Состояние гемостаза и углеводного обмена у пациентов с сахарным диабетом 2-го типа и цереброваскулярными заболеваниями

Introduction. Diabetes mellitus (DM) is associated with the formation of a prothrombotic state and is a factor in the development of cerebrovascular diseases (CVD). Hyperglycemia leads to increased formation of glycation end products (GEP) and glycation of membrane proteins of blood cells. The role of GEP in the formation of blood prothrombogenic potential in patients with CVD, both with DM type 2 and without it, has not been studied. Aim: to assess hemostatic parameters changes in patients with CVD in conjunction with glycation markers. Materials and methods. The study included 160 patients with CVD, group 1 — 80 patients with DM type 2, group 2 — 80 patients without DM. Standard biochemical profile with determination of glycemia and glycated hemoglobin levels, GEP content, ADP-induced (ADP-AT) and adrenaline-induced platelet aggregation, detailed coagulogram with determination of fibrinolytic activity (FA), fibrinolysis index and D-dimer were determined in all patients. Results. The prevalence of earlier disorders in cerebral blood circulation and hemodynamically significant stenoses of the carotid arteries were higher in patients with DM type 2 than in patients without DM. GEP level was statistically significantly higher in patients with DM — 473,0 ± 148.4 [390; 600] ng/ml vs. 325.8 ± 77.1 [250; 480] ng/ml in patients without DM that was accompanied by increasing of D-dimer content and decreasing of blood fibrinolytic properties. Parameters of platelet aggregation in patients with DM type 2 also exceeded those in patients without DM. In both groups, we revealed statistically significant negative correlations between GEP and FA (r = –0.426117), between GEP and fibrinolysis index (r = –0.36) and positive correlation between GEP and ADP-AT (r = 0.4176). Conclusion. In patients with CVD, increased GEP formation is accompanied by activation of platelet hemostasis, inhibition of fibrinolysis and contributes to the formation of prothrombogenic blood potential. 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