A 28-year-old woman with moderate persistent asthma and recurrent nasal polyps takes diclofenac for menstrual cramps. Within 30 minutes she develops intense rhinorrhoea, conjunctival injection and severe bronchospasm requiring nebulised salbutamol. An identical reaction occurred with naproxen last year. What is the pathogenetic mechanism of these episodes?
- A IgE mediated mast cell degranulation against the drug hapten
- B Cyclooxygenase inhibition shunting arachidonic acid toward excess cysteinyl leukotriene synthesis ✓
- C Complement mediated immune complex deposition in small airways
- D Delayed type IV T cell response peaking at 48 hours
Correct answer: B. Cyclooxygenase inhibition shunting arachidonic acid toward excess cysteinyl leukotriene synthesis
Explanation
This is aspirin exacerbated respiratory disease, part of Samter triad with asthma and nasal polyposis. COX inhibition reduces prostaglandin E2 braking of the 5-lipoxygenase pathway, diverting arachidonic acid toward cysteinyl leukotrienes, so reactions are cross-reactive across all NSAIDs except weak COX inhibitors like paracetamol. The onset within minutes and cross-drug pattern exclude an IgE mechanism, and the timing excludes a delayed T cell reaction.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.