Between a rock and a hard place: a high-risk patient with resistance to multiple P2Y antagonists.

Pharmacogenomics 2019 05;20(7):475-481

Department of Neurology, School of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA 35294.

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.

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Source
https://www.futuremedicine.com/doi/10.2217/pgs-2018-0201
Publisher Site
http://dx.doi.org/10.2217/pgs-2018-0201DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6563016PMC
May 2019
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