The Samter's triad consists of which combination of conditions, and aspirin sensitivity in this triad is mediated via which mechanism?

• A Asthma, nasal polyps, and penicillin allergy; IgE-mediated hypersensitivity
• B Allergic rhinitis, cystic fibrosis, and aspirin intolerance; CFTR mutation
• C Asthma, nasal polyps, and beta-blocker sensitivity; beta-2 receptor polymorphism
• D Asthma, nasal polyps, and NSAID/aspirin sensitivity; COX-1 inhibition shunting arachidonic acid towards leukotriene synthesis ✓

Explanation

Samter's triad (aspirin-exacerbated respiratory disease, AERD) is the combination of bronchial asthma, nasal polyps (eosinophilic CRS), and aspirin/NSAID intolerance. The mechanism is pharmacological (not IgE-mediated): aspirin inhibits COX-1, reducing prostaglandin E2 synthesis (which normally suppresses mast cells and eosinophils) and shunting arachidonic acid towards the 5-lipoxygenase pathway, massively increasing cysteinyl leukotriene (LTC4, LTD4) production and causing bronchoconstriction and nasal symptoms.

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.