{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T12:51:13Z","timestamp":1769172673527,"version":"3.49.0"},"reference-count":36,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2017,3,14]],"date-time":"2017-03-14T00:00:00Z","timestamp":1489449600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100006191","name":"Eski\u015fehir Osmangazi \u00dcniversitesi","doi-asserted-by":"publisher","award":["201211017"],"award-info":[{"award-number":["201211017"]}],"id":[{"id":"10.13039\/501100006191","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Basic Clin Pharma Tox"],"published-print":{"date-parts":[[2017,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Clopidogrel inhibits platelet activation and aggregation by blocking the P2Y<jats:sub>12<\/jats:sub> receptor. Dual antiplatelet therapy with clopidogrel and aspirin is recommended treatment by current guidelines for patients undergoing percutaneous interventions. Recurrent ischaemic cardiac events after this treatment showed lack of clopidogrel responsiveness. We aimed to investigate the most noticeable variants in the genes involved in clopidogrel pharmacokinetics and pharmacodynamics. A total of 347 Turkish patients who underwent percutaneous coronary interventions with stent implantation were included in our study. Platelet reactivity (<jats:styled-content style=\"fixed-case\">PRU<\/jats:styled-content>) and % inhibition were measured with VerifyNow P2Y<jats:sub>12<\/jats:sub> assay in blood samples collected from patients who took a standard dose of clopidogrel (75 mg\/day) for at least 7 days. The variants in the <jats:italic><jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>2C19<\/jats:italic>,<jats:italic> <jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>3A4<\/jats:italic>,<jats:italic> <jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>2B6<\/jats:italic>,<jats:italic> <jats:styled-content style=\"fixed-case\">ABCB<\/jats:styled-content>1<\/jats:italic>,<jats:italic> <jats:styled-content style=\"fixed-case\">ITGB<\/jats:styled-content>3<\/jats:italic> and <jats:italic><jats:styled-content style=\"fixed-case\">PON<\/jats:styled-content>1<\/jats:italic> genes were genotyped using the Sequenom Mass<jats:styled-content style=\"fixed-case\">ARRAY<\/jats:styled-content> system. When grouped, the patients with <jats:styled-content style=\"fixed-case\">PRU<\/jats:styled-content> values &gt;208 as non\u2010responsiveness to clopidogrel therapy; 104 (30%) patients were non\u2010responders and 243 (70%) patients were responders. A significant association was found between the <jats:italic><jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>2C19*2<\/jats:italic> (G636A) polymorphism and non\u2010responsiveness to clopidogrel therapy (<jats:italic>p<\/jats:italic> &lt; 0.001). An allele frequency of this single nucleotide polymorphism was high in non\u2010responders; its odds ratio was 2.92 compared with G allele (<jats:italic>p<\/jats:italic> &lt; 0.001). <jats:styled-content style=\"fixed-case\">PRU<\/jats:styled-content> values of <jats:styled-content style=\"fixed-case\">CT<\/jats:styled-content> genotypes were lower (<jats:italic>p<\/jats:italic> = 0.029) and % inhibition values of <jats:styled-content style=\"fixed-case\">CT<\/jats:styled-content> genotypes were higher (<jats:italic>p<\/jats:italic> = 0.008) compared with <jats:styled-content style=\"fixed-case\">CC<\/jats:styled-content> genotypes for the <jats:italic><jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>2C19*17<\/jats:italic> (C806T) polymorphism. None of the other genetic variants were found to be statistically associated with non\u2010responsiveness to clopidogrel and antiplatelet activity. Our findings suggest that the <jats:italic><jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>2C19*2<\/jats:italic> polymorphism is associated with non\u2010responsiveness to clopidogrel therapy and the <jats:italic><jats:styled-content style=\"fixed-case\">CYP<\/jats:styled-content>2C19*17<\/jats:italic> polymorphism enhances antiplatelet activity of clopidogrel. Depending on haplotypes of these two polymorphisms, clopidogrel\u2010treated patients can be protected or not from stent thrombosis and ischaemic events.<\/jats:p>","DOI":"10.1111\/bcpt.12763","type":"journal-article","created":{"date-parts":[[2017,1,30]],"date-time":"2017-01-30T22:56:57Z","timestamp":1485817017000},"page":"29-36","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["The <i>CYP2C19*2<\/i> and <i>CYP2C19*17<\/i> Polymorphisms play a Vital Role in Clopidogrel Responsiveness after Percutaneous Coronary Intervention: A Pharmacogenomics Study"],"prefix":"10.1111","volume":"121","author":[{"given":"Faruk","family":"Saydam","sequence":"first","affiliation":[{"name":"Department of Medical Biology and Genetics Faculty of Medicine Recep Tayyip Erdo\u011fan University Rize 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