Montelukast, a cysteinyl leukotriene receptor antagonist, is most effective in which asthma phenotype?
- A Aspirin-exacerbated respiratory disease (AERD) / Samter's triad, where shunting of arachidonic acid to 5-lipoxygenase pathway produces excess leukotrienes ✓
- B Eosinophilic asthma with blood eosinophils >300 cells/μL requiring biologic therapy
- C Neutrophilic asthma triggered by occupational sensitizers
- D Allergic bronchopulmonary aspergillosis with central bronchiectasis
Explanation
In AERD (aspirin-exacerbated respiratory disease), COX-1 inhibition by aspirin or NSAIDs blocks prostaglandin E2 synthesis, which normally suppresses the 5-lipoxygenase (5-LOX) pathway. With PGE2 inhibited, arachidonic acid is shunted toward 5-LOX, producing massive cysteinyl leukotriene (CysLT: LTC4, LTD4, LTE4) excess. These potent bronchoconstrictors trigger bronchoconstriction, nasal polyposis, and urticaria in susceptible patients. Montelukast (CysLT1 receptor antagonist) is highly effective in this phenotype and also allows aspirin desensitization. Option B describes an indication for mepolizumab/benralizumab, not primarily montelukast.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.