Abstract
Objective To investigate high platelet reactivity effective and relative strength that induced by the CYP2C19 and P2Y hotspot mutations, and explore the applicable testing methods in clinical settings. Methods A case-control study was conducted.104 patients with coronary heart disease were enrolled who administered antiplatelet agent treatment and a 300 mg loading dose of clopidogrel within 12-24h before a PCI.ADP inhibition rate was tested by TEG and flow cytometry method was used to detect VASP index (PRI) and CD62p.The citrated and heparined venous whole blood collected should be collected within 12-24 h after PCI.Genotyping was carried out by pyrophosphate method for the hotspot mutations of drug metabolism in Chinese population concluded CYP2C19 * 2 (681G> A), CYP2C19 * 3 (636G> A)and the platelet glycoprotein receptor gene concluded P2Y1 (893C> T) and P2Y12 (52G> T).According to the CYP2C19 * 2 sequencing results, patients were grouped into three groups, the wild-type group (*1/*1), the heterozygous group (*1/*2)and the homozygous group(*1/*2).Combined with other three mutation sites, platelet function was analyzed among different groups.One-Way ANOVA was used for analysis of variance between groups of different genotypes, and t test and non-parametric test were selected for statistical analysis between the two groups. Results The PRI of wild-type group (35.75±23.11)% was significantly lower (F=9.170, P 0.05) was existed on CD62p among the wild-type group (9.38±11.16)%, the heterozygous group (9.45±8.91)% and homozygous group (10.87±8.31)%.One P2Y12 (52G> T) mutation was found while no P2Y1 (893C> T) mutation was detected among 37 patients. Conclusion The risk of a low response to clopidogrel was related to the carry of CYP2C19 loss-of-function alleles, and the change can be effectively reflected by VASP analysis.(Chin J Lab Med, 2014,37:198-202) Key words: Coronary disease; Ticlopidine; Aryl hydrocarbon hydroxylases; Receptors, purinergic P2Y12; Platelet count; Microfilament proteins; Phosphoproteins; Cell adhesion molecules
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