[Experience in noninvasively quantifying hydrogen magnetic resonance imaging spectroscopic hepatic fat concentrations in patients with fatty hepatosis before and after treatment with Eslidin].

OBJECTIVE: To define the role of liver magnetic resonance (MR) spectroscopy in the evaluation of therapy for fatty hepatosis. MATERIAL AND METHODS: Spectra were studied in 49 patients (30 men and 19 women) whose mean age was 54+/-11 years. A study group consisted: 1) healthy volunteers (n = 10) and 2) patients with fatty hepatosis (n = 39) identified by clinical data. The patient group had two points: before and 6 months after treatment with Eslidin (based on polyunsaturated fatty acids). The lipid-to-water content ratio in the liver parenchyma was calculated for each patient. If its value was over 6.5%, the diagnosis of fatty hepatosis was considered verified. RESULTS: The findings showed that the ratio was not more than 3.2% in the group of healthy volunteers, which completely excluded hepatic fatty infiltration. In the patient group, the ratio was 15, 10, and 8.5% in 15, 20, and 4 cases, respectively. Reexamination revealed a reduction in fat concentrations to normal values (56,4%) in 22 patients and a more than twice (31%) decrease in 12 patients. No reduction in fat content was found in 5 (12,8%) patients. CONCLUSION: Proton MR spectroscopy is a reproducible procedure that may be used to evaluate the efficiency of treatment for fatty hepatosis. H1-spectroscopy can be used to evaluate the efficacy of some drugs for the treatment of this pathology.

[Evolution in optimization of stroke treatment].

Nowadays stroke is one of the world leading causes of mortality and disability. In process of time the evolution in view about etiology, pathogenetic mechanisms and therapy of patients with stroke has underwent pivotal changes. In this work there have been elucidated contemporary theoretical and practical aspects of stroke treatment and prophylaxis based on the results of multicenter clinical trials and experience of leading foreign and native specialists. Much attention is devoted to the pharmacotherapy of patients with stroke. It is showed that application of neuroprotective drugs is of great importance, among which antihypoxants with pleiotropic action play a crucial role (mexidol).

[The unity of pathogenesis of insulin resistance syndrome and non-alcoholic fatty disease of liver. The metabolic disorder of fatty acids and triglycerides].

The pathogenesis of non-alcoholic fatty disease of liver (steatosis) is still as unclear as a loss of hepatocytes similar to apoptosis, development of biological reaction of inflammation, its transformation into steatohepatitis with subsequent fibrosis and formation of atrophic cirrhosis. The article suggests that steatosis is developed due to higher concentration of palmitic saturated fatty acid (C 16:0) in food, intensification of its endogenic synthesis from food carbohydrates and glucose and development of insulin resistance. It is displayed in in hormone ability to activate both oxidation in cells of glucose and synthesis of oleic monoene fatty acid from palmitic saturated fatty acid (C 18:1). The insulin resistance initiates pathologic process on the level of paracrine associations of cells resulting in permanent increase of concentration of non-etherified fatty acids in intercellular medium and intensification of their passive absorption by cells. The phylogenetically ancient mitochondrions will not to oxidize glucose until non-etherified fatty acids are present in cytosol and hence there is an opportunity to oxidize them. To eliminate undesirable action of polar saturated palmitic fatty acid, the cells etherify it by spirit glyceride into triglycerides to deposit in cytosol or to secrete into blood in a form of lipoproteins of very low density. Under insulin resistance, saturated palmitic fatty acid synthesized by hepatocytes from glucose, does not further transform into oleic monoenic fatty acid. The cells are to etherify endogenic (exogenic) palmnitic saturated fatty acid into composition of aphysiologic palmitic triglycerides (saturated palmitic fatty acid in position sn-2 of spirit glyceride). At that, triglycerides of palmitat-palmitat-oleat and even tripalmitat type are formed. The melting temperature of tripalmitat is 48 degrees C and melting temperature of physiologic trioletat is 13 degrees C. The intracellular lipases factually can't hydrolyze palmitic triglycerides. So, hepatocytes, overloaded by them, are destroyed in a way similar to apoptosis. The formed corpuscles of apoptosis disorder the biologic function of endoecology and trigger biologic reaction of inflammation. At that, steatosis changes into steato-hepatitis. The prevention of steatosis consists in dramatic restriction of concentration of palmitic saturated fatty acid in food. The treatment effect is targeted to: decreasing the formation of palmitine triglycerides by force of concurrent etherification of palmitic saturated fatty acid not into triglycerides but into phosphatidylcholine (symmetric phospholipids of soya); intensification of oxidation of palmitic saturated fatty acid in peroxisomes (glytazones and fibrates); decrease of insulin resistance (binuanide metformine).