Aim. Assessment of the morphological changes of the liver on the model of non-alcoholic steatosis in laboratory animals and hemostasis parameters in animals and patients with steatosis. Materials and methods. The experimental part of the study was conducted on 18 white rats divided into 2 groups: control (intact animals) and “Steatosis” (animals with liver steatosis modeled in laboratory conditions). The clinical part was performed on 52 patients with non-alcoholic fatty liver disease (the clinical form is non-alcoholic liver steatosis), with an average age of 43.0 ± 11.1 years and a body mass index of 37.2 ± 2.6. The control group consisted of 20 practically healthy individuals. At the end of the experiment, on the 30th day, the animals were removed from the experiment, direct blood sampling was performed from the right atrium, the liver mass and mass coefficient were determined, and a histological examination of the liver was performed. Laboratory tests included the determination of the following indicators of hemostasis in blood plasma: activity of the von Willebrand factor, platelet aggregation with ADP, collagen and ristocetin; prothrombin time, Quick prothrombin, international normalized ratio, thrombin time, activated partial thromboplastin time (APTT), fibrinogen and Hageman-dependent fibrinolysis. Results. In the experiment, the mass coefficient of the liver was significantly higher in the “Steatosis” group compared to the control group (3.75 (3.38-3.99) and 3.5 (3.3-3.6), respectively) (p = 0.009). Structural reorganization of the liver confirms the development of steatosis in animals. In animals with steatosis, a change in indicators reflecting the activity of the plasma link according to the external mechanism of coagulation was found: an elongation of the prothrombin time (p = 0.034), a decrease in the prothrombin index according to Quick (p = 0.018), an increase in INR (p = 0.027). APTT and thrombin time in animals with steatosis are higher than in the control, but these changes are not statistically significant (p = 0.181 and p = 0.364, respectively). The concentration of fibrinogen, Hageman-dependent fibrinolysis, platelet aggregation with ADP and the activity of the von Willebrand factor did not have statistically significant differences when comparing the two groups. In patients with steatosis, the number of platelets did not significantly differ from the control (p = 0.082). However, there was a decrease in aggregation with collagen (p = 0.002) and with ADP (p = 0.02). Platelet aggregation with ristocetin and the activity of the von Willebrand factor was higher than in the control (p = 0.001 and p = 0.01, respectively). In patients with steatosis, there was an extension of the APTT and an increase in the concentration of fibrinogen in comparison with the control, but these indicators did not go beyond the reference values of the set. The thrombin time was significantly prolonged in patients with steatosis in comparison with practically healthy individuals (p < 0.001). Conclusion. Non-alcoholic fatty liver disease is accompanied by a violation of the functioning of both vascular-platelet and coagulation hemostasis. There is a violation of the aggregation properties of platelets, signs of endothelial damage, hepatic coagulopathy.
