Montelukast is effective in aspirin-exacerbated respiratory disease (Samter's triad) because it blocks:
- A COX-1 enzyme, preventing formation of prostaglandins that trigger bronchospasm
- B Cysteinyl leukotriene receptor 1 (CysLT1), blocking the bronchoconstriction and mucosal edema caused by LTC4/D4/E4 that accumulate due to shunting of arachidonate from COX to 5-LOX when COX is inhibited by aspirin ✓
- C 5-lipoxygenase directly, preventing leukotriene synthesis
- D H1 histamine receptors in bronchial smooth muscle, preventing aspirin-induced mast cell degranulation
Explanation
In aspirin-exacerbated respiratory disease, COX-1 inhibition by aspirin diverts arachidonic acid to the 5-lipoxygenase (5-LOX) pathway, causing overproduction of cysteinyl leukotrienes (LTC4, LTD4, LTE4). These bind CysLT1 receptors on bronchial smooth muscle and airways, causing bronchoconstriction, mucosal edema, and hypersecretion. Montelukast (a CysLT1 receptor antagonist) blocks this effect. Zileuton is the 5-LOX inhibitor (option C). Montelukast is thus a key add-on therapy for Samter's triad patients requiring NSAID-containing analgesics or who need desensitization.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.