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Complement proteins L-ficolin and M-ficolin are increased in axial spondyloarthritis patients and decrease after TNF-inhibitor treatment.

Journal of Rheumatology 2023 September 16
OBJECTIVE: We have previously reported elevated levels of the complement lectin pathway proteins L-ficolin and H-ficolin in axial spondyloarthritis (axSpA) patients compared with healthy controls. The aim of this study was to investigate these biomarkers in a cross-sectional cohort of patients suffering from low back pain (LBP). Furthermore, we aimed to investigate changes in lectin pathway protein levels after initiation of adalimumab (TNF-inhibitor) in a longitudinal cohort of axSpA patients.

METHODS: Lectin pathway protein levels (mannan-binding lectin (MBL), collectin-L1 (CL-L1), H-ficolin, L-ficolin, M-ficolin, MBL-associated serine protease (MASP)-1 MASP-2, MASP-3, MBL-associated protein (MAp)19, and MAp44) were determined in EDTA plasma in two well-characterized cohorts; 1) a clinical cross-sectional cohort of patients with LBP, including axSpA patients (n=23), patients with unspecific LBP (uLPB) with ≥ 1 SpA feature(s) (n=55), and patients with uLBP without SpA features or MRI findings suggestive of axSpA (n=64), and 2) a randomized double-blinded placebo-controlled trial cohort of axSpA patients (n=49) initiating adalimumab therapy. Lectin pathway protein levels were determined using immunoassays.

RESULTS: Plasma levels of L-ficolin and M-ficolin were significantly increased in the cross-sectional cohort of newly diagnosed axSpA patients compared with clinically relevant controls with uLBP (all p<0.05). Both L-ficolin and M-ficolin decreased significantly after adalimumab therapy (p<0.05).

CONCLUSION: L-ficolin and M-ficolin levels are elevated in newly diagnosed axSpA patients compared with clinically relevant controls. Both L-ficolin and M-ficolin levels decrease significantly after initiating adalimumab therapy. These findings provide new insights into the inflammatory processes in axSpA and support a complement perspective in the axSpA pathogenesis.

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