[The role of fraction analysis of ferritin in diagnostic of secondary hemophagocyte syndrome].

The secondary hemophagocytic syndrome is a life-threatening condition characterized by non-specifc manifestations: systemic inflammatory reaction, cytopenia, liver affection, high content of ferritin in blood serum. One of manifestations of secondary hemophagocytic syndrome is decreasing of level of glycated ferritin in blood serum expressed in percentage of total level. The detection of glycated ferritin can be applied for a differentiated diagnosis with cli9nically similar conditions, including septic process. The purpose of study was to determine clinical value of easurement of glycated ferritin for diagnostic and differentiated diagnostic of secondary hemophagocytic syndrome. The analysis was applied to samples of blood serum and clinical data of patients with diagnoses of secondary hemophagocytic syndrome (n=40), severe sepsis (n=24), cytolitic syndrome (n=36) and healthy donors (n=40). The total content of ferritin is established using rbidimetric technique ("BioSystems", Spain). The glycated ferritin was calculated. To determine level of of glycated ferritin the glycated fraction of ferritin was precipitated using concanavalin A, polymerized with sepharose 4B ("GE Healthcare", USA). The normal values of glycated ferritin made up to 78.3%-87.1%. Under secondary hemophagocytic syndrome decreasing of content of glycated ferritin made up to 25.0 ± 18.7% and was signifcantly lower than under sepsis (47.0 ±17.7%, p<0.001) and cytolytic syndrome(63.5% ±18.7%, p<0.001). According the results of ROC-analysis, the area under curve was maximal as compared with other markers of secondary hemophagocytic syndrome, including total ferritin, triglycerides, fbrinogen. At decreasing of level of glycated ferritin lower than 30.4% the applied technique provides clinical sensitivity 69%, specifcity 94.3%, accuracy 86.9% in applying differentiating diagnosis of secondary hemophagocytic syndrome. At calculation of absolute content of non-glycated ferritin it was discovered that its values correlate with concentration of triglycerides, international normalized ratio, aspartataminotransferase, alaninaminotransferase and total bilirubin in patients with secondary hemophagocytic syndrome (p<0.05). Therefore, decreasing of level of glycated ferritin permits to diagnose secondary hemophagocytic syndrome with higher accuracy.

[The chondroprotector mucosat in an integrated approach to the treatment of nonspecific back pain]. / Khondroprotektor mukosat v integrirovannom podkhode k lecheniiu patsientov s nespetsificheskoi bol'iu v spine.

A nonspecific back pain is in the vast majority of all possible cases of dorsopathies. The sources of back pain may be myogenic dysfunction, intervertebral disc pathology or osteoarthritis of the archicular (facet) joints of the spine, including myofascial pain syndrome. A differentiated approach to the treatment of spondylarthrosis is still an unsolved problem. The article discusses important issues of integration of non-drug treatment methods and drug therapy of nonspecific back pain in patients with facet syndrome. Special attention is paid to SYSADOA group chemicals, in particular chondroitin sulfate (mucosat). These drugs have proven analgesic and anti-inflammatory effects and also are able to improve the structure of the cartilaginous tissue, slowing the progression of the disease.

[Treatment of asthenic syndrome in patients with chronic brain ischemia: results of the non-interventional observational program TRIUMPH].

OBJECTIVE: To assess the severity of asthenic syndrome (AS) in chronic brain ischemia (CBI) in primary health care settings. MATERIAL AND METHODS: The study included 1170 patients with brain ischemia, aged 45-65 years, treated with phenotropil in dose 100 mg during 2 and 3 months. Clinical examination and MFI-20 subscales were administered. RESULTS AND СONCLUSION: The high incidence of asthenic syndrome was observed across all MFI-20 subscales. The decrease in asthenic syndrome severity was significant already in the end of the first month of treatment with phenotropil. Such dynamics maintained to the end of the second and third month of treatment. More than 2-fold decrease in the severity of asthenia symptoms was achieved in all subgroups 3 months after treatment. More rapid and apparent decrease in asthenic syndrome was observed in younger patients.

[Pharmacotherapy of endothelial dysfunction in patients with atherosclerotic brain ischemia].

We studied the effect of deproteinized hemoderivative of calf blood, thioctic acid and vinpocetine with piracetam on the endothelial function in patients with chronic cerebral ischemia stage III. After pharmacological treatment, there was the improvement in the endothelium properties of both large and small blood vessels. The index of occlusion that characterized the function of small vessels reached normal values while the phase shift did not approach to the reference values. This notion indicates that in cerebral atherosclerosis small arteries initially are subject to alterations to a lesser extent compared to the arteries of large and medium caliber. The most effective medicines of those used for the correction of endothelial dysfunction are deproteinized hemoderivative of calf blood and thioctic acid.

[L-carnitine treatment patients with chronic cerebral ischemia].

The purpose of this study is to investigate the effectiveness of L-carnitine treatment in patients with dodementia stage chronic cerebral ischemia. In parallel comparative clinical study included 60 patients (22 men and 38 women aged 42 to 74 years), the average age of the patients was 61.2±8.2 years. All patients received basic treatment, including antihypertensive and antiplatelet drugs. The first group consisted of 20 patients who received 1000 mg of L-carnitine per day (bilology supplement karniton). In the second group (20 patients), the drug was administered to 2000 mg per day. In the third (the control group) was carried out only basic therapy. The course of treatment was 60 days. After treatment significantly reduced the frequency of complaints of weakness, decreased performance, memory loss, headache, dizziness, unsteadiness of gait. Statistically significant differences after treatment revealed in the MMSE total score and subtests "focus" and "memory", compared to the baseline reduced the running time with all 5-tables in the test Schulte. According to questionnaire fatigue MFI-20 the main group level decreased overall, physical and mental asthenia, increased activity and the level of motivation. Revealed a dose-dependent effect of the drug.

[A search for new markers of oxidative stress in brain ischemia for the optimization of treatment approaches].

Data of literature on the role of inflammation factors in the pathogenesis of stroke are presented. The study of myeloperoxidase level in the early acute phase of ischemic stroke and dynamics of this parameter after the antioxidant treatment with the α-lipoic acid preparation berlition was carried out. It has been shown that the activation of systemic inflammation and related oxidative stress recorded in the early acute phase of brain infarction needs pharmacological treatment. Neuroprotective action of α-lipoic acid related to the prevention of damaging effect of free radicals on cell membranes and reduction of oxidative stress intensity is a pathogenetic explanation for using its preparations in ischemic brain lesions. The decrease in plasma myeloperoxidase content after the treatment with berlition may consider as a criterion of its efficacy.

[Relationship between clinical characteristics and primary and secondary products of lipid and protein peroxidation].

Recent studies showed that activation of free oxygen radicals and the resulting stress play a key role in the development of brain vascular lesions related to hypertensive disease and atherosclerosis leading to chronic cerebral ischemia. To recall, activation of oxidative stress precedes chronic cerebral ischemia and stroke. Therefore, detection of stress markers may be a step toward the development of a new method for the identification of groups at high risk of stroke among patients with the unfavourable course of cerebral ischemia. This study was focused on the relationship between lipid and protein peroxidation products and clinical manifestations of the disease.

[The role of homocysteine levels in the pathogenesis of cognitive disorders in patients with chronic cerebral ischemia].

One hundred and twenty-one patients (mean age 64.13 +/- 8.43 years) with the diagnosis of chronic cerebral ischemia were examined. Somatic and neurological examinations, biochemical blood test, plasma homocysteine measurement, CKT/MRI were carried out. Neuropsychological tests (the MMSE, a battery of frontal dysfunction tests (BFDT), the Clock drawing test, the test of speech activity, the five words test, semantic and categorical associations, the Tailor Manifest Anxiety Scale) were administered: Patients were stratified into 3 groups: group 1 included 34 patients with confirmed cognitive disorders and mild hyperhomocysteinemia (> 15 mcmol/l); group 2 consisted of 51 patients with cognitive disorders and normal levels of homocysteine (< 15 mcmol/l) and group 3 consisted of 36 controls without cognitive disorders and with normal levels of homocysteine. In group 1, the performance of neuropsychological tests was significantly lower and neurological deficit was the most severe. We found reverse correlations between homocysteine levels and severity of cognitive disorders, which were most strong for the results of BFDT, the clock drawing test and the test of speech activity. Hyperhomocysteinemia was positively correlated with the worse values of neurological status and severity of chronic cerebral ischemia.

[The free-radical processes and antioxidant therapy in brain ischemia].

A role of the free-radical processes and disturbances of oxidative-restorative blood homeostasis and nervous tissue in the pathogenesis of brain ischemic pathology and other diseases are reviewed. Attention is focused on the search for optimal ways of pharmacological correction of oxidative stress in the schemes of complex treatment of chronic blood circulation insufficiency and on the necessity of combined application of several antioxidants with different mechanisms of action which reciprocally potentiate each other. Experimental and clinical suppositions of the use of a-lipoic acid as one of the most studied antioxidant in the treatment of brain ischemia as well as the results of own studies on the preparation berlition which contains a-lipoic acid used in the neuroprotective therapy of chronic brain ischemia for correction of free-radical processes are discussed.

[Studying the hepatoprotector effect of bemithyl on a model of chronic toxic liver damage].

A prophylactic and therapeutic introduction of the synthetic adaptogen bemithyl (2-ethylthiobensimidasole hydrobromide) produces a hepatoprotector effect in rats with experimental cirrhosis. The drug exhibits an anticytolytic activity, restores liver participation in the pigment exchange, and normalizes the function of the microsomal oxidation system responsible for the metabolism of xenobiotics. The treatment with bemithyl also leads to a certain improvement of a histologic picture of the damaged liver and to a decrease in the degree of fibrosis. The drug is also capable of increasing the activity of the antioxidant system and inhibiting the process of lipid peroxidation of proteins and lipids in the liver.

[Ethomerzol as an antioxidant]. / Etomerzol kak antioksidantnoe sredstvo.

Ethomerzol (25 mg/kg, intraperitaneally, 30 min before hypoxia) prevents lipid peroxidation activation and antioxidant system suppression in brain and liver of albino rats at acute hypoxia. Injection of ethomerzol decreases accumulation of conjugated diense and malondialdehyde, increases the levels of thiols and the activities of the antioxidant enzymes in the brain and the liver. In the model biological systems in vitro ethomerzol (0.01-40 mM) inhibits of Fe2+-induced ascorbate-dependent lipid peroxidation in a non-metabolizing model, such as liposomes, similar to DMSO and Fe2+-induced ascorbate- and NADPH-dependent lipid peroxidation in the brain homogenates similar to EDTA. Thus ethomerzol exhibits antioxidant properties.

Antioxidant effects of Bemitil during acute cerebral hypoxia.

Bemitil (25 mg/kg) prevented activation of lipid peroxidation and inhibition of the antioxidant system in rat brain during acute hypoxic hypoxia.

[The effect of bemithyl in rats with experimental pneumonia]. / Effektivnost' bemitila pri éksperimental'noi pnevmonii u krys.

The tests on rats with experimental pneumonia showed that bemithyl (50 mg/kg, i.p.) reduces lethal outcome frequency, decreases the accumulation of lactate in lung tissues, and impedes activation of lipid peroxidation.

[Effect of bemethyl on the glutathione system in the rat liver in acute hypoxia]. / Vliianie bemitila na glutationovuiu sistemu v pecheni krys pri ostroi gipoksii.

The effect of bemithyl on the state of liver glutathione system was studied in rats under acute hypoxic hypoxia conditions modeled by "elevating" animals in a pressure chamber up to an altitude of 8000-11,000 m for 30 min. Bemithyl (25 mg/kg, i.p.) administered 30 min before the hypoxia onset, prevents a decrease in the content of reduced glutathione and SH groups and impedes a drop in the activity of glutathione reductase and glutathione peroxidase. By means of the inhibition analysis using actinomycin D (a protein synthesis inhibitor), it was established that the protective action of bemithyl is related to the ability of enhancing the synthesis of antioxidant enzymes in the liver glutathione system.

[Antioxidant effects of amtizol and trimetazidine in brain ischemia]. / Antioksidantnye éffekty amtizola i trimetazina pri ishemii mozga.

Effects of amtizol and trimetazidine (25 mg/kg, i.p., 30 min before and 6, 24, 48 h after the ischemia) on lipid peroxidation in the brain were studied in white rats undergoing occlusion of the common carotid arteries for 90 min, 24 h and 72 h. It was found that administration of the above drugs decreased accumulation of lipid hydroperoxides and malonic dialdehyde, corrected the activity of antioxidant enzymes in the brain after 90 min of ischemia, inhibited activation of lipid peroxidation, elevated the levels of thiol compounds, increased the activity of the glutathione antioxidant system after 24 and 72 h of ischemia.

[The antioxidant effects of amtizol and trimetazidine]. / Antioksidantnye éffekty amtizola i trimetazidina.

Experiments were conducted on rats to study the antioxidant effects of amtisol and trimethasidin (25 mg/kg) in incomplete cerebral ischemia complicated by hypoxia. Amtisol as well as trimethasidin inhibited activation of lipid peroxidation (LPO) and prevented decrease in activity of the antioxidant system. In in vitro experiments amtisol and trimethasidin blocked epinephrine auto-oxidation. Amtisol inhibited ascorbate-dependent LPO in the liposomes and metabolizing model system, inhibited fermentative NADP-dependent POL in brain tissue homogenates.

[The comparative characteristics of the metabolic effects of amtizol and trimetazidine in acute hypoxia]. / Sravnitel'naia kharakteristika metabolicheskikh éffektov amtizola i trimetazidina pri ostroi gipoksii.

Experiments were conducted on rats to study the effect of amtizol and trimetazidine on energy metabolism and lipid peroxidation in the brain, heart, and liver in acute hypoxia. Hypoxia was modelled by "raising" the animals in a pressure chamber to a "height" of 8,000-11,000 m, the exposure lasted 30 min. Equal doses (25 mg/kg) of the drugs were injected intraperitoneally 30 min before the "ascent". It was found that amtizol, just like trimetazidine, prevented energy metabolism disorders and activation of lipid peroxidation in the organs. The metabolic effects of the drugs were unidirectional, but the antioxidant activity of amtizol was pronounced more.