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Differentiating patients with psoriasis from psoriatic arthritis using collagen biomarkers


1, 2, 3, 4, 5, 6, 7, 8

 

  1. Immunoscience, Biomarkers and Research, Nordic Bioscience, Herlev, and Department of Biomedicine and Biotechnology, Technical University of Denmark, Lyngby, Denmark. shn@nordicbio.com
  2. UCD Conway Institute, School of Medicine, University College Dublin, Ireland.
  3. Immunoscience, Biomarkers and Research, Nordic Bioscience, Herlev, and University of Copenhagen, Denmark.
  4. Immunoscience, Biomarkers and Research, Nordic Bioscience, Herlev, Denmark.
  5. Immunoscience, Biomarkers and Research, Nordic Bioscience, Herlev, Denmark.
  6. Immunoscience, Biomarkers and Research, Nordic Bioscience, Herlev, Denmark.
  7. UCD Conway Institute, School of Medicine, University College Dublin, Ireland.
  8. UCD Conway Institute, School of Medicine, University College Dublin, Ireland.

CER15506
2023 Vol.41, N°3
PI 0574, PF 0580
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PMID: 35916294 [PubMed]

Received: 20/01/2022
Accepted : 02/05/2022
In Press: 28/07/2022
Published: 23/03/2023

Abstract

OBJECTIVES:
Around 30% of patients diagnosed with cutaneous psoriasis (PsC) will go on to develop psoriatic arthritis (PsA) which includes inflammation of the joints. Collagens are core proteins in all tissues, which are involved in the inflammatory process in both PsC and PsA. The aim of this study is to investigate collagen biomarkers and their potential use in separating the three patient groupings: PsC, PsA and healthy donors.
METHODS:
Healthy donors (n=41), patients with PsC (n=30) and patients with PsA (n=30) were recruited. Clinical disease parameters were recorded. Collagen remodelling was measured using ELISA immunoassays which detect the serological anabolic biomarkers quantifying formation of type I, III and IV collagen (PRO-C1, PRO-C3 and PRO-C4 respectively), and the catabolic biomarkers measuring degradation of type I, II, III, IV and X collagen (C1M, C2M, C3M, C4M and C10C respectively).
RESULTS:
Patients with PsC and PsA presented lower levels of PRO-C1 and C3M compared to healthy controls (p<0.05-p<0.0001), C1M was higher in PsA compared to healthy controls (p<0.0001) and C2M was all elevated in PsC and PsA compared to healthy controls (p=0.0002 and p=0.0004 respectively), reflecting alterations in the tissues. In addition, C1M was able to separate between PsC and PsA patients with an AUROC=0.664, indicating that this biomarker may be a biomarker of joint involvement.
CONCLUSIONS:
This work provides evidence that serum collagen biomarkers are dysregulated in PsC and PsA, as compared to healthy controls. C1M was able to differentiate patients with PsC from PsA and could be a potential biomarker of inflammatory systemic musculoskeletal involvement.

DOI: https://doi.org/10.55563/clinexprheumatol/jmt9jv

Rheumatology Article