The patient has gout, which is due to precipitation of monosodium urate crystals in joint spaces (notably the great toe) and soft tissues (causing tophi, which are often found on the external ears). Colchicine reduces the inflammation caused by the urate crystals by inhibiting leukocyte migration and phagocytosis secondary to an effect on microtubule assembly. Allopurinol and its metabolite, oxypurinol, inhibit xanthine oxidase, the enzyme that forms uric acid from hypoxanthine. Therapy with this agent should be begun 1-2 weeks after the acute attack has subsided. Aspirin competes with uric acid for tubular secretion, thereby decreasing urinary urate excretion and raising serum uric acid levels. At high doses (more than 2 gm daily) aspirin is a uricosuric. Probenecid and sulfinpyrazone are uricosuric agents, increasing the urinary excretion of uric acid, hence decreasing serum levels of the substance. Therapy with these agents should be begun 1-2 weeks after the acute attack has subsided. Ref: Grosser T., Smyth E. (2011). Chapter 34. Anti-inflammatory, Antipyretic, and Analgesic Agents; Pharmacotherapy of Gout. In B.C. Knollmann (Ed), Goodman & Gilman's The Pharmacological Basis of Therapeutics, 12e.