POS0059 COMPLEMENT PROTEINS ARE ELEVATED IN PATIENTS WITH axSpA COMPARED WITH RELEVANT CONTROLS OF PATIENTS WITH LOW BACK PAIN AND SpA-FEATURES WITHOUT AXSPA.

Background Axial spondyloarthritis (axSpA) is associated with a certain genetic predisposition, i.e., the presence of human leukocyte antigen (HLA)-B27. However, pathogenesis remains largely unexplained. Animal models ankylosing spondylitis have shown inhibition complement to be beneficial in terms limiting structural damage (1). The lectin pathway activation serves as key component innate immune system and plays pivotal role both homeostasis development. influence axSpA mainly unexplored. We have, however, previously reported elevated plasma levels proteins L-ficolin H-ficolin patients compared blood donors (2). Objectives Our aim was investigate clinical cohort compare them relevant controls that we often experience significant challenges differentiating from axSpA. Methods Plasma samples were obtained individuals suffering low back pain (LBP) including: 1) 23 axSpA, 2) 55 without experiencing SpA-features/symptoms, 3) 64 nonspecific LBP SpA-features or MRI findings suggestive Diagnosis based on multidisciplinary team conference consensus after 3.5 years follow-up (3). 10 (MBL, CL-L1, H-ficolin, L-ficolin, M-ficolin, MASP-1, MASP-2, MASP-3, MAp44, MAp19) measured by immunoassays developed in-house. Results Patient characteristics are Table 1. M-ficolin CL-L1 differed significantly patient groups (p ≤ 0.03). axSpA-patients (Figure 1). No differences observed for MBL, MAp19. correlated CRP (Spearman’s rho=0.58 p=0.004). weakly rho=0.36 p=0.003). Lectin protein did not correlate disease activity (ASDAS). (n=23) Not (n=55) Non-specific (n=64) p -value Median age, (range) 32 (19-40) 33 (19-41) (18-39) 0.75 Males, n (%) (43) 37 (67) 26 (41) 0.01 b HLA-B27 positive, 17 (74) 11 (20) 5 (8) 0.00 Inflammatory pain, 18 (78) 28 (51) 0.03 c Good response NSAID 14 (61) (31) Sacroiliitiis acc. ASAS, 22 (96) 45 (82) 0.11 Elevated CRP, 3 (13) 7 0.97 ASDAS 2.5 (1.2-3.7) 2.3 (0.8-3.8) 0.52 d Kruskal-Wallis test. all three Chi2 Mann Whitney U Figure CL-L1. Conclusion increased when control cohorts support potential pathogenic further studies needed elucidate diagnostic specific proteins. References [1]Yang, C. et al. Inhibition retards progression. Sci. Rep. (2016) doi:10.1038/srep34643. [2]Troldborg, A. H- axial spondyloarthritis: improvement identification. Clin. Exp. Immunol. (2020) doi:10.1111/cei.13374. [3]Kiil, R. M. Diagnosing multidiciplinary at years’ features according ASAS criteria. Scand. J. Rheumatol. (2021) doi:10.1080/03009742.2021.1933584. Disclosure Interests None declared