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Microarray evaluation of allergen-specific IgE in eosinophilic granulomatosis with polyangiitis
  1. Federica Bello1,
  2. Federica Maritati2,
  3. Antonella Radice3,
  4. Renato Alberto Sinico4,5,
  5. Giacomo Emmi6,
  6. Augusto Vaglio1
  1. 1Biomedical Experimental and Clinical Sciences, University of Florence, Firenze, Italy
  2. 2Nephrology, Sant'Orsola Hospital, Bologna, Italy
  3. 3Microbiology Institute, ASST Santi Paolo e Carlo, Milan, Italy
  4. 4Medicine and Surgery, Universita degli Studi di Milano-Bicocca Scuola di Medicina e Chirurgia, Monza, Italy
  5. 5Clinical Nephrology, Azienda Socio Sanitaria Territoriale di Monza, Monza, Italy
  6. 6Department of Experimental and Clinical Medicine, University of Florence, Firenze, Italy
  1. Correspondence to Dr Augusto Vaglio, University of Florence, Firenze 50139, Italy; augusto.vaglio{at}virgilio.it

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The pathogenesis of asthma and ear–nose–throat (ENT) manifestations in eosinophilic granulomatosis with polyangiitis (EGPA) is still poorly understood. Asthma is present in almost all patients with EGPA.1 Severe or uncontrolled asthma occurs in more than 40% of patients and its severity correlates with serum IgE (sIgE) levels.2 However, sIgE towards common allergens are detectable in less than one-third of patients with EGPA using conventional diagnostic tests.3 This suggests either that atopy is not a key pathogenic mechanism in EGPA or that uncommon antigens are involved. Our study assessed IgE specificity in EGPA using microarray technologies which have higher diagnostic reliability than traditional assays and offer a wider representation of the IgE repertoire.4 5 We measured sIgE towards 112 purified or biotechnologically produced allergenic molecules using the ImmunoCAP Immuno Solid-phase Allergen Chip (ISAC) (online supplemental methods). Results are reported in ISAC standardised units (ISU). The study population comprised 29 patients with EGPA, evaluated during active and inactive disease (patients’ characteristics are reported in the online supplemental table 1), 30 patients with atopic asthma, 31 with active anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) (20 with granulomatosis with polyangiitis and 11 with microscopic polyangiitis) and 30 healthy controls (online supplemental methods). Positive IgE (ISU>0.3) in at least 5% of the whole study population were detected for 35 allergen components. We assessed for each …

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Footnotes

  • Handling editor Josef S Smolen

  • Contributors FB analysed the data, created the figure and tables, and drafted the manuscript. FM contributed to data analysis and patient recruitment. AR contributed to data analysis and patient recruitment. RAS contributed to data analysis and patient recruitment. GE contributed to data analysis and to manuscript revision. AV designed the study, analysed the data, contributed to patient recruitment and revised the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

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

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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