The exact mechanism of action of colchicine in gout is not completely known, but it involves (1) a reduction in lactic acid production by leukocytes, which results in a decrease in uric acid deposition, and (2) a reduction in phagocytosis, with abatement of the inflammatory response.

Colchicine is not an analgesic, though it relieves pain in acute attacks of gout. It is not a uricosuric agent and will not prevent progression of gout to chronic gouty arthritis. It does have a prophylactic, suppressive effect that helps to reduce the incidence of acute attacks and to relieve the residual pain and mild discomfort that patients with gout occasionally feel.

In man and certain other animals, colchicine can produce a temporary leukopenia that is followed by leukocytosis.

Colchicine has other pharmacologic actions in animals: it alters neuromuscular function, intensifies gastrointestinal activity by neurogenic stimulation, increases sensitivity to central depressants, heightens response to sympathomimetic compounds, depresses the respiratory center, constricts blood vessels, causes hypertension by central vasomotor stimulation, and lowers body temperature.

Colchicine is rapidly absorbed after oral administration. Large amounts of the drug and metabolites enter the intestinal tract in bile and intestinal secretions. High concentrations of colchicine are found in the kidney, liver, and spleen, as well. Colchicine does not appear to be tightly bound to serum protein, hence the drug rapidly leaves the blood stream. Excretion occurs primarily by biliary and renal routes.

Last reviewed on RxList: 10/4/2010
This monograph has been modified to include the generic and brand name in many instances.