Abstract

Aspirin-exacerbated respiratory disease (AERD) is defined by the triad of asthma, chronic rhinosinusitis with nasal polyps (CRSwNP), and respiratory reactions to medications that inhibit cyclooxygenase-1. Of these elements, patients with AERD cite CRSwNP symptoms as the most impactful on quality of life1. Patients with AERD are less likely to respond to first-line therapy with intranasal glucocorticoids and more likely to require multiple functional endoscopic sinus surgeries (FESS) compared to aspirin-tolerant CRSwNP2. Histologically, nasal tissue eosinophil levels are higher in patients with AERD compared to those in aspirin-tolerant patients with CRSwNP3. These findings together emphasize the need for effective CRSwNP treatments and suggest a possible role for eosinophil-targeting agents in AERD. However, near-total depletion of nasal polyp tissue eosinophils with dexpramipexole failed to improve symptoms and reduce polyp burden among patients with CRSwNP, which suggests eosinophils alone may not be the primary drivers of tissue inflammation in patients with CRSwNP4,5.

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