ROLE OF OXIDATIVE STRESS IN PATHOGENESIS AND PROGRESSION OF NON-ALCOHOLIC STEATOHEPATITIS IN PATIENTS WITH CONCOMITANT CORONARY HEART DISEASE

Abstract

The aim of the study: to investigate the state of the system of oxidant-antioxidant homeostasis in patients with NASH and comorbid coronary heart disease. Material and methods. We examined 86 patients with NASH, including 30 patients with NASH and obesity of I-II degree (group 1) and 56 patients with NASH and comorbid coronary heart disease (stable angina pectoris I-II) (group 2). The control group consisted of 30 healthy individuals of the comparable age. The average age of patients was 56,6 ± 5,74 years. Results. An essential pathogenetic factor for the onset and progression of NASH in the presence of comorbid coronary heart disease is the intensification of the processes of free radical lipids oxidation that determines the degree of activity of the pathological process in the liver: the accumulation of intermediate (isolated double bonds, diene conjugates, ketodiens and conjugated trienes) and terminal (malonic aldehyde of plasma and erythrocytes) products of lipid peroxidation against the background of disintegration of the system of antioxidant protection (reduction of the content of glutathione reduced in erythrocytes, compensatory growth of catalase activity). Insufficiency and disintegration in the system of antioxidant protection is one of the main factors resulting in the increase in metabolic intoxication, while preserving of glutathione in a reduced form is necessary to prevent the inactivation of a number of enzymes, protecting the hepatocyte membranes from the effects of oxidants. The oxidation of reduced glutathione leads to decrease in the intensity of glycolysis, lowered synthesis of ATP and decline in the energy potential of hepatocytes and cardiomyocytes that is particularly undesirable for the comorbidity of NASH and coronary heart disease.