In dissertation didn’t establish significant pathomorphological differences between the ASH and NASH. The activity of NASH and ASH determines the increase in the severity of liver steatosis; an increase in the number of balloon hepatocytes and hepatocytes with Malori-Denk bodies; intensification of steatonecrosis and hepatocyte apoptosis; an increase in the number and expansion of foci of steatonecrosis in the liver, as well as immunocyte and inflammatory cell infiltration of the liver, while an indicator of the severity of the disease is perisinusoidal-pericellular and portal-Z1-3perisinusoidal fibrosis of the liver, sources of which are perisinusoidal and portal αSMA+,. vimentin +, desmin- MFB. With an increase in liver steatosis in macrophages and hepatocytes in patients with ASH, the deposition of trivalent Fe3+ and divalent Fe2+ iron increases significantly. In severe S3 steatosis, the content of lipotoxic stearic and palmitic acids and cholesterol is significantly increased in patients with NASH in the liver. Hepatocytes in NASH and ASH die by steatonecrosis, balloon cytolysis, apoptosis and ferroptosis, the death of hepatocytes early activates pericellular fibrogenesis. With the progression of fibrosis in the liver, the area of αSMA + perisinusoidal MFB, the area of Masson + extracellular matrix and deposition of type I, III and IV collagen significantly increases. At stage F2 - F3 of liver fibrosis and cirrhosis, the reparative complex of progenitor liver cells is activated with the development of a ductular reparative reaction, as a result of which the population of hepatocytes is replenished through intermediate hepatobiliary and hepatocyte-like cells, which is facilitated by the appearance of extracellular laminin, as well as pseudolobules are formed and ductules without bile accumulate in the portal tracts in case of liver cirrhosis. In 10.48% of patients with NASH and ASH develop micronodular perisinusoidal-pericellular or portal-Z1-3perisinusoidal cirrhosis, 0,57% of patients develop hepatocellular carcinoma of the liver with solid cell, trabecular and acinar patterns. With the progression of micronodular cirrhosis due to the accumulation of empty ductules, portal and bridge-like portal-portal fibrosis increases, and severe pericellular fibrosis increases in pseudolobules, which isolates hepatocytes and contributes to their steatonecrosis.
