State Of Purine Exchange And Microalbuminuria In Patients With Metabolic Syndrome

The aim of the given work was study interactions of impairments sympa-thetic – adrenal systems functional condition and processes of peroxidal oxida-tion of lipids in woman with metabolic syndrome. 107women at the age of 25-49 were observation. They were randomized into 3 groups: I (control) – 15 healthy persons, II – 43 patients with arterial hypertension, III – 49 women with arterial hypertension in combination with metabolic syndrome. The results of carried investigations showed that activation of sympathetic adrenal system and processes of peroxidal oxidation of lipids took place in metabolic syn-drome. Marked lowering of sympathetic – adrenal system key ferment catechol-amins (MAO monoaminooxidaze) desamidization activity and considerable ac-tivation of peroxidal oxidation of lipid products which have great significance in revealing the mechanism of metabolic syndrome development were observed in metabolic syndrome. This results in the prolonged toxic influence of catechola-mins on myocardium.


INTRODUCTION
Recently, we have faced a new pandemic, i.e. in medicine, a new term for metabolic syndrome (MS) has appeared and it summarizes the main factors leading to the

State Of Purine Exchange And Microalbuminuria In Patients With Metabolic Syndrome
The American Journal of Medical Sciences and Pharmaceutical Research (ISSN -2689-1026)  7,17,18,20]. MS represents a complex of interrelated disorders of carbohydrate and purine metabolism, as well as mechanisms of regulation of arterial pressure and endothelial reticula. The development of these disorders is based on a decrease in tissue sensitivity to insulin -insulin resistance (IR). This symptom complex is also known under the names "metabolic syndrome", "well-being syndrome", "polymetabolic syndrome" "syndrome X", "deadly quartet", "insulin resistance syndrome". More often than others, the names "meta -bolic syndrome "and" insulin resistance syndrome "[2,3,4,15, 18,20].
Glucose and insulin are important factors in uric acid homeostasis, in-volved in the secretion and reabsorption of uric acid. An imbalance in these in-dicators leads to either hypouricemia or hyperuricemia. So, hyperuricemia con-tributes to uricosuria, so the level of uric acid in the blood in patients with de-compensated diabetes mellitus of any type can decrease. The effects of insulin on uric acid secretion are opposite to those of glucose. At the same time, normal levels of insulin have practically no effect on renal hemodynamics, glomerular filtration, and permeability of the renal filter in relation to albumin. The hyperinsulinemia seen in IR and type 2 diabetes mellitus contributes to a decrease in the excretion of lactic acid. This was found in patients with metabolic syndrome and healthy volunteers in whom acute euglycemic hyperinsulinemia leads to transient hyperuricemia as a result of increased reabsorption of sodium and uric acid [12,13,20]. According to studies carried out in the clinic of internal diseases of the RUDN University, with daily monitoring, there was no decrease in blood pressure in patients with high hyperuricemia and a reliable relationship between the left ventricular myocardial mass index and the level of uric acid and blood serum in patients with metabolic syndrome. In patients with hypertension and left ventricular hypertrophy, the concentration of uric acid in the blood is one of the most significant determinants of left ventricular hypertrophy and indicates its resistance to standard antihypertensive therapy. The high level of uric acid is associated with the features of antihypertensive therapy in metabolic syndrome [7,8,12,14].
Consequently, hyperuricemia (HUA) and microalbuminuria (MAU) are closely interrelated processes that characterize the clinical manifestation of MS. Howev-er, studies on the state of purine metabolism and microalbuminuria in MS pa-tients are insufficient and this problem needs further comprehensive research.

PURPOSE OF THE WORK
Study of the state of purine metabolism and microalbu-minuria in patients with metabolic syndrome.

MATERIAL AND METHODS.
50 patients aged from 30 to 55 years old, suffering from MS, were examined, taking into account the risk factors and damage to organs -targets. In a hospi-tal, 18 male (34.7%) and 32 female (65.3%) patients aged 30 to 55 years were examined, who were randomized into the following 3 groups: I (control) -healthy individuals aged 25 -40 years old -15 people; II - express analyzer "Reflotron-Roche" ), blood glucose (glucose oxidase method) .The state of purine metabolism was determined enzymatically by the colorimetric method according to the level of uric acid in the blood serum on an automatic analyzer StatFax Awarenes technology INC (Italy), using rea-gents Hospitex diagnosticss.rl (Italy). The results of clinical trials were processed using the applied statistical processing programs of the Excel program, as well as by the method of variation statistics using the tables of Student's ttests. Differences between the arithmetic mean values were considered statisti-cally significant at p <0.05.

RESULTS AND DISCUSSION
In the majority of patients with MS, the disease was associated with a heredi-tary factor (31.5%), obesity (30.0%), an alimentary factor (28.4%), and low physical activity (hypodynamia -10, 1%), (Fig. 1). In the alimentary factor group, patients indicate excessive consumption of carbohydrates and fats. Excess body weight and obesity are considered the main components of MS. And at the same time, the relationship between the components of the MS is of par-ticular interest. In the examined patients, the Quetelet index (IR), body weight and the degree of abdominal obesity (AO) were determined. Measurement of the waist circumference in group I showed 78.8 ± 1.14 cm, in group II 80.3 ± 0.46, and in MC-102.5 + ± 1.5 cm (Tab -1). In patients with AH, AO was 1.9% high-er than in the control group, i.e. the figures were almost the same. When examining the IC in the control group, this indicator showed 24.3 ± 0.7 m2, and in the II group, IC was equal to 26.7 ± 1.3 m2. In the GB group, IK was higher by 4.9%, the indicators were almost the same. In MS, IC averaged 32.6 ± 0.8 m2, was higher than the indicators of the control group by 35%, indicators of the second group by 28.6%. The results obtained suggest that blood pressure and glycemic levels are related to body weight. We did not find a reliable relationship between the mag-nitude of uricemia and the level of blood pressure, but in persons with a clinical picture of metabolic syndrome without hypertension, the level of MC was sta-tistically significantly lower than in patients with a clinical picture of MS, and there was also a tendency for a lower value of this parameter in comparison with all groups of patients in which MS proceeded with AH.  Note : * р<0,05,**р<0,01,***p<0,001 In our study, hyperuricemia was detected in 52.6% of patients suffering from MS, which is slightly higher than the data of other authors. However, the frequency of violations of purine metabolism depended on the presence of concomitant components of MS: in its absence, it was only 22.2%, increased as the clinical picture of the syndrome progressed and reached a maximum of 68.6% -in patients with MS. In addition, we noted that the concentration of MC in the blood significantly correlated with the severity of obesity, hyperinsulinemia, triglyceridemia, and glycemia -parameters reflecting the state of IR.
Thus, the data obtained indicate that hyperuricemia is a metabolic disor-der and one of the components inherent in metabolic syndrome.
We examined 26 MS patients for MAU. The patients were divided into groups. The criteria for the formation of the groups were the stages of diabetic nephropathy (DN): 1 -group -patients with normoalbuminuria: urinary albumin excretion below 30 mg / day; Group 2patients with MAU: urinary albu-min excretion from 30-300 mg / day; 3 -group -patients with proteinuria (PU) detected in the study of daily excretion of protein in the urine and with preserved nitrogen excretory function of the kidneys (serum creatinine level below 110 mmol / L). The results of the study showed that MAU was expressed in pa-tients with hypertension in 22.4% of cases, in patients with MS -in 75.2% of cases.
In the presence of MS in patients, non-selective proteinuria is noted in 80.1% of cases.  Most cases of MS occur against the background of long-term coexistence of risk factors, which include an increase in triglycerides, low-density lipopro-teins (LDL-C) and a decrease in plasma HDL levels. Studies carried out in recent years on large groups of patients with MS have shown that most of the general-ly accepted risk factors retain their negative effect in the presence of dyslipidemia, i.e. against the background of an increased level of TG and cholesterol, which is the dominant biochemical factor of atherosclerosis, in particular, it was shown that the existing risk factors (age, diabetes mellitus, arterial hyperten-sion, an increase in LDL, a decrease in HDL) are risk factors for MS [2,4,5 , 7,8,12,13,16,18,20]. There are also works that emphasize that the listed param-eters cannot fully explain the variability of the clinical course of MS.
As can be seen from  According to a number of authors, it is difficult to separate MS from hyperu-ricemia, as well as to determine causal relationships, because, according to mod-ern ideas about the pathogenesis of MS, these states mutually induce the emer-gence and consolidation of each other. Hyperuricemia is detected in 25% of MS patients. The importance of the relationship between hyperuricemia and the de-velopment of MS, atherosclerosis and ischemic heart disease is evidenced by the relationship of hyperuricemia as a factor.

CONCLUSION
Thus, the data obtained indicate that hyperuricemia is a meta-bolic disorder and one of the components inherent in metabolic syndrome. The severity of GU is directly proportional to the increase in the clinical picture of MS. In patients with MS, the presence of normoalbuminuria indicates an adap-tive-compensatory vascular reaction aimed at overcoming the developing pathology of the kidneys. The presence of MAU means that the MAU stage can be reversible if treatment is started on time and will slow down the progression of DN and its transition to the stage of PU and CRF. The presence of MAU -about glomerular hypertension and a decrease in glomerular filtration.