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Is there is Need for Ubiquinone (CoQ10) Supplementation in Statin-Associated Myopathy?

机译:与他汀类药物相关的肌病是否需要补充泛醌(CoQ10)?

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Statins are currently the most effective drugs in reducing low-density lipoprotein cholesterol (LDL-C). Withtheir mechanism of action, by inhibiting 3-hydroxy-3 methylglutharyl coenzyme A reductase, statins decrease cholesterolproduction. The same biosynthetic pathway is shared by ubiquinone or coenzyme Q10. Statins block production ofdekaprenyl-4-benzoate, a precursor of coenzyme Q10 (CoQ10), which is an essential component in mitochondrialtransport system. Ubiquinone deficiency may affect oxidative phosphorylation and adenosine triphosphate production,which can subsequently result in impairing of muscle energy metabolism and contribute to development of myopathy.Statin therapy also decreases antioxidant status in the body, resulting in to increase in free radical damage to cells invarious parts of body; liver, nerves, muscles. Statins can decrease natural antioxidant protection present in our body andpredispose toxicity.Statin-associated myopathy is the most common side effect of statin treatment often lead to statin dose reduction, or therapy cessation, which can negatively affect cardiovascular risk management. The spectrum of statin-related myopathy ranges from common but clinically benign myalgia to rare but life-threatening rhabdomyolysis. Observational studies suggest that myalgia can occur in up to 10% of persons prescribed statins, whereas rhabdomyolysis continues to be rare. Statins lower circulating levels of CoQ10 up to 54%, whereas several studies did not confirmed a lowering of CoQ10 levels in muscles during statin therapy and the evidence was given also on low dose of statin therapy, which did not appear to reduce intramuscular levels of CoQ10 in symptomatic patients with statin myopathy. The conflicting results have been published on the impaired mitochondrial function, which was found during the analysis of the myocyte cells in patients treated with statins. The supplementation of CoQ10 results in increasing of serum CoQ10, but it is not clear if it relieves myopatic symptoms in statin treated patients. Yet available intervention studies reported contrasting results and just two of them proved benefit of CoQ10 supplementation. Hence coenzyme Q10 supplementation is not currently recommended for routine use in the prophylaxis of statin toxicity.
机译:他汀类药物是目前降低低密度脂蛋白胆固醇(LDL-C)的最有效药物。他汀类药物的作用机理是通过抑制3-羟基-3甲基戊二酰辅酶A还原酶来降低胆固醇的产生。泛醌或辅酶Q10具有相同的生物合成途径。他汀类药物可阻止辅酶Q10(CoQ10)的前体十氨基戊烯基-4-苯甲酸酯的生产,辅酶Q10是线粒体转运系统的重要组成部分。泛醌缺乏症可能会影响氧化磷酸化和三磷酸腺苷的产生,从而可能导致肌肉能量代谢受损并促进肌病的发展。他汀类药物疗法还可以降低体内的抗氧化剂状态,从而导致自由基损伤细胞的各个部位身体肝,神经,肌肉。他汀类药物会降低我们体内天然的抗氧化保护并增加毒性。他汀类药物相关的肌病是他汀类药物治疗的最常见副作用,通常会导致他汀类药物剂量减少或停止治疗,这可能会对心血管风险管理产生负面影响。他汀类药物相关的肌病的范围从普通但临床上良性的肌痛到罕见但危及生命的横纹肌溶解症。观察性研究表明,在处方他汀类药物的人群中,肌痛最多可发生10%,而横纹肌溶解症仍然很少见。他汀类药物可将CoQ10的循环水平降低多达54%,而几项研究并未证实他汀类药物治疗期间肌肉中CoQ10的水平降低,并且还提供了低剂量他汀类药物治疗的证据,这似乎并未降低肌肉内CoQ10的水平。在有症状的他汀类肌病患者中。关于线粒体功能受损的研究结果已经发表,这在他汀类药物治疗的患者的肌细胞分析中发现。补充辅酶Q10会导致血清辅酶Q10升高,但是尚不清楚他是否能缓解他汀类药物治疗患者的肌无力症状。然而,现有的干预研究报告了相反的结果,只有其中两个证明了辅酶Q10补充的益处。因此,目前不建议常规补充辅酶Q10来预防他汀类药物的毒性。

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