STATs assessed semi-quantitatively ranging 0 3. Results evaluated 12 (n = 6) or 6). Patients demographic clinical characteristics reported Table 1. According pathologic analysis, median 2 (IQR 4). Seven showed synovitis score≤3, other 5 cases 6. IHC analysis did not demonstrate clear association between pSTAT expression. phosphorylated form STAT1 weak all samples. Conversely, more intense fibroblasts those higher score; moreover, expressed endothelial cells presenting cellularity stronger stromal infiltration. Finally, scarcely patients. Conclusion Inflammatory infiltration course associated VEGF proliferation. – which IL-6 gp130 ligands as well pro-inflammatory cytokines - could be marker hypercellularity hypoxic metabolism tissue, context References [1]Crispino N, Ciccia F. Clin Exp Rheumatol. 2021 [2]Fearon U, et al. Nat Rev Rheumatol 2016 [3]Radner H, Ann Rheum Dis 2014 [4]Taylor W, 2006 [5]Krenn V, Histopathology Demographic N= Age, years Median (IQR) 57 (8) Gender Male:Female 9:3 BMI Ethnicity 24.6 (6.9) Caucasian N (%) 11(91.7) Asian 1 (8.3) 6 (50) Disease duration, months (I(IQR) 126 (120) Number previous bDMARDs (2) Ongoing treatment: TNF-inhibitors (41.7) JAK-inhibitors Anti-IL17 csDMARDs csDMARDS= conventional synthetic disease-modifying anti-rheumatic drugs bDMARDs= biological Acknowledgements: NIL. Disclosure Interests None Declared.