Bazhenova N. The state of platelet-plasma hemostasis in patients with arterial hypertension in combination with obesity and nonalcoholic fatty liver disease

Українська версія

Thesis for the degree of Candidate of Sciences (CSc)

State registration number


Applicant for


  • 14.01.02 - Внутрішні хвороби


Specialized Academic Board

Д 26.003.08

Bogomolets National Medical University


The dissertation is devoted to optimizing the effectiveness of early diagnosis of thrombophilic blood changes in patients with arterial hypertension (HT), stage II, with concomitant obesity and nonalcoholic fatty liver disease (NAFLD) by determining the state of hemocoagulation in these groups of patients. The results of the study confirmed the increase in spontaneous, ADP and adrenaline-induced aggregation in patients with comorbid course of HT and NAFLD, which occurs on the background of an increase in mean platelet volume. Patients with HT and its combination with NAFLD are characterized by changes in the hemostasis system with increasing blood clotting activity due to the final phase – fibrin formation versus to NAFLD, in which the initial stages of the coagulation cascade undergo the greatest changes. According to the results of highly specific tests with snake venom, activation of the coagulation potential of blood plasma in patients with HT and HT, combined with NAFLD, occurs mainly in the stage of thrombin formation. Inhibition of the fibrinolytic part of the hemostasis system is observed in HT, NAFLD and their combined course. The comorbid course of HT and NAFLD is associated with more significant inhibition of fibrinolysis. It was found that obesity is associated with an increase of platelet count and activation of the final stages of the coagulation cascade, compared with patients with body mass index (BMI)<30 kg/m2. In patients with HT hemostatic changes in obesity are exacerbated by an increase in the average volume of platelets and functional activity of platelets, hypercoagulation in the final stages of the coagulation, while both HT and its combination with NAFLD is characterized by a significant decrease in anticoagulant activity. In contrast, hemostasis in isolated NAFLD did not differ in patients with BMI<30 kg/m2 and ≥30 kg/m2, indicating a similarity of pathophysiological mechanisms of prothrombotic changes in obesity and NAFLD. Hypercholesterolemia and hypertriglyceridemia are associated with decreased anticoagulant potential and activation of coagulation in the final stages of coagulation, in addition, the increase in blood cholesterol is associated with high functional activity of platelets. Patients with comorbid course of HT and NAFLD with hypercholesterolemia have procoagulant and prothrombogenic activity of blood, but statin treatment decreases spontaneous platelet aggregation, blood coagulation potential and increases activity of anticoagulant hemostasis.


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