Non-alcoholic fatty liver disease is now recognized worldwide as a common chronic liver disease. Due to metabolic risk factors common to non-alcoholic fatty liver disease and cardiovascular disease, patients with non-alcoholic steatohepatitis are at increased risk of developing hepatic encephalopathy and cardiovascular death. The purpose of the study was to investigate the state of fibrinolysis and proteolysis system, homeostasis of nitrogen monoxide, plasma and platelet hemostasis in patients with non-alcoholic steatohepatitis, depending on the presence of comorbid coronary heart disease. Material and research methods. We examined 120 patients with non-alcoholic steatohepatitis: 30 patients with non-alcoholic steatohepatitis and obesity of I-II degree (group 1), 90 patients with non-alcoholic steatohepatitis and comorbid obesity of I-II degree and coronary heart disease (stable angina pectoris I-II) (group 2). The average age of the examined patients was 56.81±8.38 years. There were 16 (53,37 %) men and 14 (46,63 %) women in group 1. In the group 2 there were 48 (53,35 %) men and 42 (46,65 %) women. The control group consisted of 30 practically healthy persons aged from 40 to 60 years. Results and discussion. The vast majority of patients with non-alcoholic steatohepatitis and comorbid coronary heart disease showed a decrease in fibrinolytic potential of blood plasma (total (p <0.05) and enzymatic fibrinolytic activity (p <0.05), increased blood coagulation (a significant decrease of prothrombin time) (p<0.05) and increased fibrinogen content (p <0.05) in the blood, NO deficiency (p <0.05), platelet aggregation capacity (significant increase of spontaneous (p <0.05) and induced platelet aggregation (p <0.05)). Conclusions. The cause of revealed disorders of rheology and blood clotting at non-alcoholic steatohepatitis is accumulation in the systemic circulation of toxic substances, which create a high level of endotoxicosis, contribute to the release of biologically active substances, cytokines, activation of kallikrein-kinin system, the formation of plasmin and thrombin with subsequent disturbance of equilibrium between them, development of stasis, erythrocyte aggregates in an extended portal system with low blood flow velocity. The slowing of blood circulation in the liver due to the formation of microthrombuses in the microcirculatory system contributes to the deepening of organ hypoxia, processes of lipid peroxidation with subsequent damage of cell membranes and closure of the vicious circle of pathogenesis of non-alcoholic steatohepatitis and coronary heart disease progression.

Keywords: nonalcoholic steatohepatitis, coronary heart disease, fibrinolysis, proteolysis, platelet aggregation

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