Molecular mechanisms of statin intolerance.
Molecular mechanisms of statin intolerance.
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DOI：
10.5114/aoms.2016.59938
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发表时间：
2016-06-01
期刊：
影响因子：
--
通讯作者：
Banach M
中科院分区：
文献类型：
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作者：
Gluba-Brzozka A;Franczyk B;Toth PP;Rysz J;Banach M
他汀类药物在一级和二级预防中可降低心血管疾病发病率和死亡率。尽管他汀类药物有效，但由于肝毒性和肌痛/肌病等不良事件，许多人无法耐受他汀类药物。在大多数患者的情况下，肝脏和肌肉酶的轻度至中度异常似乎不是严重的不良反应，也不会超过降低冠心病风险的益处。归因于他汀类药物使用的死亡或永久性器官损伤的风险非常小，仅限于肌病和横纹肌溶解症病例。他汀类药物诱导的肌肉相关不良事件包括一种高度异质性的临床疾病，具有众多复杂的病因和各种遗传背景。每一个出现他汀类药物相关副作用的患者都不能进行包括所有这些机制的详尽分子表征。通常，唯一的解决方案是停止他汀类药物治疗/减少剂量或尝试低剂量间歇给药策略。
Statins reduce cardiovascular morbidity and mortality in primary and secondary prevention. Despite their efficacy, many persons are unable to tolerate statins due to adverse events such as hepatotoxicity and myalgia/myopathy. In the case of most patients, it seems that mild-to-moderate abnormalities in liver and muscle enzymes are not serious adverse effects and do not outweigh the benefits of coronary heart disease risk reduction. The risk for mortality or permanent organ damage ascribed to statin use is very small and limited to cases of myopathy and rhabdomyolysis. Statin-induced muscle-related adverse events comprise a highly heterogeneous clinical disorder with numerous, complex etiologies and a variety of genetic backgrounds. Every patient who presents with statin-related side effects cannot undergo the type of exhaustive molecular characterization that would include all of these mechanisms. Frequently the only solution is to either discontinue statin therapy/reduce the dose or attempt intermittent dosing strategies at a low dose.