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Calprotectin serum level is an independent marker for radiographic spinal progression in axial spondyloarthritis
  1. Maureen C Turina1,
  2. Joachim Sieper2,
  3. Nataliya Yeremenko1,3,
  4. Kristina Conrad2,
  5. Hildrun Haibel2,
  6. Martin Rudwaleit4,
  7. Dominique Baeten1,3,
  8. Denis Poddubnyy2
  1. 1Department of Clinical Immunology and Rheumatology, Academic Medical Center/University of Amsterdam, Amsterdam, The Netherlands
  2. 2Rheumatology, Med. Department I, Campus Benjamin Franklin, Charité Universitätsmedizin Berlin, Berlin, Germany
  3. 3Laboratory of Experimental Immunology, Academic Medical Center/University of Amsterdam, Amsterdam, The Netherlands
  4. 4Endokrinologikum Berlin, Berlin, Germany
  1. Correspondence to Dr Denis Poddubnyy, Rheumatology, Med. Department I, Campus Benjamin Franklin, Charité Universitätsmedizin Berlin, Hindenburgdamm 30, Berlin 12203, Germany; denis.poddubnyy{at}charite.de

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In previous works, we demonstrated that markers of systemic inflammation (elevated C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR)) are independently associated with radiographic spinal progression over 2 years in axial spondyloarthritis (axSpA) in the German spondyloarthritis inception cohort (GESPIC).1 We also found previously that calprotectin, which is secreted during monocyte infiltration into inflamed tissues, and thus, directly reflects a potentially important pathophysiological mechanism in SpA,2 ,3 and which was found to be associated with structural joint damage in psoriatic arthritis4 and in rheumatoid arthritis,5 is clearly elevated in SpA as compared to healthy controls, and decreases rapidly and consistently upon effective treatment,2 although in another work, no differences in serum calprotectin between ankylosing spondylitis patients and healthy controls could be found.6 We aimed here to assess whether serum calprotectin levels are predictive for progression of structural damage in the spine in axSpA.

Seventy-six patients (mean age 38.0±11.5 years, mean symptom duration 4.6±2.8 years, 66% males, 82% HLA-B27-positives) with definite axSpA (n=63 fulfilling the modified New York criteria for ankylosing spondylitis and n=13 patients with axSpA not fulfilling the radiographic part …

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Footnotes

  • Contributors All authors contributed to acquisition, analysis and interpretation of the data and drafting the manuscript.

  • Funding GESPIC has been financially supported by the German Federal Ministry of Education and Research (Bundesministerium für Bildung und Forschung—BMBF). As funding by BMBF was reduced according to schedule in 2005 and stopped in 2007, complementary financial support has been obtained also from Abbott/Abbvie, Amgen, Centocor, Schering-Plough, and Wyeth. Since 2010 additional support has being obtained also from ANCYLOSS (grant number FKZ 01EC1002D) and ArthroMark (grant number FKZ 01EC1009A) projects funded by BMBF.

  • Competing interests NY and DB are supported by grants from the Dutch Arthritis Foundation (Reumafonds). MCT is supported by an unrestricted fellowship grant from Janssens.

  • Ethics approval The study protocol was approved by the central ethics committee of the coordinating centre (Charité Universitätsmedizin Berlin) and by all local ethical committees of the participating centres.

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

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