[Evaluation of endothelial function and estimation of the degree of apoptosis in patients with metabolic syndrome and non-alcoholic fatty liver disease].

AIM: To evaluate endothelial function (EF) and to estimate the level of a serum apoptosis marker (caspase-8) in patients with metabolic syndrome (MS) and in those with non-alcoholic fatty liver disease (NAFLD). SUBJECTS AND METHODS: The investigation enrolled 76 patients: 43 with MS (out of them, 72.1% were found to have NAFLD) and 33 without MS and NAFLD. All the patients underwent evaluation of EF by photoplethysmography; the level of caspase-8 as one of the apoptosis markers was studied in all. RESULTS: Increased arterial stiffness was more common in a group of patients with MS. Systolic duration was higher in these patients (p < 0.05). In these patients, an occlusion test revealed the significantly more marked signs of endothelial dysfunction (ED), which correlated with some cardiovascular diseases (CVD), and hepatic steatosis (p < 0.05). The mean level of caspase-8 was significantly higher in the group of MS patients (p < 0.05). There was a positive correlation between caspase-8 levels and hepatic and pancreatic steatosis, obesity, aortic atherosclerosis, type 2 diabetes mellitus, and gastroesophageal reflux disease (p < 0.05). CONCLUSION: The study group of MS patients (among whom, there was a preponderance of those with NAFLD) had, firstly, higher arterial stiffness more frequently (as evidenced by photoplethysmography), secondly, longer systolic duration, which may be a risk factor for CVD; thirdly, more pronounced ED. Fourthly, according to the data of a study of caspase-8 levels, its indicator may serve as a prognostic marker for the development of CVD and NAFLD. It was, fifthly, shown that the administration of statins might reduce the degree of apoptosis.

[[Current approaches to diagnosing and treating nonalcoholic fatty liver disease].

Nonalcoholic fatty liver disease (NAFLD) is associated with major cardiovascular risk factors, such as type 2 diabetes mellitus, obesity, dyslipidemia, hypertension, and insulin resistance, and has been recently considered to be a new component of metabolic syndrome and it serves as a criterion for the hepatic manifestation of the latter. The review considers the present-day views and approaches to diagnosing and treating NAFLD and its dangerous manifestation - fibrosis (sclerosis), which may lead to cirrhosis and hepatocellular carcinoma. Fibrogenesis is a widespread and universal process that is a final path of chronic inflammation of and damage to different tissues (including those of the liver and cardiovascular system). Although the mechanisms for developing NAFLD remain unclear, insulin resistance, an obesity-related slowly progressive inflammatory response, and elevated levels of free fatty acids with their lipotoxicity along with possible genetic, dietary, and environmental (lifestyle) factors play a key role in the pathogenesis of this disease. So it is important for patients at high risk for NAFLD or with existing liver disease to pay attention to their life style, proper balanced diet, and slow and gradual weight loss. At present there are drugs that can improve liver function. Success in NAFLD therapy will be determined by the identification of the most significant pathogenetic factors in a specific patient and by the purposeful action on them.