Marcoff Leo, Thompson Paul D
Section of Cardiology, Department of Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
J Am Coll Cardiol. 2007 Jun 12;49(23):2231-7. doi: 10.1016/j.jacc.2007.02.049.
Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are currently the most effective medications for reducing low-density lipoprotein cholesterol concentrations. Although generally safe, they have been associated with a variety of myopathic complaints. Statins block production of farnesyl pyrophosphate, an intermediate in the synthesis of ubiquinone or coenzyme Q10 (CoQ10). This fact, plus the role of CoQ10 in mitochondrial energy production, has prompted the hypothesis that statin-induced CoQ10 deficiency is involved in the pathogenesis of statin myopathy. We identified English language articles relating statin treatment and CoQ10 levels via a PubMed search through August 2006. Abstracts were reviewed and articles addressing the relationship between statin treatment and CoQ10 levels were examined in detail. Statin treatment reduces circulating levels of CoQ10. The effect of statin therapy on intramuscular levels of CoQ10 is not clear, and data on intramuscular CoQ10 levels in symptomatic patients with statin-associated myopathy are scarce. Mitochondrial function may be impaired by statin therapy, and this effect may be exacerbated by exercise. Supplementation can raise the circulating levels of CoQ10, but data on the effect of CoQ10 supplementation on myopathic symptoms are scarce and contradictory. We conclude that there is insufficient evidence to prove the etiologic role of CoQ10 deficiency in statin-associated myopathy and that large, well-designed clinical trials are required to address this issue. The routine use of CoQ10 cannot be recommended in statin-treated patients. Nevertheless, there are no known risks to this supplement and there is some anecdotal and preliminary trial evidence of its effectiveness. Consequently, CoQ10 can be tested in patients requiring statin treatment, who develop statin myalgia, and who cannot be satisfactorily treated with other agents. Some patients may respond, if only via a placebo effect.
他汀类药物（3-羟基-3-甲基戊二酰辅酶A还原酶抑制剂）是目前降低低密度脂蛋白胆固醇浓度最有效的药物。尽管总体安全，但它们与多种肌病主诉有关。他汀类药物可阻断法尼基焦磷酸的生成，而法尼基焦磷酸是辅酶Q10（CoQ10）合成过程中的一种中间体。这一事实，再加上CoQ10在线粒体能量产生中的作用，促使人们提出假说，即他汀类药物诱导的CoQ10缺乏与他汀类药物性肌病的发病机制有关。我们通过检索截至2006年8月的PubMed，确定了与他汀类药物治疗和CoQ10水平相关的英文文章。对摘要进行了审查，并详细研究了涉及他汀类药物治疗与CoQ10水平关系的文章。他汀类药物治疗可降低循环中的CoQ10水平。他汀类药物治疗对肌肉内CoQ10水平的影响尚不清楚，且关于他汀类药物相关性肌病症状患者肌肉内CoQ10水平的数据很少。他汀类药物治疗可能会损害线粒体功能，运动可能会加剧这种影响。补充CoQ10可提高循环中的CoQ10水平，但关于补充CoQ10对肌病症状影响的数据很少且相互矛盾。我们得出结论，没有足够的证据证明CoQ10缺乏在他汀类药物相关性肌病中的病因学作用，需要进行大规模、设计良好的临床试验来解决这个问题。不建议在接受他汀类药物治疗的患者中常规使用CoQ10。然而，这种补充剂没有已知风险，并且有一些轶事和初步试验证据表明其有效。因此，对于需要接受他汀类药物治疗、出现他汀类药物性肌痛且无法用其他药物得到满意治疗的患者，可以试用CoQ10。一些患者可能会有反应，即便只是通过安慰剂效应。
