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Calprotectin as a marker of inflammation in patients with early rheumatoid arthritis
  1. Maria Karolina Jonsson1,2,
  2. Nina Paulshus Sundlisæter2,
  3. Hilde Haugedal Nordal1,3,
  4. Hilde Berner Hammer2,
  5. Anna-Birgitte Aga2,
  6. Inge Christoffer Olsen2,
  7. Karl Albert Brokstad3,
  8. Désirée van der Heijde2,4,
  9. Tore K Kvien2,
  10. Bjørg-Tilde Svanes Fevang1,3,
  11. Siri Lillegraven2,
  12. Espen A Haavardsholm2,5
  1. 1Bergen Group of Epidemiology and Biomarkers in Rheumatic Diseases, Department of Rheumatology, Haukeland University Hospital, Bergen, Norway
  2. 2Department of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway
  3. 3Broegelmann Research Laboratory, Department of Clinical Science, University of Bergen, Bergen, Norway
  4. 4Leiden University Medical Center, Leiden, The Netherlands
  5. 5Institute of Health and Society, University of Oslo, Oslo, Norway
  1. Correspondence to Dr Maria Karolina Jonsson, Department of Rheumatology, Haukeland University Hospital, Postboks 1400, NO-5021 Bergen, Norway; jonssonmk{at}gmail.com

Abstract

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)-naïve 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.

Trial registration number NCT01205854; Post-results.

  • early rheumatoid arthritis
  • inflammation
  • ultrasonography

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Footnotes

  • Contributors All authors were involved in drafting the article or revising it critically for important intellectual content and approved the final manuscript to be submitted and agreed to be accountable for all aspects of the work. Conception and design of the study: EAH, SL, MKJ, B-TSF, ICO, HBH, DvdH and TKK. Acquisition of data: MKJ, EAH, ABA, HBH, KAB and DvDH. Analysis and interpretation of data: MKJ, EAH, SL, B-TSF, NPS, HHN, A-BA, KAB and ICO.

  • Funding MKJ reports grants from Norwegian Extra Foundation for Health and Rehabilitation, the Borgny Kleppe Legacy, the Western Norway Regional Health Authority and non-financial support from Calpro AS during the conduct of the study. ICO has received grants from Pfizer. TKK has received fees for speaking and/or consulting from AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Epirus, Hospira, Merck-Serono, MSD, Mundipharma, Novartis, Oktal, Orion Pharma, Hospira/Pfizer, Roche, Sandoz and UCB and received research funding to Diakonhjemmet Hospital from AbbVie, BMS, MSD, Pfizer, Roche and UCB. EAH has received research funding from Pfizer, UCB, Roche, MSD and AbbVie, honorariums as a speaker from Pfizer, UCB, Roche and AbbVie, and honorariums for development of educational material from Pfizer and has sat on advisory boards for Pfizer.

  • Competing interests All authors have completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf (available at request from the corresponding author) and declare that NPS, HHN, HBH, A-BA, KAB, DvdH, B-TSF and SL have no competing interests.

  • Patient consent Obtained.

  • Ethics approval The Regional Committee for Medical and Health Research Ethics South-East; reference number 2010/744.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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