Colchicine apparently exerts its effect by reducing the inflammatory response to the deposited crystals and also by diminishing phagocytosis. Colchicine diminishes lactic acid production by leukocytes both directly and by diminishing phagocytosis, thereby interrupting the cycle of urate crystal deposition and inflammatory response that sustains the acute attack. The precise biochemical step that is affected by colchicine is not yet known. The antimitotic activity of colchicine is unrelated to its effectiveness in the treatment of acute gout, as indicated by the fact that trimethylcolchicinic acid, an analog of colchicine, has no antimitotic activity except in extremely high doses. It is effective in relieving the pain of acute attacks, especially if therapy is begun early in the attack and in adequate dosage.
Many therapists use colchicine as interval therapy to prevent acute attacks of gout.
It has no effect on nongouty arthritis or on uric acid metabolism. The intravenous use of colchicine is advantageous when a rapid response is desired or when gastrointestinal side effects interfere with oral administration of the medication. Occasionally, intravenous colchicine is effective when the oral preparation is not. After the acute attack has subsided, the patient can usually be given colchicine tablets by mouth. Colchicine should not be given in the presence of combined renal and hepatic disease.