Samter's triad (also called aspirin-exacerbated respiratory disease, AERD) consists of which three components, and what is the underlying eicosanoid mechanism?

• A Nasal polyps + asthma + aspirin sensitivity; mechanism = COX-1 inhibition causing leukotriene (LTC4/LTD4) excess due to arachidonic acid shunting to the lipoxygenase pathway ✓
• B Nasal polyps + asthma + aspirin hypersensitivity; mechanism = COX-2 upregulation with prostaglandin E2 excess
• C Rhinitis + eczema + penicillin allergy; mechanism = IgE-mediated
• D Sinusitis + bronchiectasis + situs inversus (Kartagener's syndrome)

Explanation

Samter's triad (AERD) = nasal polyps + intrinsic asthma + aspirin/NSAID sensitivity (COX-1 inhibitors). When COX-1 is inhibited, arachidonic acid is shunted into the 5-lipoxygenase (5-LOX) pathway, generating excess leukotrienes (LTC4, LTD4, LTE4), which are potent bronchoconstrictors and pro-inflammatory mediators causing bronchoconstriction and nasal reactions within 30–180 minutes of aspirin ingestion. Leukotriene modifiers (montelukast) are useful adjuncts; dupilumab and aspirin desensitization are emerging treatments.

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.