The author analyzes the neuroendocrine relationships between the true adrenergic and cholinergic neuromediators and peptide neuromediators, on the one hand, and neurosecretory neurons regulating gonadotropin and prolactin secretion, on the other. About 30 neuromediators of different origin are characterized with due consideration for their localization in the CNS structures, involvement in the production and secretion of gonadotropin releasing factor, gonadotropins, prolactin, and, hence, the function of the reproductive system in general. The impact of the hormone background of sex steroids in the system of these intricate relationships is analyzed. The author presents his own findings and published data on the time course of catecholamine levels in hypothalamic structures involved in the regulation of the pituitary gonadotropic function and analyzes correlations between changed levels of sex steroids and gonadotropins in the blood and the time course of changes of catecholamines and luteotropin releasing factor in the hypothalamus. Possible mechanisms of coordination of different neuromediators of adrenergic origin and amino neuromediators with different mechanisms of action during the regulation of normal function of the reproductive system are discussed. The author assesses the efficacy of treating disorders of the reproductive system caused by the CNS disorders by combinations of sex hormones and neurotropic agents.

The sufficiency of vitamins С, A, E. B2, B$, and carotenoids was assessed in 32 patients of both sexes with non-insulin-dependent diabetes on home diets, in spring 1996. A deficit of group В vitamins (56-66%) and carotenoids (50%) was detected in the majority (68.8%) of examinees, while the levels of vitamins C, A, and E were sufficient. Hence, improvement of the vitamin status of diabetics is a most important component of treatment.

Effects of long glurenorm therapy on daily arterial pressure (AP), central hemodynamics, and diastolic function of the left ventricle were assessed in patients with non-insulin-dependent diabetes with stages I and II essential hypertension. The patients were divided in 2 groups: group I (n=24) treated with manilil (5-20 mg/day) and nifedipin (20-50 mg/day) and group II (n=24) treated with glurenorm (60-150 mg/day). Control groups consisted of diabetics without arterial hypertension: group III, glurenorm, and group IV, manilil. AP decreased in 88% of patients in groups I and II during the second week of treatment, the maximal decrease was observed by the and of week 12. Decrease of AP in groups I and II was paralleled by a decrease of the total peripheral resistance, improvement of leftventricular diastolic function, and no effect of myocardial contractility. One probable mechanism of the hypotensive and vasodilating effect of glurenorm is decrease of basal insulin level, whose values were higher in groups I and II in comparison with the control and correlated with daily AP values.

Epidemiological screening has been carried out in West Siberia in order to assess the prevalence of iodine deficiencies. The incidence of goiter was assessed, iodine excretion with the urine measured in children, and levels of neonatal thyrotropic hormone (TTH) measured in the course of screening for congenital hypothyrdsis. The findings confirmed the significance of measuring TTH in the newborns for detecting the degree of iodine deficit. The incidence of increased TTH level (more than 25 IU/liter) in the newborns of West Siberia (1.69%) is notably higher than in previously screened provinces of Canada and Australia without iodine deficit and Southern Poland cities with a moderate iodine deficit. Analysis of the frequency distribution of neonatal TTH levels in various geographical regions of the Tyumen district indicates a higher incidence of iodine deficiencies near and beyond the Polar Circle and in the Urals. These findings coincide with previous data on increased incidence of goiter and decreased iodine excretion with the urine in these regions. Monitoring of TTH levels within the framework of program of screening for congenital hypothyrosis can be used to assess the prevalence of iodine deficiencies in the population.

The clinical significance of measuring thyroid antibodies has been evaluated. With this aim in view, 47 patients with diffuse toxic goiter (DTG) (46 women and 1 man) aged 15 to 65 were examined. Antibodies to TTH receptors were detected in 85 patients with decompensated DTG by the radioligand method based on assessment of blocking of TTH binding to its receptor in the presence of patient’s serum. Antibodies to thyroglobulin (TG) were detected in 55.6% patients before therapy. Blood level of TG was increased in 42% of patients. Antibodies to the microsomal fraction (MS) were detected in 59% of patients. The activity of antibodies to TTH receptor depended on the disease severity, degree of the thyroid enlargement, and size of goiter. The incidence of antibodies to TG and their titers did not depend on the severity of thyrotoxicosis or size of goiter. The incidence of antibodies to MS increased only with enlargement of goiter. The incidence and titers of antibodies gradually decreased in the course of mercasolyl therapy of DTG. After 6 months antibodies to TTH receptors were found in 57% of patients, their activity being decreased, too. The incidence of anti-MS antibodies dropped to 45%, whereas the rate of detection of antibodies to TG was virtually the same. One year after therapy antibodies to TTH receptors were found in 29.4%> of patients. The rate of detection of antibodies to TG and MS decreased to 25 and 20%o, respectively. Hence, a high rate of detection of antireceptor antibodies in DTG and the relationship between the thyroid status and the titer of these antibodies confirm their leading role in the pathogenesis of the disease. The presence of antibodies to TG and MS in no more than half of the patients with DTG and absence of a clear-cut correlations between these antibodies and various clinical hormonal parameters of the disease indicates their significance solely as markers of the autoimmune process in the thyroid but does not specify the nature of its involvement. Antibodies to TTH receptors are the most informative immunological test for the diagnosis of DTG and the markers of immunological remission of the disease.

The aim of this study was to assess the efficacy of various methods for monitoring the intake of 100 pg potassium iodide for preventing endemic goiter. The study was carried out in a region with slight and moderate iodine deficit. A total of 104 children aged 10-11 years were examined. Group 1 children were administered 100 \ig of iodine 5 times a week, group 2 had the same dose daily, and group 3 were controls. After 3months the mean concentrations of iodine increased in group 1 from 4.9 ig/liter to normal values (12 ig/liter), in group 2 the content of iodine in the urine increased from 5.3 to 9.9 ig/liter, which means that slight iodine deficiency was still present, and in the controls urinary iodine content increased to 7.8 ig/liter. After 6 months, iodine excretion with the urine was somewhat decreased in all the groups; the most probable cause of this decrease was irregular intake of the drug. Six months after the drug was discontinued, the content of iodine in the urine was below the initial level. The incidence of thyroid enlargement decreased approximately by half in both groups treated with iodine drugs, despite the fluctuations in renal iodine excretion: from 13.8 to 7.1% in group 1 and from 23.3 to 12.5%> in group 2. In the controls the incidence of thyroid enlargement did not change. Thus, we demonstrated a high efficacy of potassium iodide for preventing and treating endemic goiter in regions with slight and moderate iodine deficiency. However, this method requires great accuracy, because irregular intake of the drug deteriorates the results of treatment.

Examinations of 14 healthy males, including measurements of the main adrenal and testicular androgens and their precursors, estradiol, and pituitary gonadotropic hormones in the peripheral blood, revealed that the levels of the main adrenal and testicular androgens do not correlate. Assessment of the hormonal status of 24 patients with hypogonadism showed that a deficit in the production of testicular androgens is not compensated for by hyperproduction of adrenal androgens. Testosterone production in patients with acquired anorchism, who were never administered substitute androgen therapy, is about 1/12 of this hormone’s production in health. Hence, the secretion of testicular and adrenal androgens is regulated by different mechanisms.

According to special, but not always complete reports and relevant studies, one in ten adult residents of Russia suffers from a particular digestive system disease (P. Grigoryev // Med. Newspaper. - 1996. - April 24). Their timely identification was facilitated by the widespread introduction of endoscopic studies into clinical practice using standardized methods for evaluating the results. At the same time, endoscopic examinations are still often carried out without necessarily obtaining a biopsy for subsequent histological and, more importantly, immunohistochemical studies. The latter allows you to more objectively judge the etiological causes of the disease, among which endocrine occupy a special place.

Binding of [³H]-16a-cyclohex-3'-enoprogesterone (I) and [³ H]-progesterone (II) with soluble fraction proteins of the rat uterus is compared. I specifically reacts with progesterone receptor but not with other proteins. Its affinity to the receptor assessed from K_d (11.6+2.0 nM), Kj (15 nM) values and relative competitive'activity (0.89+0.35 and 0.33+0.04 with [³H]-I and [³H]-II, respectively) is just negligibly inferior to the affinity of the natural hormone (K_d=6.9+2.6 nM, Kj=8.5 nM, relative competitive activity =1). The dissociation of [³H]-I and [³H]-II complexes with the receptor was biphasic with similar constants of dissociation rate (kf_I=1.8x.lO'⁵C'¹; кД=4.5*10'⁴ C¹). Specific features of [³H]-I reaction with the receptor in comparison with [³H]-II are a lesser share of rapidly dissociating [³H]-I complexes and a lower capacity of [³H]-I to prevent the receptor degradation. It is probable that the detected features reflect the differences in the receptor conformation and are associated with the selectivity of I action.

The author hypothesizes a probable causative role of alteration of ascorbic acid concentration in the brain in the development of mental disease in diabetics. In order to verify this hypothesis, ascorbic acid was measured in the brain cortex of rats 21 days after induction of streptozotocin diabetes or 1 h after intraperitoneal injection of glucose in a dose of 5 g/kg. Ascorbic acid level was increased both in diabetes (456+26 yg/g tissue versus 415+37 \vg/g in the control, p<0.01) and in acute hyperglycemia (475+54 \tg/g versus 406+65 \xg/g in the control, p<0.001). This confirmed that changed concentration of ascorbic acid in the brain can promote the development of a mental disease in diabetics. In the liver the concentration of ascorbic acid was decreased in streptozotocin diabetes (by 17%), p<0.001) and increased in acute hypoglycemia (by 24%, p<0.01). The findings permit us to hypothesize that hypoglycemia inhibits the production of ascorbic acid from the liver to the blood in rats and impedes the transport of ascorbic acid through the gut wall into the blood in humans.

Diabetes mellitus is a clinically and genetically heterogeneous disease characterized by absolute or relative insulin deficiency and (or) peripheral tissue resistance to the hormone. Each of these disorders individually or in various combinations reduces tissue glucose consumption and increases the concentration of this monosaccharide in the patient’s blood. The state of hyperglycemia is a necessary and, over time, sufficient condition for the development of the so-called late complications of diabetes mellitus (mainly vascular - diabetic angiopathies). These chronic complications of diabetes are the main cause of high disability and mortality in patients, thus representing not only a serious medical and social, but also an economic problem [60]. This problem is exacerbated by the fact that recently there has been a tendency to an increase in the incidence of diabetes [42], the expected prevalence of which by 2010 will be about 215 million people [59]. In addition, the most common form of the disease, non-insulin-dependent (type II) diabetes mellitus (NIDDM), is characterized by delayed diagnosis and under-detection of the disease in the general population, leading to a significantly underestimated estimate of its prevalence [29, 30].

Atherosclerosis and related disorders of carbohydrate metabolism go beyond narrow cardiological problems and, in one way or another, are the subject of close attention of doctors of various specialties, including endocrinologists. In everyday practice, most endocrinologists leave the solution of issues related to hyperlipidemia “for later”, because, first, for many decades, full compensation for diabetes and hypothyroidism - conditions in which secondary hyperlipidemia is most common - was difficult ; secondly, there were no effective and safe means for treating hyperlipidemia, which made generations of doctors skeptical about the possibility of real correction of lipid metabolism disorders. Improving the methods for compensating for diabetes mellitus and the possibilities for treating hypothyroidism have brought clinicians to the problem of the need for additional therapy with lipid-lowering drugs, so the pathogenesis and treatment of hyperlipidemia are of great interest to them.