Colchicine's mechanism in acute gout differs from that of NSAIDs because colchicine:
- A Binds tubulin dimers, preventing polymerisation into microtubules and thereby inhibiting neutrophil chemotaxis, degranulation, and NLRP3 inflammasome assembly ✓
- B Inhibits xanthine oxidase, reducing uric acid synthesis
- C Blocks interleukin-1beta (IL-1β) directly by occupying its receptor on synovial macrophages
- D Inhibits COX-2-mediated prostaglandin synthesis in inflamed synovial tissue
Correct answer: A. Binds tubulin dimers, preventing polymerisation into microtubules and thereby inhibiting neutrophil chemotaxis, degranulation, and NLRP3 inflammasome assembly
Explanation
Colchicine binds beta-tubulin and prevents microtubule polymerisation. This disrupts neutrophil chemotaxis, phagocytosis of urate crystals, and the cytoskeletal rearrangements needed for NLRP3 inflammasome assembly and IL-1β processing. NSAIDs block COX; anakinra/canakinumab block IL-1β; allopurinol and febuxostat inhibit xanthine oxidase. Colchicine's mechanism is independent of prostaglandin synthesis.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.