Abstract

The nature of violations of the hemostatic system in liver cirrhosis is complex, often unpredictable and concerns all its links – vascular-platelet, coagulation and fibrinolysis. It is now well established that patients with cirrhosis may experience both bleeding and thrombosis. The mechanisms of blood clotting disorders in this case are very complex, since defects simultaneously occur both in the procoagulant system and in the anticoagulation system. Aim to study the factors and mechanism of the development of hemostasis imbalance in patients with liver cirrhosis based on the analysis of scientific literature, to determine the information content of existing laboratory tests for the study of hemostasis and the features of correction of hemostasis disorders depending on hyper- or hypocoagulation. It is generally accepted that cirrhosis results in a state of hypocoagulation with an increased tendency to bleeding. However, a number of publications do not support this opinion, and the interpretation of laboratory parameters is explained by the standard methodology, where the procoagulant and antifibrinolytic systems of hemostasis are insufficiently studied. Many researchers have established a state of hypercoagulability in liver cirrhosis, leading to intra- and extrahepatic thrombosis. The cause of bleeding, primarily from varicose veins of the esophagus and stomach, is not hypocoagulation as such, but rupture of varices due to hemodynamic disturbances with increased portal pressure, one of which is thrombosis. Accordingly, therapeutic tactics should be aimed, first of all, not at normalizing laboratory tests, but at eliminating the pathogenetic mechanisms of hemostatic imbalance that occur in liver cirrhosis. At the same time, drug correction should be directed not at individual links of the hemostasis system - pro or anticoagulant, but at the correction of hemostatic imbalance as a whole. Conclusions. To date questions about the nature of changes in the hemostasis system in liver cirrhosis, their relationship with hemorrhagic complications or thrombosis, the principles of drug correction remain open, requiring further research in this direction.

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