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辅酶Q10:它有临床作用且有必要进行检测吗?

Coenzyme Q10: is there a clinical role and a case for measurement?

作者信息

Molyneux Sarah L, Young Joanna M, Florkowski Christopher M, Lever Michael, George Peter M

机构信息

Clinical Biochemistry Unit, Canterbury Health Laboratories, Christchurch, New Zealand.

出版信息

Clin Biochem Rev. 2008 May;29(2):71-82.

PMID:18787645
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2533152/
Abstract

Coenzyme Q(10) (CoQ(10)) is an essential cofactor in the mitochondrial electron transport pathway, and is also a lipid-soluble antioxidant. It is endogenously synthesised via the mevalonate pathway, and some is obtained from the diet. CoQ(10) supplements are available over the counter from health food shops and pharmacies. CoQ(10) deficiency has been implicated in several clinical disorders, including but not confined to heart failure, hypertension, Parkinson's disease and malignancy. Statin, 3-hydroxy-3- methyl-glutaryl (HMG)-CoA reductase inhibitor therapy inhibits conversion of HMG-CoA to mevalonate and lowers plasma CoQ(10) concentrations. The case for measurement of plasma CoQ(10) is based on the relationship between levels and outcomes, as in chronic heart failure, where it may identify individuals most likely to benefit from supplementation therapy. During CoQ(10) supplementation plasma CoQ(10) levels should be monitored to ensure efficacy, given that there is variable bioavailability between commercial formulations, and known inter-individual variation in CoQ(10) absorption. Knowledge of biological variation and reference change values is important to determine whether a significant change in plasma CoQ(10) has occurred, whether a reduction for example following statin therapy or an increase following supplementation. Emerging evidence will determine whether CoQ(10) does indeed have an important clinical role and in particular, whether there is a case for measurement.

摘要

辅酶Q(10)(CoQ(10))是线粒体电子传递途径中的一种必需辅助因子,也是一种脂溶性抗氧化剂。它通过甲羟戊酸途径内源性合成,也可从饮食中获取。CoQ(10)补充剂可在健康食品店和药店非处方购买。CoQ(10)缺乏与多种临床疾病有关,包括但不限于心力衰竭、高血压、帕金森病和恶性肿瘤。他汀类药物,即3-羟基-3-甲基戊二酰辅酶A(HMG)-CoA还原酶抑制剂疗法,可抑制HMG-CoA向甲羟戊酸的转化,并降低血浆CoQ(10)浓度。检测血浆CoQ(10)的依据是其水平与治疗结果之间的关系,如在慢性心力衰竭中,它可能识别出最有可能从补充疗法中获益的个体。在补充CoQ(10)期间,应监测血浆CoQ(10)水平以确保疗效,因为不同商业制剂之间的生物利用度存在差异,且已知个体间CoQ(10)吸收存在差异。了解生物学变异和参考变化值对于确定血浆CoQ(10)是否发生了显著变化很重要,例如他汀类药物治疗后降低或补充后升高。新出现的证据将确定CoQ(10)是否确实具有重要的临床作用,特别是是否有检测的必要。

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