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Nonsteroidal anti-inflammatory drugs (NSAIDs) can induce hypersensitivity reactions with various clinical manifestations including acute/delayed reactions and three common phenotypes, NSAID/aspirin-exacerbated respiratory disease (NERD or AERD) with/without chronic rhinosinusitis (CRS) and nasal polyps, NSAID-exacerbated cutaneous disease (NECD). NSAID-induced urticaria/angioedema (NIUA). NIAU is commonly combined with anaphylaxis and named as NIUAA. The major pathogenic mechanism is the inhibition of cyclooxygenase-1 with a reduction in prostaglandin E2 levels, leading to the overproduction of cysteinyl leukotrienes and activation of inflammatory cells, including eosinophils and mast cells.

To confirm the diagnosis, provocation testing via the oral route or inhalation remains the gold standard; in vitro diagnostic methods are still not available. Essential managements are: (1) avoidance of cross-reacting NSAIDs along with the use of alternative analgesics; (2) pharmacologic treatment should follow standard guidelines in patients with underlying asthma/rhinitis (NERD, CRS), and urticaria (NECD). Aspirin desensitization and biologic treatment can be done when indicated.

Delayed reactions, including fixed drug eruptions, maculopapular eruptions, and severe cutaneous adverse reactions, are rare and mediated by T-cell responses. Symptomatic treatment with avoidance is essential. NSAID is a cofactor of food-dependent exercise-induced anaphylaxis. In this talk, we will update various clinical phenotypes and discuss practical issues faced in real clinical practice.