Abstract

Ingestion of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin can trigger acute bronchoconstriction and the incidence of NSAID- exacerbated respiratory disease (NERD), formerly Aspirin-intolerant asthma (AIA), rises from 7% in asthma generally to over 15% in severe asthma and up to 30% in severe asthmatics with nasal polyposis. NSAIDS inhibit the synthesis of prostanoids by blockade of cyclooxygenase (COX). Acute reactions to NSAIDs can be life threatening and may be associated with rhinoconjunctival and dermal symptoms. The selectively for COX-1 inhibition determines the ability of NSAIDs to induce NERD. Pathologically, the bronchial and nasal airways of patients with NERD show chronic eosinophilia, with evidence of eosinophil and mast cell activation during acute reactions. The etiology of NERD is unclear, but involves inhibition by NSAIDs of prostaglandin E2 synthesis that would normally suppress local inflammatory reactions. The consequent synthesis of cysteinyl-leukotrienes and other leukocyte-derived mediators contributes to bronchoconstriction and other acute features. Recent evidence also implicates a role for type 2 (T2) inflammation in subtypes of NERD. Treatment of NERD involves avoidance of NSAIDs combined with conventional management of underlying asthma with combination inhaled corticosteroids/long-acting β2-agonists along with leukotriene modifiers and potentially anti-T2-directed antibody therapy. Controlled desensitization with regular doses of an NSAID can provide protection against acute reactions.

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