Colchicine treats acute gout flares. Its primary anti-inflammatory mechanism in gout is:

• A Inhibiting xanthine oxidase to reduce uric acid synthesis
• B Blocking prostaglandin synthesis via COX-1 inhibition in synovial tissue
• C Binding tubulin dimers and inhibiting neutrophil microtubule polymerisation, impairing chemotaxis and inflammasome activation ✓
• D Competitively blocking urate reabsorption at URAT-1 in renal proximal tubule

Explanation

Colchicine binds beta-tubulin and prevents microtubule polymerisation. This disrupts neutrophil functions critically dependent on an intact cytoskeleton: migration (chemotaxis) to the joint, phagocytosis of monosodium urate crystals, and NLRP3 inflammasome assembly (which would otherwise produce IL-1beta to amplify the inflammatory cascade). Colchicine does not lower urate levels and has no COX inhibitory activity. Xanthine oxidase is inhibited by allopurinol/febuxostat; URAT-1 is blocked by lesinurad and benzbromarone.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.