Rationale:

• As monosodium urate is mobilized from the soft tissues and joints, a supersaturated solution is present around these deposits that causes equilibrium between crystal formation and dissolution.
• The surfaces of new crystals are efficient in activating complement and initiating the inflammation cascade and promoting new gout attacks.
• These effects are down-regulated over time, as serum proteins deposited on the crystal surfaces “hide” the crystals.

Evidence:

• In a placebo-controlled study, prophylaxis with colchicine reduced attacks of acute gout by more than 50% over 6 months in patients given probenecid as the uric acid-lowering therapy (56).
• Reductions in the number and severity of gouty flares were seen in a placebo-controlled trial of colchicine for prophylaxis at the initiation of allopurinol for uric acid-lowering therapy (57).
• Three reviews give recommendations for use of colchicine in different clinical settings (58) and how to prevent colchicine toxicity (59; 60).
• The case of a patient taking colchicine who developed rhabdomyolyisis has been published (61).

Comments:

• Athough NSAIDs have not been specifically studied as prophylactic agents, they may be preferable when concomitantly treating an acute gout attack and pain from joint damage (osteoarthritis) that has already occurred.