INFLUENCE OF INTEGRIN BETA-3 GENE MUTATION AND TYPE 2 DIABETES MELLITUS ON PLATELET`S HEMOSTASIS IN PATIENTS WITH ACUTE AND CHRONIC CORONARY SYNDROMES
Keywords:platelet aggregation, diabetes mellitus, polymorphism
Introduction. The reactivity of the platelet component of hemostasis has been recently considered as the leading link in the development, course and formation of complications of many diseases. And in this regard, the most frequent and threatening combination to date is coronary heart disease and type 2 diabetes mellitus. It is the vascular complications of diabetes that are considered the most common cause of early disability and death of this cohort of patients. Authors emphasized in their study the exceptional role of platelets in the pathogenesis of coronarothrombosis and the importance of glycoprotein receptors in its implementation, which allows us to state the importance of a genetic predisposition to the course of the disease according to this scenario. The aim of the study was to establish the characteristics of platelet hemostasis changes in patients with coronary heart disease with concomitant type 2 diabetes mellitus, depending on the T1565C polymorphism of the GPIIIa gene. Materials and Methods. Analyzing modern genomic bases (National Center for Biotechnology Information, Online Mendelian Inheritance in Man) among the SNP genes involved in the pathogenesis of cardiovascular diseases, we selected the platelet integrin beta-3 gene. The gene is localized on the long (q) arms of chromosome 17 (17q21.32), has 15 exons, and the DNA site where thymine is replaced by cytosine at position 1565 is designated as the genetic marker T1565C (rs5918). As a result of this substitution, the biochemical properties of the GPIIIa protein are changed, in which the amino acid leucine is replaced by proline at position 33 (Leu33Pro). Results. The results of platelets functional activity obtained in the study allow us to consider type 2 diabetes mellitus in patients with acute and chronic coronary syndromes as an additional risk factor in the formation of increased aggregation potential precisely in the cohort of patients with hetero- and, especially, homozygous mutation of the C-allele of the integrin beta 3 gene.
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