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. 2003 Nov;112(5):877-82.
doi: 10.1016/j.jaci.2003.08.009.

Features of airway remodeling and eosinophilic inflammation in chronic rhinosinusitis: is the histopathology similar to asthma?

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Features of airway remodeling and eosinophilic inflammation in chronic rhinosinusitis: is the histopathology similar to asthma?

Jens U Ponikau et al. J Allergy Clin Immunol. 2003 Nov.

Abstract

Background: Asthma and chronic rhinosinusitis (CRS) coexist clinically in >50% of patients with CRS. Although epithelial damage and basement membrane thickening are well-known features of airway remodeling in asthma, they have not been described in CRS.

Objective: In this study, we tested the hypothesis that histopathologic features of asthma, namely, the chronic eosinophilic inflammation, epithelial damage, and basement membrane thickening of the airway mucosa, are also present in sinonasal specimens from patients with CRS.

Methods: We examined histologic specimens from 22 randomly selected patients with refractory CRS undergoing endoscopic sinus surgery and 4 healthy control subjects. The shedding of the epithelium and basement membrane thickening were evaluated by 3 independent observers' scores of hematoxylin-and-eosin staining. Eosinophilic inflammation was monitored with immunohistochemistry for eosinophil major basic protein. A novel, computerized method objectively analyzed confocal microscopic images of major basic protein immunofluorescence to determine areas with the least and most inflammation per specimen.

Results: Specimens from all patients with CRS (22/22) revealed epithelial damage (shedding) and basement membrane thickening. Strikingly heterogeneous eosinophilic inflammation, which did not differ between allergic and nonallergic patients, was detected in all patients with CRS and was absent in all healthy control subjects.

Conclusion: The histopathologic findings of asthma, namely, heterogeneous eosinophilic inflammation and features of airway remodeling, are also present in CRS. These findings, coupled with the common clinical coexistence of both diseases, suggest that the same pathologic disease process is manifest as CRS in the sinonasal tissue and as asthma in the lower airway.

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