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A Method to Study the C924T Polymorphism of the Thromboxane A2 Receptor Gene
Published on: April 1, 2019
Evaluation of response to clopidogrel in patients with CYP2C19*2/*3 polymorphisms and its association with miR-19b
Shiva Eskandarian1, Alireza Zafarani2, Parisa Tandel1
1Department of Hematology and Blood Banking, Diagnostic Laboratory Sciences and Technology Research Center, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran.
Background:
Clopidogrel is a widely used antiplatelet drug for treating acute coronary syndrome. Its metabolism primarily involves the CYP2C19 isoenzyme, with CYP2C192 and CYP2C193 alleles associated with reduced metabolic activity. MicroRNAs, particularly miR-19b, have been linked to cardiovascular disease, but their role in clopidogrel metabolism remains unclear.
Methods:
A cross-sectional study was conducted on 50 middle-aged patients on clopidogrel therapy. Platelet aggregation was measured using adenosine diphosphate-induced assays, while CYP2C19*2/*3 polymorphisms were analyzed via RFLP-PCR. The expression of miR-19b was assessed using Real Time-PCR. Statistical analyses were performed to evaluate the relationship between genetic variations, platelet aggregation, and miR-19b expression.
Results:
The study revealed that 68% of the patients had wild-type genotypes, while 26% had CYP2C19*1/3, 4% had CYP2C193/3, and 2% had CYP2C191/2 genotypes. Patients with CYP2C191/3 polymorphisms exhibited significantly higher mean platelet aggregation compared to those with wild-type genotypes, suggesting a reduced response to clopidogrel treatment. Additionally, the expression of miR-19b did not show significant variation across the different genotypes, indicating that miR-19b may not play a substantial role in clopidogrel metabolism.
Conclusion:
Patients with CYP2C19*1/*3 polymorphisms have a reduced response to clopidogrel, emphasizing the importance of genetic testing to personalize antiplatelet therapy. The lack of association between miR-19b expression and clopidogrel metabolism suggests that miR-19b is not a critical factor in treatment response.

