Colchicine prevents acute gout flares by a mechanism distinct from xanthine oxidase inhibitors and uricosurics. The mechanism is:
- A Inhibiting solubilisation of monosodium urate crystals in synovial fluid
- B Binding tubulin dimers and inhibiting microtubule polymerisation, thereby preventing neutrophil chemotaxis, degranulation, and NLRP3 inflammasome activation ✓
- C Blocking IL-1β receptor, reducing downstream inflammatory signalling
- D Inhibiting phospholipase A2, reducing prostaglandin and leukotriene synthesis in synovium
Correct answer: B. Binding tubulin dimers and inhibiting microtubule polymerisation, thereby preventing neutrophil chemotaxis, degranulation, and NLRP3 inflammasome activation
Explanation
Colchicine binds to β-tubulin, preventing tubulin polymerisation. This disrupts microtubule-dependent processes: neutrophil migration (chemotaxis), phagocytosis of urate crystals, and assembly of the NLRP3 inflammasome — which is the key platform for IL-1β processing in gout. Colchicine does not lower serum uric acid. Canakinumab targets the IL-1β receptor. Corticosteroids and NSAIDs are anti-inflammatory by different mechanisms. Colchicine also prevents pseudogout (CPPD crystal disease) flares by the same mechanism.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.