Indicators of the hemostasis system and markers of endothelial damage in patients with steatosis and liver fibrosis

Abstract

Introduction. According to the analysis of indicators of the hemostasis system in liver pathology, there are multidirectional data in the literature, which may be associated with the examination of patients with varying degrees of severity and etiology of the process. Aim. The aim of the study was to study the indicators of hemostasis and markers of endothelial damage in patients with non-alcoholic steatosis and liver fibrosis of viral etiology. Materials and methods. A total of 64 people were examined. The first group included 32 patients with non-alcoholic liver steatosis on the background of obesity of 1–2 degrees, with an average age of 46.3 ± 4.3 years (12 men and 20 women). The second group consisted of 22 patients with liver fibrosis on the background of chronic hepatitis C (HCV) with an average age of 36.8 ± 4.7 years (12 men and 10 women). The control group included 10 practically healthy individuals with an average age of 38.9 ± 5.3 years without liver pathology. The number of platelets, platelet aggregation with ADP inducers, collagen and ristocetin, functional activity of Willebrand factor (vWF), coagulation hemostasis and fibrinolysis system, and serum concentration of vascular endothelial growth factor (VEGF) were determined. Statistical processing of the obtained data was carried out using the program “Stat2015”. Results. Induced platelet aggregation in steatosis and liver fibrosis significantly decreased with ADP agonists and collagen against the background of a normal platelet count. In both study groups, signs of endothelial damage with a tendency to increase the functional activity of vWF and VEGF hyperproduction were found. An elongation of thrombin time was also recorded, more significantly in patients with steatosis. Conclusion. Patients with non-alcoholic liver steatosis and liver fibrosis on the background of HCV are characterized by disorders in the vascular-platelet (endothelial damage and thrombocytopathy in the form of platelet hypocoagulation) and coagulation (hypocoagulation) links of hemostasis.