Hsu Wei-Chih, Chen Wei-Hung, Chang Ming-Tsung, Chiu Hou-Chang
Department of Neurology, Shin-Kong WHS Memorial Hospital, Taipei, Taiwan.
Clin Neuropharmacol. 2002 Sep-Oct;25(5):266-8. doi: 10.1097/00002826-200209000-00008.
Colchicine and 3-hydroxy-3-methy-glutaryl coenzyme A (HMG-CoA) reductase inhibitors are well known to cause myopathy. Myotoxicity is dose-dependent in both drugs; therefore, the onset of symptoms usually takes months or years. We report the case of a patient with chronic renal failure who had been taking simvastatin for 2 years and developed acute weakness 2 weeks after the start of treatment with colchicines for recurrent gout. The electromyography and elevated muscle enzymes indicated that his symptoms were caused by myopathy. When this patient stopped taking both drugs, his weakness resolved rapidly. Acute myopathy induced by combination therapy with colchicines and simvastatin is rare. In patients with chronic renal failure, co-administration of colchicine with simvastatin may accelerate the onset of myopathy because CYP3A4 (part of cytochrome P450) is crucial in the breakdown of both drugs. When adding colchicine to a medication regimen that includes a HMG-CoA reductase inhibitor for patients with renal insufficiency, drugs that are metabolized outside the CYP3A4 system (e.g., fluvastatin and pravastatin) should be selected instead.
秋水仙碱和3-羟基-3-甲基戊二酰辅酶A（HMG-CoA）还原酶抑制剂众所周知会引起肌病。这两种药物的肌毒性均呈剂量依赖性；因此，症状通常在数月或数年后出现。我们报告了一例慢性肾衰竭患者，该患者服用辛伐他汀2年，在开始使用秋水仙碱治疗复发性痛风2周后出现急性肌无力。肌电图和肌肉酶升高表明其症状由肌病引起。当该患者停用这两种药物后，肌无力迅速缓解。秋水仙碱与辛伐他汀联合治疗引起的急性肌病较为罕见。在慢性肾衰竭患者中，秋水仙碱与辛伐他汀合用可能会加速肌病的发作，因为细胞色素P450的一部分CYP3A4在这两种药物的分解中起关键作用。对于肾功能不全且正在服用HMG-CoA还原酶抑制剂的患者，当在药物治疗方案中添加秋水仙碱时，应选择在CYP3A4系统外代谢的药物（如氟伐他汀和普伐他汀）。
