Complement Proteins L-Ficolin and M-Ficolin Are Increased in Patients With Axial Spondyloarthritis and Decrease After Tumor Necrosis Factor Inhibitor Treatment

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

  • Clara Elbæk Mistegaard
  • Anne Troldborg
  • Annette Hansen
  • Steffen Thiel
  • Anne Grethe Jurik
  • Rosa M. Kiil
  • Alice A. Christiansen
  • Berit Schiøttz-Christensen
  • Oliver Hendricks
  • Susanne Juhl Pedersen
  • Inge Juul Sørensen
  • Østergaard, Mikkel
  • Anne Gitte Loft

Objective. We have previously reported elevated levels of the complement lectin pathway proteins L-ficolin and H-ficolin in patients with axial spondyloarthritis (axSpA) compared with healthy controls. The aim of the present study was to investigate these biomarkers in a cross-sectional cohort of patients suffering from low back pain (LBP). Further, we aimed to investigate changes in lectin pathway protein levels after initiation of adalimumab (ADA; a tumor necrosis factor inhibitor) in a longitudinal cohort of patients with axSpA. Methods. Lectin pathway protein levels (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 were determined in 2 well-characterized cohorts: (1) a clinical cross-sectional cohort of patients with LBP, including patients with axSpA (n = 23), patients with unspecific LBP (uLBP) with ≥ 1 SpA features (n = 55), and patients with uLBP without SpA features or magnetic resonance imaging findings suggestive of axSpA (n = 64); and (2) a randomized double-blinded, placebo-controlled trial cohort of patients with axSpA (n = 49) initiating ADA 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 patients with axSpA compared with clinically relevant controls with uLBP (all P < 0.05). Both L-ficolin and M-ficolin decreased significantly after ADA therapy (P < 0.05). Conclusion. L-ficolin and M-ficolin levels are elevated in newly diagnosed patients with axSpA compared with clinically relevant controls. Both L-ficolin and M-ficolin levels decrease significantly after initiating ADA therapy. These findings provide new insights into the inflammatory processes in axSpA and support the involvement of complement in axSpA pathogenesis.

OriginalsprogEngelsk
TidsskriftJournal of Rheumatology
Vol/bind51
Udgave nummer1
Sider (fra-til)31-38
Antal sider8
ISSN0315-162X
DOI
StatusUdgivet - 2024

Bibliografisk note

Funding Information:
The study was supported by The Danish Rheumatism Association. 1C.E. Mistegaard, MD, Department of Rheumatology, Aarhus University Hospital, Aarhus, Department of Clinical Medicine, Aarhus University, Aarhus, Institute of Regional Health Research, University of Southern Denmark, Odense, and Department of Biomedicine, Aarhus University, Aarhus; 2A. Troldborg, MD, PhD, Department of Rheumatology, Aarhus University Hospital, Aarhus, Department of Clinical Medicine, Aarhus University, Aarhus, and Department of Biomedicine, Aarhus University, Aarhus; 3A. Hansen, BA, S. Thiel, PhD, Department of Biomedicine, Aarhus University, Aarhus; 4A.G. Jurik, MD, PhD, R.M. Kiil, MD, PhD, Department of Clinical Medicine, Aarhus University, Aarhus, Institute of Regional Health Research, University of Southern Denmark, Odense, and Department of Radiology, Aarhus University Hospital, Aarhus; 5A.A. Christiansen, MD, PhD, O. Hendricks, MD, PhD, Institute of Regional Health Research, University of Southern Denmark, Odense, and Danish Hospital for Rheumatic Diseases, Sonderborg; 6B. Schiøttz-Christensen, MD, PhD, Research Unit of General Practice, University of Southern Denmark, Odense; 7S.J. Pedersen, MD, PhD, I.J. Sørensen, MD, PhD, Copenhagen Center for Arthritis Research (COPECARE), Center for Rheumatology and Spine Diseases, Centre of Head and Orthopedics, Rigshospitalet Glostrup, Glostrup; 8M. Østergaard, MD, PhD, Copenhagen Center for Arthritis Research (COPECARE), Center for Rheumatology and Spine Diseases, Centre of Head and Orthopedics, Rigshospitalet Glostrup, Glostrup, and Department of Clinical Medicine, University of Copenhagen Faculty of Health and Medical Sciences, Copenhagen; 9A.G. Loft, MD, PhD, Department of Rheumatology, Aarhus University Hospital, Aarhus, Department of Clinical Medicine, Aarhus University, Aarhus, and Institute of Regional Health Research, University of Southern Denmark, Odense, Denmark. The authors declare no conflicts of interest relevant to this article. Address correspondence to Dr. C.E. Mistegaard, Department of Biomedicine, Aarhus University, Høegh-Guldbergs Gade 10, 8000 Aarhus, Denmark. Email: clarjo@rm.dk. Accepted for publication September 1, 2023.

Publisher Copyright:
© 2024 The Journal of Rheumatology.

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