Zileuton is used in aspirin-exacerbated respiratory disease (AERD/Samter's triad). Its mechanism that specifically addresses the pathophysiology of AERD is:

• A Blockade of leukotriene receptors CysLT1 and CysLT2 preventing bronchoconstriction
• B Inhibition of phospholipase A2 preventing arachidonic acid release from membranes
• C COX-1 inhibition at low doses selectively blocking pathological prostaglandin formation
• D Inhibition of 5-lipoxygenase preventing synthesis of all leukotrienes including LTB4 and cysteinyl leukotrienes ✓

Explanation

In AERD, aspirin inhibits COX, shunting arachidonic acid into the 5-lipoxygenase pathway with overproduction of cysteinyl leukotrienes (LTC4, LTD4, LTE4) causing bronchoconstriction and nasal polyps. Zileuton directly inhibits 5-lipoxygenase (5-LOX), blocking synthesis of ALL leukotrienes including LTB4 (neutrophil chemotaxis) and cysteinyl leukotrienes. Montelukast/zafirlukast block only CysLT1 receptors (leukotriene receptor antagonists), so zileuton provides more complete blockade of the pathway.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.