Kassardjian Charles D, Tian Xia, Vladutiu Georgirene, Wong Lee-Jun, Milone Margherita
Department of Neurology, Mayo Clinic, Rochester, MN, USA.
Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
J Neurol Sci. 2014 Dec 15;347(1-2):380-2. doi: 10.1016/j.jns.2014.10.037. Epub 2014 Oct 31.
Ranolazine is a medication indicated for treatment of chronic angina and is a partial inhibitor of the fatty acid β-oxidation. We present an adult patient who developed subacute progressive muscle weakness and exercise-induced myalgia, soon after increasing the daily dose of ranolazine, in the setting of therapy with simvastatin. CK persisted normal throughout the duration of the weakness and muscle biopsy showed a lipid storage myopathy for which no underlying genetic defect was identified. Discontinuation of both drugs resulted in clinical improvement. Although simvastatin may have contributed to the myopathy, the temporal relation between the increase in ranolazine dose and the onset of the weakness would favor ranolazine as major culprit for the weakness.
雷诺嗪是一种用于治疗慢性心绞痛的药物，是脂肪酸β氧化的部分抑制剂。我们报告一名成年患者，在增加雷诺嗪每日剂量后不久，在接受辛伐他汀治疗的情况下，出现了亚急性进行性肌无力和运动诱发的肌痛。在肌无力持续期间，肌酸激酶一直正常，肌肉活检显示为脂质贮积性肌病，未发现潜在的基因缺陷。停用这两种药物后临床症状改善。虽然辛伐他汀可能促成了肌病，但雷诺嗪剂量增加与肌无力发作之间的时间关系表明，雷诺嗪是肌无力的主要罪魁祸首。
