The incidence of type 1 diabetes mellitus (T1DM) is increasing in many countries of the world, the average annual increase in the frequency of the disease in European children is 3.4% at the age of 0-14 and 6.3% at the age of 0-5. The increase in the incidence of type 1 diabetes at an early age has a definite effect on the whole society as a whole, increasing the burden both on the patients themselves and their families, in particular, leading to an earlier development of complications. Since these changes in the development of diabetes have occurred too quickly to be due to changes at the genetic level, they are most likely a consequence of environmental changes.

Insulin therapy is a pharmaceutical treatment used for patients with diabetes to normalize blood glucose level. In patients receiving insulin therapy, optimization of blood glucose levels can be achieved using various types of insulin and various methods, such as MDI (multiple daily injections) and CSII (continuous subcutaneous insulin infusion). This review describes actual key features of CSII for diabetes patients.

Congenital adrenal hypoplasia is a rare clinical variant of primary adrenal insufficiency. Two forms of this disease are known, one of which is inherited in an autosomal recessive manner (including IMAGe syndrome - a combination of adrenal hypoplasia with intrauterine growth retardation, metaphysical dysplasia and abnormal genital structure, OMIM 300290), and the other has X-linked nature of inheritance (DAX-1 gene defect). X-linked adrenal hypoplasia is relatively more common and studied in more detail.
Congenital X-linked adrenal hypoplasia is manifested by a combination of primary adrenal insufficiency and hypogonadotropic hypogonadism and is caused by defects in the DAX-1 gene (measurement-sensitive sex reversal, adrenal hypoplasia congenital, critical region on the X chromosome, gene-1).

In 1973 and 1976 2 cases of endocrine ophthalmopathy (EO) after external irradiation of the anterior surface of the neck due to a tumor (Hodgkin's lymphoma) was described. Further observations showed that treatment of Graves' disease (BG) with radioactive iodine (¹³¹I) can worsen the course of EO. So, L. De Groot et al., Observing 264 patients after exposure to ¹³¹I for BG, found progression of EO in 4% of patients after the 1^st course of therapy and in 12% after subsequent sessions.

Later the appearance or significant progression of EO in  patients treated with ¹³¹I has been observed. Some studies have shown that the progression of EO after treatment with ¹³¹I without glucocorticoids administration can be observed in 18–30% of cases. Along with this, there is an opinion that ¹³¹I does not affect the incidence of clinical symptoms in the orbit and that hypothyroidism that occurs after it does not lead to the progression of eye symptoms. The relationship between treatment and the onset or progression of EO is not clear. Nevertheless, there is evidence of an adverse effect of an elevated level of antibodies to the thyroid stimulating hormone receptor in the blood serum after ¹³¹I training for EO.

The paper deals with the study of a correlation of grelin, growth hormone, insulin, Caros index, lipid spectrum, anthropometric characteristics in patients with obesity and overweight. Seventy-six young obese males aged 18 to 23 years were examined. A control group included 15 apparently healthy individuals of the same age. This cohort of patients was found to have a significantly reduced level of grelin that tended to decrease with the increased grade of obesity. The established hyperinsulinemia and decreased Caros index suggest that young obese young males are insulin-resistant.

Weight-based dosing of growth hormone (GH) is the standard of therapy in short children although insulin-like growth factor-I (IGF-I) is a major mediator of GH actions on growth. Objective: to test whether the IGF-I levels achieved during GH therapy are determinants of the growth responses to GH therapy. This was a two-year open-label, randomized IGF-I concentration-controlled trial. Prepubertal short children [n = 172; mean age 7.53 years; mean height SD score (HT-SDS - 2.64] with low IGF-I levels (mean IGF-I SDS - 3.56) were randomized to receive one of two GH dose-titration arms in which GH dosage was titrated to achieve an IGF-I SDS at the mean [IGF(low) group, n = 70) or the upper limit of the normal range [+2 SDS, IGF(high) group, n = 68] or to a comparison group of conventional GH dose of 40 mg/kg/day (n = 34). The multicenter study was performed in the outpatient centers. The primary outcome measure was to determine changes in HT-SDS during 2-year therapy. One hundred and forty-seven patients completed the trial. Target IGF-I levels were achieved in the dose-titration arms within 6-9 months. The changes in HT-SDS were +1.0, +1.1, and +1.6 for conventional, IGF(low), and IGF(high), respectively, with IGF(high) showing significantly greater linear growth response (p < 0.001), compared with the two other groups). The IGF-I(high) arm required higher doses ( > 2.5 times) than the IGF-I(low) arm, and these GH doses were highly variable (20-346 mg/kg/day). Multivariate analyses suggest that the rise in IGF-I SDS significantly impacted height outcome along with the GH dose and the pretreatment peak-stimulated GH level. IGF-I-based GH dosing is clinically feasible and allows maintaining serum IGF-I concentrations within the desired target range. Titrating the GH dose to achieve higher IGF-I target results in improved growth responses, although at higher average GH doses.

The purpose of the study was to comprehensively analyze glycemic control in type 2 diabetes (T2D) patients who were first given glucose-reducing therapy. Glidiab MB and Diabeton MB caused a comparable reduction in glycemic control parameters: the level of HbA1c, fasting glycemia, and mean glycemic levels as shown by the results of its continuous glucose monitoring system (CGMS) study. The lower glycemic level was not accompanied by weight gain and it improved lipid spectrum parameters. The readings of monthly self-control of glycemia were transformed to its deviation from the goal range (ADRR) that and the hyper- and hypoglycemia indices calculated from the continuous glycemic control were used to evaluate glycemic lability not reflected by HbA1c. In this connection ADRR may be used to evaluate the efficiency of sugar-reducing therapy and in the examined groups it proved to be low, which generally reflects the stable course of the disease in new cases of T2D. The mean glycemic value calculated from CGMS data virtually coincides with the mean glycemia estimated from glycemic self-control readings both on the day of continuous glucose monitoring and in the month to come before and after CGMS study. In this connection the latter is justified only when the continuous glycemic curve undergoes a complex analysis. The complex analysis of the continuous glycemic curve includes symmetrization of the continuous glycemia scale; calculation of hyper- and hypoglycemic indices, hourly diurnal hyperglycemic index and hourly glycemic variations (Poincare method). The use of this procedure could compare the glucose-reducing effect of the two drugs within the framework of a short-term study.

The effects of Dibicor (taurine) were studied in 20 patients with type 2 diabetes (T2D) with a disease duration of 1 to 9 years and a mean body weight of 93.8±16 kg who received concomitant therapy (monotherapy with sulfonylurea (n = 7), novonorm (n = 1), sulfonylurea with metformin (n = 7); one patient was on diet therapy). Addition of Dibicor to the therapy following 3 months caused a statistically significant reduction in fasting and postprandial glycemia (from 7.9 to 6.3 mmol/l and from 7.9 to 6.9 mmol/l, respectively). Glycated hemoglobin decreased from 7.8 to 7.05% (p = 0.062). Lipid metabolic parameters improved after 3-month course of therapy. There was also a statistically significant fall in microalbuminuria from 0.082 to 0.054 g/day (p = 0.042). The administration of Dibicor can significantly improve T2D compensation.

The aim of the study was to reveal a relationship between gustatory sensitivity to phenylthiocarbamide (PTC) and thyroid disease. The distribution of PTC sensitivity was studied in 198 healthy individuals, 100 patients with autoimmune thyroiditis (AIT), 139 patients with nodular euthyroid goiter, and 100 patients operated on for thyroid cancer. There was a statistically significant decrease in the number of PTC-resistant male and females patients in the thyroid cancer group and an increase in the proportion of PTC-resistant male patients in the AIT and nodular euthyroid goiter groups.

Thyrotoxicosis of newborns, observed in less than 1% of pregnant women with Graves disease, is due to transplacental transfer of stimulating antibodies to the thyroid stimulating hormone receptor (rTSH). The clinical picture manifests itself in the first days of a child’s life, is transient in nature and, as a rule, ends with a full recovery as the maternal antibodies to rTSH disappear from the bloodstream of the newborn. However, in addition to the "classic" autoimmune thyrotoxicosis, cases of congenital and familial non-autoimmune thyrotoxicosis, which are caused by inherited activating mutations of the gene encoding rTSH - TSHR, have been described. This article presents its own observation.

The Wilms tumor gene (WT1) encodes a transcription factor that plays a key role in the laying and differentiation of the kidneys and gonads. Mutations of the WT1 gene were detected in patients with the WAGR complex (Wilms tumor, aniridia, urogenital pathology, mental retardation), Denis-Drach syndrome (early renal failure, diffuse mesangial sclerosis, varying degrees of gonadal dysgenesis, high risk of Wilms tumor) and Fraser syndrome. The latter is characterized by a fully female phenotype with karyotype 46XY, focal segmental glomerulosclerosis with the development of renal failure in the 2^nd decade of life, gonads in the form of cords and a high risk of gonadoblastoma. The presence of a heterozygous point mutation, which alters the donor site of splicing of the intron 9 of the WT1 gene, is also typical of Fraser syndrome. We present a case of characteristic clinical manifestations of Fraser syndrome in a patient in whom the diagnosis was confirmed by the detection of a mutation in the WT1 gene.

75 years have passed since the birth and 51 years of scientific and pedagogical and medical activity of one of the leading endocrinologists in our country, the founder of university endocrinology, the founder and first head of the endocrinology department of the Russian State Medical University (RSMU), honored worker of a higher school of the Russian Federation, honored doctor RF, Professor Vladimir Potemkin.

November 10, 2008 marks the 80th anniversary of the birth and 61 years of work as an academician! NAS and AMS of Ukraine, the Russian Academy of Medical Sciences, Honored Worker of Science and Technology of Ukraine, laureate of the State Prize of Ukraine, Doctor of Medical Sciences, Professor, Head of the Department of Diabetology, Deputy Director for Clinic of the Institute of Endocrinology and Metabolism named after V.P. Komissarenko of the Academy of Medical Sciences of Ukraine Andrey  Efimov.

October 25, 2008 100th anniversary of the birth of a major Soviet endocrinologist, corresponding member of the Academy of Medical Sciences of the USSR, professor Anatoly Anatolyevich Voitkevich.