The following is a summary of “Complement Proteins L-Ficolin and M-Ficolin Are Increased in Patients With Axial Spondyloarthritis and Decrease After Tumor Necrosis Factor Inhibitor Treatment,” published in the January 2024 issue of Rheumatology by Mistegaard et al.

Building upon prior findings of elevated L-ficolin and H-ficolin in Axial Spondyloarthritis (axSpA), these complement lectin pathway proteins were investigated in a cross-section of patients with Low Back Pain (LBP).

Researchers conducted a retrospective study to analyze complement lectin pathway protein profiles in a cross-section of LBP sufferers and a longitudinal cohort of axSpA patients receiving adalimumab (ADA) treatment.

They assessed lectin pathway protein levels, including mannan-binding lectin (MBL), collectin liver 1, H-ficolin, L-ficolin, M-ficolin, MBL-associated serine protease (MASP)-1, MASP-2, MASP-3, MBL-associated protein 19 (MAp19), and MAp44, in EDTA plasma in two well-defined cohorts. The first cohort comprised patients with LBP, with subgroups including axSpA (n = 23), unspecific LBP (uLBP) with ≥ 1 SpA features (n = 55), and uLBP without SpA features or MRI findings suggestive of axSpA (n = 64). The second cohort included 49 axSpA patients in a double-blinded, placebo-controlled ADA therapy trial. Immunoassays determined lectin pathway protein levels.

The results showed a significant elevation in plasma levels of L-ficolin and M-ficolin in the cross-sectional cohort of newly diagnosed axSpA patients compared with clinically relevant controls with uLBP (all P<0.05). Following ADA therapy, both L-ficolin and M-ficolin exhibited a substantial decrease (P<0.05).

The investigator concluded that new axSpA diagnoses showed elevated L-ficolin and M-ficolin, but adalimumab treatment lowered them, implying these proteins play a role in axSpA inflammation and treatment.

Source: jrheum.org/content/51/1/31