A 45-year-old asthmatic with nasal polyposis and aspirin sensitivity presents with recurrent nasal polyps after two prior polypectomies. This clinical triad is known as Samter's triad (aspirin-exacerbated respiratory disease). The pathomechanism primarily involves:
- A IgE-mediated mast cell degranulation to aspirin as a true allergic reaction
- B Aspirin-induced IL-4 production leading to Th2-dominant B-cell class switching to IgG4
- C Aspirin inhibiting COX-2 causing prostaglandin E2 deficiency with paradoxical TXA2 excess
- D COX-1 inhibition by aspirin shunting arachidonic acid to the 5-lipoxygenase pathway, overproducing leukotriene C4/D4/E4 causing bronchoconstriction and eosinophilic mucosal inflammation ✓
Explanation
Samter's triad (AERD) is a non-allergic pseudo-allergy caused by COX-1 inhibition by aspirin/NSAIDs, not IgE-mediated. When COX-1 is blocked, arachidonic acid is shunted entirely to the 5-lipoxygenase pathway, massively overproducing cysteinyl leukotrienes (LTC4, LTD4, LTE4), which are potent bronchoconstrictors and eosinophil chemoattractants. Prostaglandin E2 (which normally suppresses mast cells) is also depleted. Management includes leukotriene receptor antagonists (montelukast), aspirin desensitization, and dupilumab (anti-IL-4/IL-13) which is now approved for AERD-associated nasal polyps.
Reference: Dhingra Diseases of Ear, Nose and Throat, 7th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.