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Serum cytokine and chemokine levels in patients with eosinophilic granulomatosis with polyangiitis, hypereosinophilic syndrome, or eosinophilic asthma


1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18

 

  1. Vasculitis Clinic, Division of Rheumatology, Mount Sinai Hospital, Toronto, ON, Canada. cpagnoux@mtsinai.on.ca
  2. Division of Respirology, St. Joseph’s Healthcare, McMaster University, Hamilton, ON, Canada.
  3. Department of Medical Imaging, Department of Statistical Sciences, University of Toronto, ON, Canada.
  4. Division of Rheumatology, St. Joseph’s Healthcare, McMaster University, Hamilton, ON, Canada.
  5. Vasculitis Clinic, Division of Rheumatology, Mount Sinai Hospital, Toronto, ON, Canada.
  6. Health Informatics Institute, University of South Florida, Tampa, FL, USA.
  7. Systemic Autoimmunity Branch, National Institutes of Health, NIAMS, Bethesda, MD, USA.
  8. Division of Rheumatology, University of Utah, Salt Lake City, UT, USA.
  9. Department of Rheumatic and Immunologic Diseases, Cleveland Clinic, Lerner College of Medicine, Cleveland, OH, USA.
  10. Division of Rheumatology, University of Pennsylvania, Philadelphia, PA, USA.
  11. Division of Rheumatology, University of Pittsburg, PA, USA.
  12. Section of Rheumatology, Boston University School of Medicine, Boston, MA, USA.
  13. Division of Rheumatology, Johns Hopkins University, Baltimore, MD, USA.
  14. Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, MN, USA.
  15. Division of Rheumatology, University of Pennsylvania, Philadelphia, PA, USA.
  16. Division of Rheumatology, Mayo Clinic College of Medicine, Rochester, MN, USA.
  17. Department of Medical Imaging, Department of Statistical Sciences, University of Toronto, ON, Canada.
  18. Division of Rheumatology and Department of Biostatistics, Epidemiology, and Informatics, University of Pennsylvania, Philadelphia, PA, USA.

for the Vasculitis Clinical Research Consortium

CER11251
2019 Vol.37, N°2 ,Suppl.117
PI 0040, PF 0044
Clinical aspects

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PMID: 30652675 [PubMed]

Received: 17/03/2018
Accepted : 22/05/2018
In Press: 14/01/2019
Published: 21/05/2019

Abstract

OBJECTIVES:
The pathogenesis of eosinophilic granulomatosis with polyangiitis (EGPA) remains poorly understood, and may overlap with eosinophilic asthma and primary hypereosinophilic syndrome (HES). The aim of this study was to analyse a panel of serum cytokines and chemokines as markers of disease activity in patients with these conditions.
METHODS:
The levels of 54 cytokines and chemokines were measured in the sera of 40 patients with active EGPA, 10 of these patients during inactive disease, 6 patients with HES, 8 with asthma, and 10 healthy controls. Serum cytokine/chemokines measured included interleukin (IL)-1α, 1β, 3, 4, 5, 6, 8, 13, 15, 17A, 17E(25), 18, 23 and 33, soluble IL-2 receptor alpha, eotaxin-1 (CCL11), -2 (CCL24) and -3 (CCL26), macrophage-derived chemokine (MDC/CCL22), macrophage inflammatory protein (MIP)-1a and -1b, and tumour necrosis factor (TNF)-α. Results were compared between disease and control groups using regression analysis, with Bonferroni correction for multiple comparisons (significant p value ≤0.00093).
RESULTS:
Significant differences were observed only in serum levels of MDC, IL-8, MIP-1a and -1b, TNF-α, each of which were lower in patients with active EGPA than in healthy controls (p<0.0001). Differences between patients with active disease and other disease groups did not reach significance. Paired comparisons between sera from patients with active or inactive EGPA showed no significant difference for any of the studied cytokines or chemokines.
CONCLUSIONS:
No clear difference in the serum levels of measured cytokines and chemokines helped distinguish between active EGPA or inactive EGPA, or other disease or control groups.

Rheumatology Article

Rheumatology Addendum