Observational analysis reveals nasal polyps and chronic rhinosinusitis in patients with eosinophilic granulomatosis with polyangiitis, indicating treatment challenges.
Objective: Comorbid chronic rhinosinusitis (CRS) can be observed during the maintenance phase of eosinophilic granulomatosis with polyangiitis (EGPA), particularly during the tapering of oral corticosteroid (OCS) dosages, even when treated with mepolizumab (MPZ). Control of the comorbid CRS might be key for the remission of EGPA with lower OCS dosages, but the clinical features remain unclear. This study retrospectively investigated the clinical features of comorbid CRS during the EGPA maintenance phase. Methods: 11 patients were included in this study. Clinical data, including details of the EGPA treatment, were analyzed. The histopathological eosinophilic count was assessed to determine the phenotype of the comorbid CRS. To assess the severity, the criteria defining primary eosinophilic CRS (eCRS) were used: a histopathological eosinophilic count ≥10 per high-power field. Results: The median SNOT-22 score (interquartile range [IQR]) was 23 (15−55), and six (55%) patients were classified into the moderate/severe category of SNOT-22 stratification. Nine (82%) patients had nasal polyps (NPs). Six (55%), seven (64%), six (55%), and two (18%) patients received inhaled corticosteroids, MPZ, immunosuppressants, and nasal corticosteroids, respectively. All patients received OCS, and the median value (IQR) was 4 (1−5) mg/day. In absolute eosinophil count (AEC) of blood tests, one patient (9%) exhibited blood eosinophilia (AEC ≥500/μL), and the median value (IQR) was 52 (29−371) /μL. In the histopathological eosinophilic count of the sinonasal mucosa, 10 (91%) patients met the diagnostic criteria for primary eCRS, with a median value (IQR) of 136 (78−134) cells/high-power field. Conclusions: NPs with eosinophilic inflammation without blood eosinophilia can be observed during the maintenance phase of EGPA. Current treatments, including MPZ for EGPA and its comorbidities, may be insufficient to control comorbid CRS. Endotypic investigation of the sinonasal mucosa is required to elucidate its pathophysiology.
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Ishikawa et al. (2025) studied this question.
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