Balkan Journal of Medical Genetics

EFFECTS OF CYP2C19 AND P2Y12 GENE POLYMORPHISMS ON CLINICAL RESULTS OF PATIENTS USING CLOPIDOGREL AFTER ACUTE ISCHEMIC CEREBROVASCULAR DISEASE
Sen HM1,*, Silan F2, Silan C3, Degirmenci Y4, Ozisik Kamaran HI1
*Corresponding Author: Halil Murat Sen, M.D., Department of Neurology, School of Medicine, Çanakkale Onsekiz Mart Üniversity, Barboros Mah., Terzioðlu Kampüsü, Týp Fakültesi, Çanakkale, Turkey. Tel : +90-286-218-37-38. Fax : +90-286-218-00-18. E-mail: hmuratsen@gmail.com
page: 37

INTRODUCTION

Clopidogrel is used as a prophylactic monotherapy to prevent the development of a new attack of ischemic cerebrovascular disease (ICVD) [1]. Stroke is a major cause of disability and death, and affects nearly 16 million people globally each year [2]. As ICVD cause a high rate of morbidity and mortality, the importance of effective prophylactic treatment increases. The clinical benefits of clopidogrel occur due to its inhibition of thrombocyte activation and aggregation [3,4]. Clopidogrel is actually a prodrug and transforms to active metabolite through CY2C19 enzyme in the cytochrome P450 (CYP450) enzyme family in the liver. As a result of CYP2C19 gene polymorphism, the transformation of clopidogrel to active metabolite reduces [5]. The CYP2C19 *1 allele is a wild type allele linked to enzyme activity [6]. The most frequently seen variant causing reduced enzyme activity are the CYP2C19*2 allele and the less frequently seen CYP2C19*3 allele [7]. The *1/*1 wild type produces normal metabolism, heterozygous *1/*2 and *1/*3 produce mild metabolic disorders and *2/*2, *2/*3 and *3/*3 produce severe metabolic disorders [8]. P2Y12 receptors are found in the platelet membranes and play a role in adenosine diphosphate (ADP)-induced platelet aggregation [9]. The aim of the active clopidogrel metabolite is the ADP platelet receptor P2Y12, thus irreversibly inhibiting ADP linkage to platelets. As a result platelet activation and aggregation is inhibited [10,11]. The ADP-induced platelet aggregation varies between individuals [12]. The causes of these individual differences are genetic factors [13]. Patients with a P2Y12 gene polymorphism using clopidogrel with peripheral artery disease have been shown to develop more cerebral ischemic events than those without polymorphism [14]. Again, it has been reported that myocardial infarctus, stent thrombosis, and ischemic stroke development were higher in those with CYP2C19 gene polymorphisms compared to those without a polymorphism [15]. In acute coronary syndrome, stent patients with P2Y12 and CYP2C19 single gene polymorphisms have been shown to have negative clinical results linked to unresponsiveness to clopidogrel; however, patients with a combination of both polymorphisms had worse clinical results [16]. In our study, we planned to research the clinical effects of CYP2C19 and P2Y12 gene polymorphisms in our ICVD patients who take clopidogrel.

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