The problem of non-alcoholic fatty liver disease, metabolic syndrome and atherosclerosis: from the unity of pathogenesis to the possibility of ursodeoxycholic acid correction

Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver pathologies, the prevalence of which is steadily increasing worldwide. Cardiovascular disease (CVD) is another group of common diseases that have similar pathophysiological mechanisms with NAFLD. CVD and NAFLD occur against the background of metabolic syndrome, systemic insulin resistance, oxidative stress, altered lipid metabolism. The course of both diseases predisposes to the development of endothelial dysfunction and formation/instability of atherosclerotic plaques. The progression of NAFLD is associated with an increase of the thickness of intima-media complex and calcification of coronary arteries, which is accompanied by an increased risk of subclinical and clinically significant atherosclerosis development. Patients with NAFLD have a high cardiovascular risk, the maximum increase of which should be expected in patients with severe fibrosis (F3–F4 on the NAFLD Fibrosis Score scale). Ursodeoxycholic acid reduces the severity of systemic inflammatory response and oxidative stress, improves lipid metabolism, increases the hypolipidemic effect of statins, reduces the degree of hyperglycemia and insulin resistance, inhibits the formation of atherosclerotic plaques, has vasodilating effect. The presence of significant pleiotropic properties in combination with apparent cytoprotective, choleretic, antiapoptic, anticholestatic, immunomodulatory activity allows to include ursodeoxycholic acid in NAFLD treatment, non-alcoholic steatohepatitis in order to reduce the clinical manifestations of atherosclerosis and prevent CVD progression.