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

Abstract

BackgroundAxial spondyloarthritis (axSpA) is associated with a certain genetic predisposition, i.e., with the presence of human leukocyte antigen (HLA)-B27. However, the pathogenesis remains largely unexplained. Animal models of ankylosing spondylitis have shown inhibition of complement to be beneficial in terms of limiting structural damage (1). The lectin pathway of complement activation serves as a key component of the innate immune system and plays a pivotal role in both homeostasis and development. The influence of complement in axSpA is mainly unexplored. We have, however, previously reported elevated plasma levels of the lectin pathway proteins L-ficolin and H-ficolin in patients with axSpA compared with blood donors (2).ObjectivesOur aim was to investigate plasma levels of lectin pathway proteins in a clinical cohort of patients with axSpA and compare them to relevant controls that we often experience significant challenges in differentiating from axSpA.MethodsPlasma samples were obtained from individuals in a cohort of patients suffering from low back pain (LBP) including: 1) 23 patients with axSpA, 2) 55 patients without axSpA experiencing SpA-features/symptoms, and 3) 64 patients with nonspecific LBP without SpA-features or MRI findings suggestive of axSpA. Diagnosis of axSpA was based on multidisciplinary team conference consensus after 3.5 years of follow-up (3). Plasma levels of 10 lectin pathway proteins (MBL, CL-L1, H-ficolin, L-ficolin, M-ficolin, MASP-1, MASP-2, MASP-3, MAp44, and MAp19) were measured by immunoassays developed in-house.ResultsPatient characteristics are shown in Table 1. Plasma levels of lectin pathway proteins L-ficolin, M-ficolin and CL-L1 differed significantly in the patient groups (p ≤ 0.03). L-ficolin and M-ficolin were elevated in axSpA-patients compared with patients with SpA-features without axSpA and nonspecific LBP patients (Figure 1). CL-L1 was elevated in axSpA-patients and patients with SpA-features without axSpA compared with nonspecific LBP patients (Figure 1). No significant differences were observed for MBL, H-ficolin, MASP-1, MASP-2, MASP-3, MAp44, and MAp19. L-ficolin levels correlated with CRP in axSpA-patients (Spearman’s rho=0.58 p=0.004). M-ficolin levels correlated weakly with CRP in nonspecific LBP patients (Spearman’s rho=0.36 p=0.003). Lectin pathway protein levels did not correlate with disease activity (ASDAS).Table 1.Patient characteristicsaxSpA (n=23)Not axSpA (n=55)Non-specific low back pain (n=64)p-valueMedian age, years (range)32 (19-40)33 (19-41)32 (18-39)0.75aMales, n (%)10 (43)37 (67)26 (41)0.01bHLA-B27 positive, n (%)17 (74)11 (20)5 (8)0.00bInflammatory back pain, n (%)18 (78)28 (51)0.03cGood response to NSAID14 (61)17 (31)0.01cSacroiliitiis on MRI acc. ASAS, n (%)22 (96)45 (82)0.11cElevated CRP, n (%)3 (13)7 (13)0.97ASDAS (range)2.5 (1.2-3.7)2.3 (0.8-3.8)0.52da compared by Kruskal-Wallis test.b all three groups compared by Chi2 test.c compared by Chi2 test.d compared by Mann Whitney U test.Figure 1.Plasma levels of L-ficolin, M-ficolin and CL-L1.ConclusionL-ficolin and M-ficolin are increased in patients with axSpA when compared with relevant control cohorts of patients with LBP or with SpA-features without axSpA. Our findings support a potential pathogenic role for complement in axSpA, however, further studies are needed to elucidate the diagnostic potential of the specific complement proteins.