A 28-year-old asthmatic woman develops acute bronchospasm, urticaria, and nasal polyps within an hour of taking aspirin for musculoskeletal pain. Her serum IgE is normal. What is the mechanism of this reaction?

• A IgE-mediated type I hypersensitivity to aspirin acting as a hapten
• B COX-1 inhibition shunts arachidonic acid through 5-lipoxygenase, generating excess cysteinyl leukotrienes ✓
• C Aspirin inhibits histamine degradation, causing histamine accumulation in airways
• D Aspirin directly antagonises beta-2 adrenoceptors in bronchial smooth muscle

Explanation

Aspirin-exacerbated respiratory disease (AERD, Samter's triad) is a pharmacological, not immunological, reaction — hence normal IgE. COX-1 inhibition by aspirin reduces prostaglandin E2, which normally suppresses 5-lipoxygenase (5-LOX) activity. Without this brake, arachidonic acid is diverted through 5-LOX to produce excess cysteinyl leukotrienes (LTC4, LTD4, LTE4), which potently cause bronchospasm, mucosal oedema, and urticaria. The reaction occurs with any non-selective NSAID but not with selective COX-2 inhibitors, which confirms the mechanism.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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