In recent years, numerous epidemiological studies have reported a rising incidence of cardiovascular disease in patients with comorbid course of non-alcoholic fatty liver disease and cardiovascular diseases, which is the main cause of death of these patients. The purpose of the study was to establish the clinical and biochemical features of the course of non-alcoholic steatohepatitis (NASH) with comorbid obesity of I-II degree and coronary heart disease (CHD) compared with the course of NASH on the background of obesity without comorbid CHD. Material and methods. We examined 86 patients with NASH. 30 patients with NASH and obesity of I-II degree (group 1), 56 patients with NASH, comorbid obesity of I-II degree and CHD (stable angina pectoris of I-II functional classes) (group 2). To determine the dependence of the course of NASH with CHD, the groups of patients were randomized according to age, sex and degree of obesity. The average age of patients was 55.9 ± 5.68 years. The control group consisted of 30 practically healthy persons of the corresponding age. Results and discussion. The obtained results showed that the clinical picture of NASH was characterized by multi symptoms of manifestations and low intensity of clinical manifestation of syndromes with predominance of astheno-vegetative, dyspeptic syndromes, hepatomegaly, hyper- and dyslipidemia, insulin resistance on the background of mild cytolysis and mesenchymal inflammation. During ultrasonographic examination of the liver in patients with NASH, we detected hepatomegaly, medium-grained transformation and hyperechogenicity of the liver parenchyma, dorsal fading of echoes as a result of diffuse fatty infiltration, visual impairment of the intrahepatic vessels and diaphragm. Conclusion. The main factors of the development and progression of NASH on the background of comorbid CHD are the violation of the lipid profile of the blood (increase in the content of total cholesterol, triglycerides, proatherogenic fraction of low density lipoproteins on the background of reduction of anti-atherogenic high-density lipoproteins) and glucose metabolism (postprandial hyperglycemia, insulin resistance) which ultimately promote the early development of adverse cardiovascular events.
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