Endometrial hyperplasia is a benign pathology of the uterine mucosa, characterized by certain histological changes, characterized as simple and complex, non-atypical and atypical forms. Hyperplastic processes of endometrium, according to various authors, in the structure of gynecological pathology make up 15 to 40%. Clinically, the endometrial hyperplasia manifest by uterine bleeding. Maternal bleeding that is not susceptible to hormonal, symptomatic, and hemostatic therapy, leads to chronic post-hemorrhagic anemia and is the indication for surgical intervention. Consequently, systemic disorders of the hemostasis parameters on the background of uterine bleeding with endometrial hyperplasia, in particular the regulation of the aggregate state of blood systems, require further research to identify new pathogenetic links and develop correction methods.
Materials and methods.
State of platelet-vascular hemostasis was assessed by the percentage of platelets adhesion in the blood and by the index of spontaneous platelet aggregation. Total potential coagulation of blood, plasma fibrinolytic activity, plasminogen potential activity, antiplasmin, fibrinogen in blood plasma, the activity of antithrombin III, the concentration of soluble fibrin monomer complexes in the blood was determined by reagents made by Simko Ltd company (Ukraine). Using the «Thromboelastohraph ACG» machine we identified parameters of thrombin clotting rate, thromboelastograph K constant, specific platelets convolution constants, a- angle and coagulation composite index.
Results. In women with anemia of ІІІ-rd degree against background of the uterine bleeding, at high activity of primary hemostasis, structural and chronometric hypocoagulation develops; it is predefined by the acute decreasing of fibrinogen in the blood. The principal reason of hypofibrinogenaemia is the excessive activating of non-fermentative fibrinolysis. In conclusion, changes in the system of regulation of the aggregate state of blood in women with severe degree of anemia are the display of subclinical inopexia that develops as a result of thrombocytes high functional activity.
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