进退两难：一位对多种P2Y拮抗剂耐药的高危患者。
Between a rock and a hard place: a high-risk patient with resistance to multiple P2Y antagonists.
作者信息
Davis Brittney H, Dillon Chrisly, Cai Anping, Williams Iii Lance A, Pamboukian Salpy V, Limdi Nita A
机构信息
Department of Neurology, School of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA 35294.
Department of Pathology, Division of Laboratory Medicine, University of Alabama at Birmingham, Birmingham, AL, USA 35249.
出版信息
Pharmacogenomics. 2019 May;20(7):475-481. doi: 10.2217/pgs-2018-0201.
Impaired response to P2Y receptor antagonists, such as clopidogrel and prasugrel, can have devastating consequences for patients that require prolonged or indefinite therapy with these agents, including those with a left ventricular assist device (LVAD). While loss-of-function (LOF) alleles in have been elucidated as contributing to high on treatment platelet reactivity (HTPR) during clopidogrel therapy, genetic variations in the metabolic pathway of prasugrel have not been shown to elicit this same effect. Moreover, limited studies have assessed the effect of coexisting genetic variations in pharmacokinetic and pharmacodynamic pathways. Herein, we report a left ventricular assist device patient exhibiting high on treatment platelet reactivity during clopidogrel and prasugrel therapy. Genotyping revealed variants in pharmacokinetic (), and pharmacodynamic pathways, with multiple variants in P2Y, the target receptor.
对P2Y受体拮抗剂（如氯吡格雷和普拉格雷）反应受损，对于需要长期或无限期使用这些药物进行治疗的患者，包括使用左心室辅助装置（LVAD）的患者，可能会产生灾难性后果。虽然已阐明某些基因的功能丧失（LOF）等位基因会导致氯吡格雷治疗期间出现高治疗中血小板反应性（HTPR），但尚未证明普拉格雷代谢途径中的基因变异会引发同样的效果。此外，仅有有限的研究评估了药代动力学和药效学途径中共存基因变异的影响。在此，我们报告了一名左心室辅助装置患者，在氯吡格雷和普拉格雷治疗期间表现出高治疗中血小板反应性。基因分型显示药代动力学（）和药效学途径存在变异，靶受体P2Y中有多个变异。
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