Alayli Gamze, Cengiz Kivanç, Cantürk Ferhan, Durmuş Dilek, Akyol Yeşim, Menekşe Elif B
Department of Physical Medicine and Rehabilitation, Medical Faculty, Ondokuz Mayis University, Samsun, Turkey.
Ann Pharmacother. 2005 Jul-Aug;39(7-8):1358-61. doi: 10.1345/aph.1E593. Epub 2005 May 24.
To report a case of acute myopathy after concomitant use of colchicine and pravastatin.
A 65-year-old woman was admitted to the hospital with an acute episode of gout. She had been taking pravastatin 20 mg once daily for 6 years. On admission, blood urea nitrogen and serum creatinine levels were 48 mg/dL and 1.3 mg/dL, respectively. Colchicine 1.5 mg/day was added to the treatment regimen, but 20 days after the initiation of colchicine therapy, symmetrical proximal muscle weakness developed in the woman's legs. Physical examination, laboratory findings, and electromyelogram findings suggested myopathy. The Naranjo probability scale indicated a probable relationship between myopathy and combined therapy. Seven days after discontinuation of colchicine and pravastatin, the patient's weakness improved and enzyme levels returned to normal. Colchicine was restarted at 1.0 mg/day 5 days later; no myopathy occurred.
Hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) and colchicine are known to cause myopathy. Most of the statins and colchicine are biotransformed in the liver primarily by the CYP3A4 system, which may increase the risk of myopathy when concurrent therapy is used. However, pravastatin is not primarily metabolized by cytochrome P450 isoenzymes. The cause of myopathy in our patient may be related to the interaction of colchicine and pravastatin via P-glycoprotein. In addition, the presence of mild renal dysfunction could have contributed to the development of myopathy.
We suggest that clinicians be aware that neuromuscular toxicity can occur in patients with mild renal dysfunction with combined use of colchicine and pravastatin.
报告一例秋水仙碱与普伐他汀联合使用后发生急性肌病的病例。
一名65岁女性因痛风急性发作入院。她每日服用20mg普伐他汀，已服用6年。入院时，血尿素氮和血清肌酐水平分别为48mg/dL和1.3mg/dL。治疗方案中加用了秋水仙碱，每日1.5mg，但在秋水仙碱治疗开始20天后，该女性双下肢出现对称性近端肌无力。体格检查、实验室检查结果及肌电图检查结果提示为肌病。Naranjo概率量表显示肌病与联合治疗之间可能存在关联。停用秋水仙碱和普伐他汀7天后，患者肌无力症状改善，酶水平恢复正常。5天后，秋水仙碱以每日1.0mg的剂量重新开始使用；未发生肌病。
已知羟甲基戊二酰辅酶A还原酶抑制剂（他汀类药物）和秋水仙碱可引起肌病。大多数他汀类药物和秋水仙碱主要在肝脏中通过CYP3A4系统进行生物转化，联合使用时可能增加肌病风险。然而，普伐他汀并非主要通过细胞色素P450同工酶代谢。我们患者发生肌病的原因可能与秋水仙碱和普伐他汀通过P-糖蛋白的相互作用有关。此外，轻度肾功能不全的存在可能促使了肌病的发生。
我们建议临床医生应意识到，轻度肾功能不全患者联合使用秋水仙碱和普伐他汀时可能发生神经肌肉毒性。
