Abstract

Colchicine is a very ancient anti-inflammatory drug mainly indicated for the treatment and prophylaxis of gout and familial Mediterranean fever. Its mode of action is not completely elucidated but depends on microtubule formation, thereby affecting mitosis and other microtubule-dependent functions. It has a bioavailability of 25% to 50% when administered orally. Colchicine and its metabolites are excreted through the urinary and biliary tracts. Gastrointestinal side effects occur early and are most common manifestations of colchicine toxicity. Severe colchicine toxicity results in multiple organ failure, convulsions, coma, and death. Colchicine is metabolized by cytochrome P450 3A4 and is also a substrate for the P-gp transporter. Thus, if colchicine is co-administered with inhibitors of CYP3A4 and/or P-gp its systemic concentrations may be altered and may increase the risk for colchicine toxicity. These potential drug-drug interactions need a careful monitoring and a dosage adjustment. In conclusion, colchicine can be considered to be a relatively safe and effective medication when used in appropriate dosage in patients with normal kidney and liver function and if the drug-drug interactions are carefully considered.

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