4.7 Article

Calprotectin as a marker of inflammation in patients with early rheumatoid arthritis

期刊

ANNALS OF THE RHEUMATIC DISEASES
卷 76, 期 12, 页码 2031-2037

出版社

BMJ PUBLISHING GROUP
DOI: 10.1136/annrheumdis-2017-211695

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资金

  1. Norwegian Extra Foundation for Health and Rehabilitation
  2. Borgny Kleppe Legacy
  3. Western Norway Regional Health Authority
  4. Pfizer
  5. AbbVie
  6. Biogen
  7. BMS
  8. Boehringer Ingelheim
  9. Celgene
  10. Celltrion
  11. Eli Lilly
  12. Epirus
  13. Hospira
  14. Merck-Serono
  15. MSD
  16. Mundipharma
  17. Novartis
  18. Oktal
  19. Orion Pharma
  20. Hospira/Pfizer
  21. Roche
  22. Sandoz
  23. UCB

向作者/读者索取更多资源

Objectives Calprotectin is an inflammatory marker of interest in rheumatoid arthritis (RA). We evaluated whether the level of calprotectin was associated with disease activity, and if it was predictive of treatment response and radiographic progression in patients with early RA. Methods Plasma from disease-modifying antirheumatic drug (DMARD)-naive patients with RA fulfilling 2010 American College of Rheumatology/European League Against Rheumatism classification criteria with symptom duration <2 years was analysed for calprotectin at baseline, and after 1, 3 and 12 months. All patients received treat-to-target therapy, as part of a randomised controlled strategy trial (ARCTIC). The association between calprotectin, erythrocyte sedimentation rate (ESR) and C reactive protein (CRP) and measures of disease activity were assessed by correlations. We used likelihood ratios and logistic regression models to assess the predictive value of the baseline inflammatory markers for treatment response and radiographic damage. Results 215 patients were included: 61% female, 82% anti-citrullinated peptide antibody positive, mean (SD) age 50.9 (13.7) years and median (25, 75 percentile) symptom duration 5.8 (2.8, 10.5) months. Calprotectin was significantly correlated with Clinical Disease Activity Index (r=0.32), ESR (r=0.50) and ultrasonography power Doppler (r=0.42) before treatment onset. After 12 months of treatment, calprotectin, but not ESR and CRP, was significantly correlated with power Doppler (r=0.27). Baseline levels of calprotectin, ESR and CRP were not predictive of treatment response, but high levels of calprotectin were associated with radiographic progression in multivariate models. Conclusions Calprotectin was correlated with inflammation assessed by ultrasound before and during DMARD treatment, and was also associated with radiographic progression. The data support that calprotectin may be of interest as an inflammatory marker when assessing disease activity in different stages of RA.

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