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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 …
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.
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