A patient with acute gout is treated with colchicine. The drug's anti-inflammatory mechanism in gout specifically involves:
- A Binding to tubulin heterodimers and preventing their polymerisation, disrupting neutrophil microtubule-dependent functions including crystal phagocytosis and inflammasome assembly ✓
- B Inhibition of xanthine oxidase, reducing uric acid production during the acute attack
- C Blockade of P2X7 ATP receptor on neutrophils, preventing NLRP3 activation
- D Inhibition of prostaglandin synthesis by competing with arachidonic acid at COX active sites
Explanation
Colchicine binds to tubulin heterodimers (alpha-beta tubulin) and prevents their polymerisation into microtubules. This disrupts multiple neutrophil functions critical to acute gout: it inhibits neutrophil chemotaxis toward urate crystals, impairs phagocytosis of crystals by pseudopod formation (which requires microtubule dynamics), and disrupts NLRP3 inflammasome assembly (which is microtubule-dependent). The net effect is dramatic reduction of neutrophil-driven acute inflammation in the joint. Colchicine does not lower uric acid levels and has no effect on prostaglandin synthesis or P2X7 receptors as primary mechanisms.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.