A 32-year-old woman with asthma and recurrent nasal polyposis develops intense bronchospasm, flushing, and rhinorrhoea within 30 minutes of taking ibuprofen for menstrual cramps. Which mechanism best explains this reaction?
- A IgE-mediated hypersensitivity to salicylate hapten
- B COX-1 inhibition diverting arachidonic acid toward cysteinyl leukotrienes ✓
- C Direct mast cell degranulation by prostaglandin metabolites
- D Complement-mediated bradykinin release
Explanation
Aspirin-exacerbated respiratory disease (Samter triad: asthma, nasal polyps, NSAID intolerance) results from pharmacological inhibition of COX-1, which shunts arachidonic acid down the 5-lipoxygenase pathway, producing excess cysteinyl leukotrienes that trigger bronchospasm. It is a pseudoallergic reaction, so IgE-mediated mechanisms and complement pathways do not apply, and reactions occur with any potent COX-1 inhibitor, not just aspirin. Leukotriene receptor antagonists partially protect these patients.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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Written and medically reviewed by the StethoPrep medical team.