Lack of effect of common single nucleotide polymorphisms in leukotriene pathway genes on platelet reactivity in patients with diabetes
Copyright policy )Lack of effect of common single nucleotide polymorphisms in leukotriene pathway genes on platelet reactivity in patients with diabetes
The aim of the present study was to investigate the effect of genetic polymorphisms in candidate genes within the leukotriene (LT) pathway on platelet reactivity and the concentration of selected LTs in diabetic patients treated with acetylsalicylic acid (ASA). The study cohort consisted of 287 Caucasians with type 2 diabetes who had received treatment with ASA tablets (75 mg/day) for at least three months. Platelet reactivity analyses were performed using VerifyNow aspirin and PFA‑100 assays. The measured LTs included leukotriene B4 (LTB4) and leukotriene E4 (LTE4). Genotyping for the selected 25 single nucleotide polymorphisms (SNPs) within six genes of the LT pathway was performed using a Sequenom iPLEX platform. No statistically significant association was observed between the investigated SNP genotypes, platelet reactivity and measured LTs in the patient cohort. The results of our study suggest that certain polymorphisms of the LT pathway are not associated with altered platelet reactivity and the measured LTs in diabetic patients treated with ASA.
Blood Platelets, Epoxide Hydrolases, Leukotriene E4, Male, Arachidonate 5-Lipoxygenase, Aspirin, Genotype, 5-Lipoxygenase-Activating Proteins, Middle Aged, Arachidonate 12-Lipoxygenase, Leukotriene B4, Cohort Studies, Diabetes Mellitus, Type 2, Gene Frequency, Arachidonate 15-Lipoxygenase, Humans, Female, Alleles, Aged, Glutathione Transferase
Blood Platelets, Epoxide Hydrolases, Leukotriene E4, Male, Arachidonate 5-Lipoxygenase, Aspirin, Genotype, 5-Lipoxygenase-Activating Proteins, Middle Aged, Arachidonate 12-Lipoxygenase, Leukotriene B4, Cohort Studies, Diabetes Mellitus, Type 2, Gene Frequency, Arachidonate 15-Lipoxygenase, Humans, Female, Alleles, Aged, Glutathione Transferase
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