During an acute gout attack, colchicine is prescribed. Colchicine's anti-inflammatory effect in acute gout is primarily due to:
- A Inhibition of prostaglandin synthesis by blocking COX-1 and COX-2
- B Binding to tubulin dimers, preventing microtubule polymerisation and impairing neutrophil chemotaxis and degranulation ✓
- C Blocking IL-1beta receptor on synovial macrophages
- D Inhibiting NLRP3 inflammasome assembly directly
Explanation
Colchicine binds to tubulin dimers and prevents their polymerisation into microtubules. Since neutrophil migration (chemotaxis), phagocytosis, and degranulation all depend on intact microtubule-dependent cytoskeletal function, colchicine selectively inhibits neutrophil influx into the synovial space—attenuating the acute inflammatory response to urate crystals. It also inhibits crystal-induced IL-1beta secretion downstream of inflammasome activation but does not directly block the NLRP3 inflammasome (canakinumab and anakinra target IL-1beta itself). It has no COX-inhibiting activity.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.