Annotation. Polytrauma is considered the main cause of death among people younger 45 years. Among trauma patiens 15-20% regularly take alcohol, close to 32% of patients who needed intensive therapy to alcohol withdrawal syndrome (AWS), and 5-20% of the progressed to alcohol delirium. The aim of the study is to analyze the dynamics of autoimmune response to markers of neurodestruction in the blood of patients with moderate polytrauma and alcohol withdrawal, complicated by alcohol delirium and assessment of cognitive functions depending on the method of sedation. The study involved 80 patients with moderate polytrauma with alcohol withdrawal, complicated by alcohol delirium. The median age was 45 years (39-54). Patients in Group 1 (n=40) were given dexmedetomidine as a sedation method, and in Group 2 (n=40) diazepam sedation was used according to the symptom-trigger protocol. The content of antibodies to neuron-specific enolase (NSE), myelin basic protein (MBP), total human brain antigen (THBA), S-100 calcium were determined by enzyme-linked immunosorbent assay on days 1, 3, 7 and 14 after alcohol delirium. Assessment of cognitive function was performed (after withdrawal from sedation if present) on days 4 and 14 using the Montreal Cognitive Assessment Scale (MoCa). Mathematical processing of the obtained results was performed in accordance with the generally accepted methods of statistical analysis. The critical value of the significance level (p) was taken as ≤5%. Signs, the distribution of which differed from normal, are presented in the form of Me (median), the confidence interval within the first and third quarters [QI - QIII]. To assess the causal role of various factors in the development of lesions used χ-square with the inclusion of the Yates correction and the odds ratio. In the first 24 hours after the manifestation of AD, the levels of autoantibodies in the two groups of patients did not differ significantly from the level of healthy volunteers. Estimation of the level of antibodies to the S-100B protein showed that in group 1 this indicator increased by a maximum of 24.4% and amounted to 15.8 [14.7 - 17.6], while in the second group increased by 32.6% and became 17.5 [15.3 - 19.7]. From the 7th day, the number of antibodies began to decrease in both groups and was 15.6 [13.6 - 16.8] in group 1 and 16.3 [14.1-19.2] in group 2 on the 7th day, and 14.0 [11.6 - 15.3] and 15.2 [ 13.1 - 18.3], respectively, on the 14th day after hospitalization in ICU. The level of antibodies to NSE was maximum on the 3rd day of the study and was 29.8 [28.4 - 31.8] in patients of group 1, which is higher than the initial level by 26.8%, and in patients of group 2 was 31.6 [29.5 -33.2], which exceeds baseline by 33.9% (p=0.0114 between groups 1 and 2). Subsequently, there was a decrease in the level of antibodies to NSE on the 7th and 14th day after the onset of AD, while maintaining a significant difference between the comparison groups. Antibodies to MBP did not differ between groups up to and including day 3, but were significantly higher than in healthy volunteers. On the 7th day, the level of antibodies to MBP in group 1 was 26.8 [24.4 - 28.8], which corresponded to the values of the control group, and in group 2 was 29.3 [27.7 - 31.5], which is significantly more than the first group (p = 0.0017). In the study on day 14, this trend was maintained: the level of antibodies to OBM among patients in group 2 was 28.6 [27.0 - 30.8], while in group 1 it was 26.2 [23.7 - 28.2]. Antibody levels to THBA on day 3 were significantly higher than baseline and were 30.8 [28.4 - 34.5] in group 1 and 32.7 [30.6 - 36.1] in group 2 (p=0.0056). On day 7 and day 14, the number of antibodies THBA in patients of group 1 did not differ significantly from the control group, while in patients of group 2 they were significantly higher on day 7 - 31.5 [29.4 - 34.9] and normalized on day 14. When analyzing the results of the MoCa test after eliminating the main manifestations of alcohol withdrawal syndrome (4 days after admission to ICU), the number of points in the study groups was significantly lower than the control values: in group 1 1.3 times (p <0.0001), in group 2 – 1.6 times (p<0.0001). The differences between the studied groups of patients are significant (p = 0.000087). Thus, the use of dexmedetomidine for the sedation of patients with hypertension and polytrauma reduces autumnal neurodestruction, which improves the prognosis for the restoration of cognitive function.
The first part of the review presents data on the content of magnesium in organs and tissues of the human body, the role of magnesium in the implementation of multiple functions, and the peculiarities of its intake and excretion from the body. A significant part of the review is devoted to methods for determining the concentration of magnesium in biological fluids of the human body. The advantages, disadvantages and limitations of various methods are presented. The most common methods for studying the concentration of magnesium in biological fluids of the body, which are used in clinical medicine all over the world, are photometric methods with dyes. The role of the fraction of ionized magnesium in the body, the content of which is determined electrochemically, is still uncertain. Cellular magnesium studies are extremely complex and time-consuming. Cells of different organs and tissues normally contain very different amounts of magnesium. It is not possible to judge about the presence of magnesium deficiency in the body by its concentration in plasma or serum. To detect a decrease in the tissue content of magnesium, tests with magnesium load and the subsequent observation of the rate of its excretion from the body are used. The causes for the development of hypomagnesemia are extremely numerous. The main of them are: any severe stress, restriction of magnesium intake into the body, an increase in its losses through the gastrointestinal tract and the kidneys in various pathological conditions. The formation of hypomagnesemia is facilitated by therapy with numerous medications, which are very widely used in clinical practice, and especially in the intensive care. Studies on the distribution of magnesium in the body after its intravenous administration have shown that, despite the large size of hydrated magnesium ions, they can not only paradoxically quickly spread in the extracellular water space, but most likely are also able to quickly penetrate through cell membranes, spreading in the intracellular water compartment.
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