Histological and histochemical features of the liver in patients with non-alcoholic steatohepatitis depending on the presence of coronary heart disease

Abstract

The aim of the study — investigation of pathohistological and histochemical features of changes in liver tissue with nonalcoholic steatohepatitis (NASH) and comorbid obesity and coronary heart desease (CHD) in comparison with the course of NASH on the background of obesity.Material and methods. Eighteen specimens of the autopsy material of the liver of patients with NASH were taken for the study, including 9 persons with NASH and 9 — with NASH and comorbid CHD. The morphological examination of the liver was carried out according to the standard method. The sections were stained with hematoxylin and eosin for inspection purposes. To identify the components of connective tissue, we used the techniques of staining histological sections by chromotrope aqueous blue according to the method of N. Z. Slinchenko and bromphenol blue based on Mikel Calvo method.Results. In the presence of NASH with comorbid obesity and CHD, the percentage of hepatocytes with steatosis is 2.5 times higher (p<0.05) compared to NASH without myocardial pathology. The comorbidity of NASH with CHD significantly increases the percentage of hepatocytes in the state of granular or hydropic dystrophy (in 1.2 times (p<0.05)) and the percentage of hepatocytes with signs of death — mainly necrosis (1.6 times (p<0.05))), sometimes apoptosis. In patients with NASH, the overall percentage of hepatocytes in the state of alteration (dystrophy, necrosis or apoptosis) is significantly lower (60.9%) (p<0.05) than in patients with NASH and CHD (99.4%). Comorbidity of NASH, obesity and CHD in 100% of cases reported in hepatocyte lipofuscinosis compared to 33.3% of NASH cases without CHD (p<0.009). Comorbid CHD with NASH and obesity leads to an increase in the connective tissue volume in the liver parenchyma — in 2.1 times compared with NASH (p<0.05), as well as to a higher degree of its maturation.Conclusion. In patients with nonalcoholic steatohepatitis and coronary heart disease develop changes that are in close pathogenetic interconnection and manifested by venous stasis, liver hypoxia and sustained activation of free radical processes. These processes lead to persistent considerable morphological long standing changes in the liver tissue with growth and compaction, a greater degree of connective tissue maturation, and are associated with activation of liver fibroblasts.