Colchicine Mechanism — SCE Rheumatology MCQ
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Correct answer: D — Binding to tubulin and inhibition of microtubule polymerisation
Colchicine binds tubulin and prevents microtubule polymerisation. This disrupts microtubule-dependent neutrophil functions — chemotaxis, adhesion and recruitment — and impairs NLRP3 inflammasome activation, blunting the interleukin-1 beta-driven response to monosodium urate crystals. It does not alter serum urate, so it treats the flare rather than the underlying hyperuricaemia. Cyclo-oxygenase inhibition is the mechanism of NSAIDs, an alternative first-line flare therapy, which is why option E is tempting. Xanthine oxidase inhibition describes allopurinol and febuxostat, and direct interleukin-1 beta neutralisation describes biologics such as canakinumab, used in refractory gout; neither is colchicine's action. Complement C5 inhibition (eculizumab) treats complement-mediated disorders and has no role in crystal arthritis.
Reference: Dalbeth N, Lauterio TJ, Wolfe HR. Mechanism of action of colchicine in the treatment of gout. Clinical Therapeutics 2014;36(10):1465–79. https://pubmed.ncbi.nlm.nih.gov/25151572/