Colchicine is used for acute gout attacks. Its primary mechanism in reducing gouty inflammation is:

• A Competitive inhibition of xanthine oxidase, reducing uric acid synthesis
• B Binding to tubulin dimers, preventing microtubule polymerisation and thereby blocking neutrophil chemotaxis and degranulation ✓
• C Inhibition of COX-2 in neutrophils, reducing prostaglandin-mediated inflammation
• D Activation of PPARγ in macrophages, suppressing IL-1β release

Explanation

Colchicine binds β-tubulin and prevents tubulin polymerisation into microtubules. Because neutrophil chemotaxis, phagocytosis, degranulation, and IL-1β secretion all depend on intact microtubule-dependent cytoskeletal function, colchicine impairs the neutrophil response to urate crystals without directly blocking xanthine oxidase or COX enzymes. It also inhibits NLRP3 inflammasome activation, reducing IL-1β maturation. Xanthine oxidase inhibition is allopurinol/febuxostat. COX-2 inhibition is celecoxib/indomethacin. PPARγ activation is not a primary mechanism of colchicine.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.