The role of coenzyme Q10 in statin-associated myopathy - A systematic review
The role of coenzyme Q10 in statin-associated myopathy - A systematic review
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DOI：
10.1016/j.jacc.2007.02.049
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发表时间：
2007-06-12
影响因子：
24
通讯作者：
Thompson, Paul D.
中科院分区：
文献类型：
--
作者：
Marcoff, Leo;Thompson, Paul D.
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。虽然一般安全，他们已与各种肌病的投诉。他汀类药物阻断焦磷酸法呢酯的产生，焦磷酸法呢酯是合成泛醌或辅酶Q10（CoQ 10）的中间体。这一事实，加上辅酶Q10在线粒体能量产生中的作用，促使他汀类药物诱导的辅酶Q10缺乏参与他汀类药物肌病的发病机制的假设。我们通过PubMed检索到2006年8月，确定了与他汀类药物治疗和辅酶Q10水平相关的英文文章。摘要进行了审查，并详细检查了他汀类药物治疗和辅酶Q10水平之间的关系的文章。他汀类药物治疗降低循环水平的辅酶Q10。他汀类药物治疗对肌内辅酶Q10水平的影响尚不清楚，他汀类药物相关肌病症状患者肌内辅酶Q10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。补充可以提高辅酶Q10的循环水平，但关于辅酶Q10补充对肌病症状的影响的数据是稀缺和矛盾的。我们的结论是，没有足够的证据证明辅酶Q10缺乏在他汀类药物相关肌病中的病因作用，需要大型，精心设计的临床试验来解决这个问题。CoQ 10的常规使用不能推荐给他汀类药物治疗的患者。然而，这种补充剂没有已知的风险，并且有一些轶事和初步试验证据证明其有效性。因此，辅酶Q10可以在需要他汀类药物治疗的患者中进行测试，这些患者患有他汀类药物肌痛，并且不能用其他药物进行满意的治疗。一些患者可能会有反应，即使只是通过安慰剂效应。
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.