The cost efficiency of neonatal screening for congenital hypothyroidism has been estimated. The cost of one newborn screening Is 99.37 rubles and that of detection of a patient with congenital hypothyroidism are 430,582.67 rubles. The state's negative profits due to patients disability, which includes social security benefits and undone gross domestic product, have been stated to be 5,687,356 0 rubles per disabled person. The cost efficiency of neonatal screening is determined by the absence of a need for social payments and by the amount of gross domestic product, which are made by these patients due to their preserved working ability and it is 5.35 rubles per ruble invested in a screening program

The purpose of the study was to evaluate moxonidme therapy on the daily profde of blood pressure (BP), insulin sensitivity, glucose tolerance, carbohydrate and lipid metabolic parameters, and vascular endothelial function in patients with metabolic syndrome (MS) and grade 1 arterial hypertension (AH). The study included 20 patients (8 males and 12 females) aged 44.85±5.87 years, who had MS and grade 1 AH. All the patients took moxonidine in a dose of 0.2 mg twice daily. Body weight and waist and hip circumferences were measured, a biochemical blood study (lipid profile, glucose, uric acid, liver tests) and oral glucose tolerance lest determining endogenous insulin and C-peplide were performed, leptin and blood vasoactive hormones were estimated, and office BP measurement and 24-hour BP monitoring were made at baseline and after 12-week therapy. Target BP could be achieved in 90% of the patients. After therapy, there were significant body weight losses, improved daily BP profile, increased glycemic index, and better lipid profile. In addition, moxonidine therapy caused significant decreases in vasoconstrictive hormones and leptin and an elevation in nitric oxide levels. Along with antihypertensive activity, moxonidine exerts a positive effect on insulin sensitivity, lipid metabolism, and endothelial function in patients with MS and AH.

Based on the analysis of the classifications of endocrine ophthalmopathy (EOP), described in the literature and their many years' own observations of patients with this condition, the authors propose their classification. EOP is divided into 3 forms, 2 of which may be characterized by the compensation of a pathological process and by the stages of its development (from active cellular infiltration to end-stage fibrosis). The former of the forms (exophthalmic thyrotoxicosis) frequently regresses during endocrinological therapy. Edematous exophthalmos and endocrine myopathy may be complicated by an irreparable loss of visual functions and working capacity. These patients should be treated by ophthalmologists, by obligatorily keeping in mind the compensation of a pathological process and the stage of its development.

Ninety-five preschool age children living in an iodine deficiency area were examined. Neonatal screening forcongenital hypothyroidism showed that 79 and 16 children had a thyroid-stimulating hormone (TSH) level of 20-50 and 51-100 uIU/ml, respectively, which became normal in the first 6 months of life. A control group comprised 35 children of the same age who had a TSH level of as high as 20 uIU/ml. A study of thyroid function revealed subclinical hypothyroidism in 16.8% of cases and an isolated increase in free triiodothyronine with the normal levels of TSH and free T_«. Volumetry Indicated detected thyroid hypoplasia in 36.8% of the children. In the study group, the neuropsychological development Index was 90-110scores in 38(40.0%) children, 80-89 scores in 24(25.3%), and less than 80 scores In 33 (34.7%). The found changes in the pituitary-thyroid system in the study group determine a risk for thyroid disease and cognitive defects, which requires a follow-up of such children and drug correction of thyroid function.

In patients with coronary heart disease (CHD) and periodically recorded impaired fasting glycemia, the Incidence of impaired glucose tolerance and type 2 diabetes mellitus was 61.6 and 17.8%, respectively. CHD patients with a history of carbohydrate metabolic disturbance were observed to have hyperinsulinemia on fasting and 2 hours after glucose load. In these patients, ambiguous changes were found in C-peptide 2 hours following glucose load. Changes were ascertained in the lipid spectrum.

Lipoid adrenal hyperplasia (LAH) is a most severe type of congenital adrenal cortical dysfunction (CACD). In this type of CACD, there is defect in the conversion of cholesterol to pregnenolone, as a consequence the production of all steroid hormones was impaired in both the adrenals and gonads. Defects of the STAR gene encoding for a steroidogenic acute regulatory (StAR) protein underlie the disease in most cases. Until the present time, there have been no reports on cases of LAH in the Russian literature. The diagnosis of LAH was established by the authors in three genetic girls aged 2.3 years, 6 and 7 months who had a normal structure of the external genitalia and in whom the disease was marked by manifestations of primary hypoadrenocorticism at the age of 21, 2, and 10 days, respectively. A hormonal study failed to show elevated levels of Cortisol and 17-hydroxyprogesterone in response to adrenocorticotropic hormone stimulation. A molecular genetic study revealed the following STAR gene defects: P129AC/W250X, IVS5-1G, and W147X, respectively. Р129ЛС, IVSS, and W147X mutations have not been earlier described. The data of the observation emphasizes the need of including LAH into the algorithm of differential diagnosis of CACD in children with the normal female structure of the external genitalia. The molecular genetic analysis should be prominent in diagnosing LAH, by taking into account the lack of hormonal markers of the disease.

The study was undertaken to define the frequency of nonclasslcal 21-hydroxylase deficiency confirmed by CYP21 gene mutations in girls with pubertal hyperandrogenlsm, to estimate the value of clinical and hormonal markers of nonclasslcal 21-hydroxylase deficiency. Eighty-five girls aged 5-17 years who had hyperandrogenlsm (pubertas precox, hirsutism, acne vulgaris). All the examinees underwent adrenocorticotropic hormone (ACTH) (Synacthen-depot) test. After detecting the hormonal markers oj"nonclassical21-hy-droxylase deficiency (the baseline level of 17- О HP being was above 9 nmol/l and/or above 45 nmol/l after A CTH stimulation), the authors analyzed the most common CYP21 gene mutations. The frequency of nonclassical 21-hydroxylase deficiency supported by CYP21 mutations In the girls with hyperadrogenlsm was 8.3%. There were no clinical differences between the nonclassical form of 21-hydroxylase deficiency and other forms of hyperandrogenlsm. The high baseline 17-OHP ( > 20 nmol/l) is the most specific hormonal marker of nonclasslcal 21-hydroxylase deficiency. Glucocorticoid therapy is indicated for patients with substantially accelerated growth and bone maturation and in those with menstrual irregularities as oligomenorrhea or amenorrhea.

The state of enzymatic and non-enzymatic components of the antioxidative defense system (ADS) and lipid peroxidation was studied in the homogenates of the brain of rats with diabetes melhtus (DM) on days 30, 60, and 90 after administration of alloxan. There was a decrease in the buffer capacity of ADS: reductions in the activities of superoxide dismutase (on DM days 60 and 90), glutathione peroxidase and antiradical activity (on day 90) and glutathione reductase (in all periods of DM). This was followed by the progressive enhancement of lipid peroxidation processes, achieving the maximum magnitude on day 90 of DM (as estimated by the level of malonic dialdehyde). Concurrent brain tissue ultrastructural analysis revealed slightly pronounced oxidative lesions of all cell elements, which enhanced by day 90 of DM. The most marked changes were found in the neuroglial cells, in astrocytes in particular, as compared with cerebral microvascular neurons and endotheliocytes. Administration of the a-lipoic acid agent espa-lipon to rats with DM produced a significant positive effect on the state of the ADS components, promoted the elimination of active manifestations of abnormal processes in the neuroglial cells and neurons and the development of compensatory and reducing processes

Hypoglycemic coma was induced with 40 U of insulin per kg body weight. The animals experiencing 7 hypoglycemic comas at 2-day intervals and killed during the last coma were found to have elevated serum levels of free fatty acids, urea, and uric acid; hepatic glycogen levels remained normal. In the liver, the activities of aspartate aminotransferase (EC 2.6.1.1), alanine aminotransferase (EC 2.6.1.2), glutaminase (EC 3.5.1.2), glutamate dehydrogenase (EC 1.4.1.3), succinate dehydrogenase (EC 1.3.99.1), and lactate dehydrogenase (EC 1.1.1.27) were enhanced and the rate of lactate generation increased when glucose and glycogen were used as substrates. Such changes were absent in initially healthy animals during the first hypoglycemic coma. They are indicative of increases in the catabolism of amino acids and in the activation of gluconeogenesls in the rats experiencing insulin hypoglycemia many times and they are associated with the stimulation of the contramsular apparatus in hypoglycemia