The present paper deals with late results of the treatment of patients with Cushing's disease by proton beam irradiation of the pituitary gland. Retrospective analysis included results of hormonal assays in 197 patients (161 women and 36 men) with verified Cushing's disease who had undergone proton therapy at the Endocrinological Research Centre. The age of the patients prior to irradiation varied from 17 to 54 years (mean 29±12.1). Duration of the follow up period ranged from 1 to 24 years. Each patient was first examined 6 month after irradiation, then annually for 5 years, and thereafter during episodic visits to the clinic of Endocrinological Research Centre. Trophic hormones (ACTH, GH, prolactin, LH, FSH, TSH) as well as cortisol, estradiol, testosterone, and free thyroxin were determined in peripheral blood; in addition, free cortisol was measured in daily urine. ACTH and cortisol were measured twice daily (at 8 a.m. and 11 p.m.) to characterize diurnal dynamics of these hormones. Complete remission of the primary disease was documented based on the results of hormonal assays in 164 (83.6%) patients 0.5-3 (mean 1.5±1.8) years after irradiation; remission without subsequent impairment of the pituitary trophic activity was achieved in 43 (21.8%) patients. Different combinations of post-treatment side effects (hypopituitarism) were recorded in 100 (50.1%) patients while 54 (27.4%) others had only one function affected by radiation. The following disorders of hormonal function of the pituitary and peripheral glands developed: adrenal insufficiency in 58 (29.7%) patients, secondary hypothyroidism in 66 (22.8%), hypogonadism in 93 (47.4%), and hyperprolactinemia in 72 (36.7%). Adrenal insufficiency was the first adverse event to develop after proton therapy (within 0.5-12.0, mean 2.5±2.3, years). It was followed by elevation of prolactin levels and decrease of gonadotropins (within 1.0-7.2, mean 3.0±2.9, years and 0.8-11.8, mean 3.0±3.1, years respectively). Secondary hypothyroidism was the last to develop (within 1.3-12.3, mean 5.0±3.2, years after treatment). It is concluded that biochemical monitoring hormonal changes coupled to the evaluation of the patient's clinical conditions is a very important component of long-term (throughout the lifespan) dynamic observation of patients with Cushing's disease necessary for the timely detection of manifestations of hypopituitarism and initiation of relevant treatment.

The objective of the present study was to evaluate the efficiency and safety of the treatment of girls presenting with Turner syndrome by recombinant growth hormone Rastan (Farmstandart-UfaVITA). A total 29 girls in this condition were available for observation. Their chronological age at the time of diagnosis averaged 7.9±1.2 years at the time of diagnosis and 9.8±1.6 at the onset of therapy; the bone age was 7.5±1.1 years. Duration of the treatment was 24 months. Recombinant somatotropin was used in the form of lyophilisate (1.33 mg) to prepare a solution for subcutaneous injections at a dose of 0.05 mg/kg of body weight. The solution was administered daily at evening hours. The mean growth rate of the patients with Turner syndrome was estimated at 4.2±0.6 cm/year prior to Rastan therapy, 8.7±0.6 cm/year during the first 12 months of the treatment, and 6.1±1.2 cm/yr in the second year. Overall, the height of the girls increased by 0.84 SD within the two years. No adverse effects of therapy were documented. It is concluded that the use of recombinant somatotropin Rastan is an efficacious and safe therapeutic modality for the acceleration of growth in girls with Turner syndrome.

This paper reports the results of a study of lymphocyte apoptosis in the blood of 81 patients presenting with autoimmune thyropathies, such as autoimmune thyroidism (AIT) and Grave's disease (GD). It was shown that AIT in patients with hypothyroidism and DTG is associated with an increased number of CD95+ lymphocytes «doomed» to apoptose. Moreover, AIT and DTG conditions are characterized by an elevated level of serum tumour necrosis factor-alpha (TNF-α). In euthyroid patients with AIT, this rise is accompanied by a decrease in the interferon-gamma (IFN-γ) level. Hypotyroid patients with AIT exhibit positive relationship between an increased number of CD95+ lymphocytes in blood and serum TNF-α levels.

The objective of the present study was to evaluate effects of iron deficiency anemia in pregnant women on the effectiveness of iodine prophylaxis; the secondary objective was to develop standard prophylactic iodine dose schedule for these patients. The study included two groups of pregnant women treated either with a daily dose of 200 mcg potassium iodide (group 1, n=32) or with 300 mcg potassium iodide/day (group 2, n=68). In all of them, blood TSH, free thyroxin and antithyroid peroxidase antibody levels were measured along with iodine excretion in urine. Thyroid volume was determined by ultrasound. Diagnosis of anemia was based on the results of clinical blood analysis including hemoglobin level, erythrocyte count, hematocrit, and mean hemoglobin content of red blood cells. Iron deficiency was estimated from serum iron and ferritin (SF) levels. Treatment with potassium iodide during pregnancy resulted in a significant increase of the median urine iodine level to 260.9 mcg/l and 143.7 mcg/l in groups 1 and 2 respectively (p<0.05). It means that iodine excretion in urine during pregnancy is directly related to the efficiency of prophylaxis; it is optimal in women consuming daily at least 300 mcg of potassium iodide. Of all hematological parameters, the serum ferritin level undergoes the largest deviation (decrease) from the normal value. It was below 15 ng/ml in 24 (31.2%) patients with the median urine iodine level of less than 150 mcg/l and in 10 (11.1%) patients with the median urine iodine level higher than 150 mcg/l (a three-fold difference).

This work was designed to study effects of leptin and/or ghrelin in combinations characteristic of different trimesters of pregnancy on the expression of membrane molecules and apoptosis of lymphocyte in the peripheral blood of women. Leptin was shown to decrease the relative number of activated Th-cells and apoptosis of lymphocytes. Moreover, it either increased or decreased the number of CD16+CD56+NK and CD16+CD56+NKT cells depending on the dose but did not change the number of T-lymphocytes CD4+CD25bright. In contrast, ghrelin caused a dose-dependent increase in the number of activated Th-cells and enhanced lymphocyte apoptosis but did not influence the number of CD16+CD56+NK, CD16+CD56+NKT cells, and T-lymphocytes CD4+CD25bright. Simultaneous administration of both hormones in combinations known to occur in the first and second trimesters of pregnancy did not change percentage of activated Th-cells, the relative number of CD16+CD56+NK and CD16+CD56+NKT cells or apoptosis of lymphocytes. However, they stimulated expression of CD25 on Th-cells and CD16 on NK-cells.

It is shown that combined treatment with thyroxin and diazepam permits to avoid negative effect of either drug on the bone tissue. Mutual regulation of thyroxin and diazepam activities is mediated through their competitive binding to common receptors. It is hypothesized that the key factor in this process is steric availability of the receptor; in other words, close localization of thyroxin and diazepam targets may interfere with simultaneous activation of receptors by the two ligands and account for the effects of their combined administration described in the present work.

Deficiency of type II 5-alpha reductase (5-ARII) is known to be responsible for abnormal sexual differentiation in boys. Of primary importance is differential diagnosis between this condition and incomplete form of androgen resistance. In the latter case, adaptation to male gender is highly undesirable because of inefficiency of androgen therapy. In contrast, such adaptation is socially justified in patients with type II 5-alpha reductase deficiency; sometimes, it permits to preserve fertility. The cases reported in this paper demonstrate low diagnostic value of the T/DHT ratio (at least as determined by the immunoenzyme assay) and emphasize the necessity of analysis of the SRD5A2 gene in all patients with suspected deficiency of type II 5-alpha reductase.

The present review deals with the treatment of main nosological forms of primary hyperaldosteronism, such as aldosteron-producing adenoma (APA) and idiopathic hyperaldosteronism (IHA). Much attention is given to perioperative management of APA patients for whom surgical treatment is the method of choice. Idiopathic hyperaldosteronism characterized by bilateral macro- and micronodular changes dictates the necessity of medicamentous therapy, in the first place with antagonists of mi­neralocorticoid receptors (e.g. spironolactone). Pharmacological standards of drug therapy are described for patients with IHA and those with APA in whom surgical treatment is impracticable.

The current concept of obesity as a heterogeneous condition is discussed. Such interpretation provides a basis for distinguishing a group of obese subjects without metabolic disturbances (metabolically healthy obese (MHO) subjects) and another one including subjects with normal body weight and signs of hormonal and metabolic disorders (metabolically obese normal weight (MONW) subjects). A separate subgroup is represented by obese patients with deficit of muscular mass and force (sarcopenic obesity). Potential mechanisms underlying development of these conditions are considered along with selected applied aspects of this problem.

The influence of various medicinal preparations on the function of the hypothalamo-pituitary-thyroid axis is discussed. Thyroidal status at different somatic diseases is considered alongside the efficiency of substitution therapy with thyroid hormones for the management of hypothyroidism.