SYNDROME IN WOMEN IN PERIMINOPAUSE

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Julian Poole
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1 УДК Kodirova G.I., Kholikova D.S., Toshtemirova I.M. Andijan State Medical Institute Uzbekistan, Andijan сity Кодирова Г.И., Холикова Д.С., Тоштемирова И.М. Андижанский государственный медицинский институт Узбекистан, г. Андижан METABOLIC SYNDROME IN WOMEN IN PERIMINOPAUSE Abstract: This article discusses the relationship between the state of the sympathetic adrenal system and the processes of lipid peroxidation in women of fertile age with a metabolic syndrome Key words: metabolic syndrome, arterial hypertension, sympathetic-adrenal system, lipid peroxidation, monoamine oxidase, catecholamines, malonic dialdehyde, fenofibrates. МЕТАБОЛИЧЕСКИЙ СИНДРОМ У ЖЕНЩИН В ПЕРИМЕНОПАУЗЕ Аннотация: В этой статье обсуждается взаимосвязь между состоянием системы симпато-надпочечников и процессами перекисного окисления липидов у женщин фертильного возраста с метаболическим синдромом Ключевые слова: метаболический синдром, артериальная гипертония, симпатико-адреналовая система, перекисное окисление липидов, моноаминоксидаза, катехоламины, малоновый диальдегид, фенофибраты. The metabolic syndrome (MS) today is the most acute medical and social problem of the present and is seen not only as a frequent pathology, but also as a lifethreatening condition, since cardiovascular complications of MS are the leading cause of death worldwide, according to WHO. Of great interest at the present time are metabolic disorders in estrogen deficiency states in women, as well as the contribution of each individual component to the formation of cardiovascular pathology and the direct influence of the constituents of MS on each other, as these issues have not been sufficiently studied to date. The menopause period is a complex stage in the life of a woman, as it reflects a

2 direct transition to the aging of the organism and, in addition, is accompanied by multiple metabolic disturbances. The course of metabolic disorders in estrogen deficiency states has a number of features, such as: an increase in body weight in the perimenopausal period, triggering a cascade of pathological reactions leading to the formation of metabolic disturbances; aggravation and progression of the course of individual components of the MS, if they exist before the onset of menopause and involvement of new organs in the pathological process, which contributes to the development of complications of MS; the direct effect of estrogen deficiency on the process of mutual weighting of the MC component flow, which contributes to the formation of "vicious circles". The most significant increase in the prevalence of MS components in women is observed at the age of years. Data have been obtained that the high incidence of individual MS components in the Northwest region is also high in the perimenopausal period, as in the general population: arterial hypertension (AH) was found in 58.39%, hypercholesterolemia in 47%, hyperglycemia - mia - in 7.3%, in the absence of hypertension, increased body weight / obesity - in 51% of cases (26.9% and 24.1%, respectively). With the onset of menopause, the risk of developing cardiovascular diseases (CVD), type 2 diabetes mellitus (DM) is significantly increased, and in women in the period of peri- and menopause suffering from type 2 diabetes, the risk of cardiovascular disease increases by a factor of 3-7 compared with healthy women of the same age [11]. An increase in the incidence of CVD in the perimenopause has been shown with an increase in BMI: BMI %, BMI %, BMI %, BMI 35-39, 9-50%, BMI> 40-67% [10]. In women in the menopausal period, a combined cardiovascular pathology often develops, the formation of which begins with the first years of menopause, which significantly increases the risk of fatal complications. According to the Framingham study, the incidence of acute coronary events is increased 12-fold in postmenopausal women compared with women of reproductive age. A prospective study of ARIC showed a

3 two-fold increase in the risk of developing ischemic stroke in both men and women with MS. The concept of the formation of the menopausal metabolic syndrome. The contribution of estrogen deficiency to the formation of cardiovascular pathology. The concept of the formation of the menopausal metabolic syndrome in women is proposed by C. P. Spenser et al. in It is based on estrogen deficiency and, as a consequence, abdominal redistribution of adipose tissue, the onset of lipid and carbohydrate metabolism disorders, pathological changes in the hemostasis system, and the formation of insulin resistance (IR). According to some authors, approximately 60-65% of women in the perimenopausal period have a sharp increase in body weight, triggering a cascade of pathological processes in the body, leading to the formation of MC. According to other data, dynamic monitoring of a group of 1000 women during the menopause revealed no changes in body weight in 44% of patients, a decrease in 16%, and an increase in only 40%. E. T. Roelhman and A. Tchernof showed that in women after 48 years the rate of basal metabolism decreases by 4-5% for each decade, which requires increased control of body weight in women of this age group to prevent the development of obesity. Studies show that the nature of fat deposition in women in menopause does not depend on the degree of obesity and age, but depends only on the cessation of ovarian function: in early postmenopausal women, the fat volume in the thigh region is more by 36%, and the volume of intra-abdominal fat by 49% compared with women with preserved ovarian function [21]. In 2009, the International Diabetes Federation, with the participation of the American National Heart, Lung and Blood Institute, the American Heart Association, the World Heart Federation, the International Society for Atherosclerosis, the International Society for the Study of Obesity, the criteria for diagnosing MS were updated. According to the new criteria, MS can be diagnosed if there are any of the following three of the following: hypertriglyceridemia ( 150 mg / dl or 1.7 mmol / L) or normal triglyceride levels with appropriate therapy. This circumstance casts doubt on the validity of the concept of C. P. Spenser et al. about the menopausal metabolic syndrome and suggests the need for further study of the problem of metabolic disorders. It has been shown experimentally that

4 estrogens exert a direct effect on the cardiovascular system, affecting the vascular endothelium and cardiomyocytes, as well as the mediated effect, by acting on lipid, carbohydrate metabolism and hemostasis system. The perimenopausal period as an estrogen-deficient state contributes to aggravation of endothelial dysfunction due to impaired synthesis of nitric oxide and stimulation of the opening of calcium channels in the cell membranes of smooth muscle cells of vessels, increased rigidity of the vascular wall, manifested by lower compliance and higher pulse-wave velocity, vascular wall, leading to a change in the elastin / collagen ratio and proliferation of smooth muscle cells. Estrogen deficiency leads to the activation of the reninangiotensin system, resulting in increased plasma renin and angiotensin-converting enzyme activity, blood levels of angiotensin-2 and the number of receptors to it increase. The onset of menopause also contributes to the activation of the sympathetic nervous system. Hypercatecholamineemia leads to an increase in heart rate and increased vascular tone. It has been shown experimentally that the administration of estrogens to women after ovariectomy has been removed eliminates sympathicotonia. In hyperinsulinemia (GI) in menopausal women who do not receive hormone replacement therapy with sex steroids, the platelet aggregation capacity increases: the concentration of camp and cgmp in platelets decreases, thromboxane synthesis increases, concentration of procoagulants increases, concentrations and activity of antithrombotic factors decrease. Women with preserved ovarian function have a higher level of proconvertin compared to men, but lower levels of fibrinogen in the blood and a lower activity of the tissue plasminogen activator and plasminogen activator inhibitor-1, which provides a lower risk of arterial thrombosis due to the action of estrogens. In addition, estrogens help increase the level of high-density lipoprotein (HDL) and inhibit circulation and accumulation of low-density lipoprotein (LDL) in the arterial wall, inhibit the accumulation of lipids in macrophages and convert them into foam cells. Thus, hypoestrogenia, having a complex effect on the cardiovascular system, leads to endothelial dysfunction, increased blood pressure, left ventricular hypertrophy (LVH), and vascular wall remodeling, contributes to the equilibrium

5 shift in the thrombus-fibrinolysis system, thereby increasing the risk development of cardiovascular diseases. Obesity as a component of MS. His contribution to the pathogenesis of cardiovascular pathology in women. It has been established that the risk of developing diseases associated with obesity is largely determined by the distribution of adipose tissue in the body [11]. It is also important that insulin resistance occurs in 88% of patients with android obesity, regardless of the degree of obesity 42, while 32% of persons with obesity obesity have MI, and mainly, with obesity of 3-4 degrees [ 25]. Obesity promotes an increase in the rate of androgen metabolism and an increase in the rate of their production, and with abdominal obesity, the testosterone production rate is significantly higher than in the case of the gynoid type of subcutaneous fat distribution. Literature: Medicus.ru:

Term-End Examination December, 2009 MCC-006 : CARDIOVASCULAR EPIDEMIOLOGY

MCC-006 POST GRADUATE DIPLOMA IN CLINICAL CARDIOLOGY (PGDCC) 00269 Term-End Examination December, 2009 MCC-006 : CARDIOVASCULAR EPIDEMIOLOGY Time : 2 hours Maximum Marks : 60 Note : There will be multiple