Objective: To report a case of drug interaction leading to rhabdomyolysis. Case Summary: A 65-year old woman suf-fering from chronic atrial fibrillation was treated with amiodarone and acenocoumarol. Two weeks after a...Objective: To report a case of drug interaction leading to rhabdomyolysis. Case Summary: A 65-year old woman suf-fering from chronic atrial fibrillation was treated with amiodarone and acenocoumarol. Two weeks after administration of conventional dosage of colchicine for pericarditis, the patient developed rhabdomyolysis. colchicine-induced rhabdomyolysis was suspected. Colchicine was stopped and the patient underwent supportive therapy. Clinical symptoms improved rapidly. Discussion: Colchicine-induced neuromuscular toxicity and rhabdomyolysis have been reported with chronic treatment in therapeutic doses. Concomitant use of several drugs with colchicine may potentiate the development of myopathy. In our case, a co-administration of colchicine, a well known substrate of cytochrome P450 3A4 and P-glycoprotein, and amiodarone had possibly precipitated rhabdomyolysis. Amiodarone may increase colchicine toxicity by a dual mechanism. Amiodarone inhibits P-glycoprotein which may theoretically result in increased intrace- llular colchicine concentrations and decreased hepatic and renal excretion of the drug. Conclusion: Amiodarone may potentiate the development of colchicine-induced rhabdomyolysis.展开更多
文摘Objective: To report a case of drug interaction leading to rhabdomyolysis. Case Summary: A 65-year old woman suf-fering from chronic atrial fibrillation was treated with amiodarone and acenocoumarol. Two weeks after administration of conventional dosage of colchicine for pericarditis, the patient developed rhabdomyolysis. colchicine-induced rhabdomyolysis was suspected. Colchicine was stopped and the patient underwent supportive therapy. Clinical symptoms improved rapidly. Discussion: Colchicine-induced neuromuscular toxicity and rhabdomyolysis have been reported with chronic treatment in therapeutic doses. Concomitant use of several drugs with colchicine may potentiate the development of myopathy. In our case, a co-administration of colchicine, a well known substrate of cytochrome P450 3A4 and P-glycoprotein, and amiodarone had possibly precipitated rhabdomyolysis. Amiodarone may increase colchicine toxicity by a dual mechanism. Amiodarone inhibits P-glycoprotein which may theoretically result in increased intrace- llular colchicine concentrations and decreased hepatic and renal excretion of the drug. Conclusion: Amiodarone may potentiate the development of colchicine-induced rhabdomyolysis.
