Endocrine ophthalmopathy (EOP) is a multidisciplinary problem at the intersection of endocrinology and ophthalmology. The patients presenting with this condition experience deficit of adequate medical aid due to the poor cooperation between ophthalmologists and endocrinologists. There are practically no specialized centres in this country where the patients with EOP could receive the combined treatment of this pathology including the surgical intervention. Taken together, late diagnostics and delayed seeking the efficacious medical assistance, the absence of stable compensation of the functional disorders of the thyroid gland, erroneous identification of the phase of the disease, and incorrect choice of the methods for its treatment, the lack of coordination and consistency in the actions of ophthalmologists and endocrinologists are responsible for the low effectiveness of EOP treatment. On the other hand, the absence of the unified approach to diagnostics and treatment of endocrine ophthalmopathy, the necessity of introducing the international experience gained in this field into the routine clinical practice and pooling efforts of representatives of different medical disciplines (endocrinologists, ophthalmologists, radiologists, endocrine surgeons, and neurosurgeons) created the prerequisites for the solution of the EOP problems and gave impetus to the development of the recommendations being proposed.

The proposed clinical recommendations discuss the modern approaches to diagnostics and treatment of the diseases with the clinical picture of thyrotoxicosis.

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At present, four main types of autoimmune polyglandular syndromes (APS) are distinguished. Type 1 APS is associated with candidiasis, primary hypoparathyroidism, and primary adrenal insufficiency developing in the childhood as a result of mutations in the AIRE gene. Type 2 APS involves primary adrenal insufficiency in combination with autoimmune thyroid diseases and/or type 1 diabetes mellitus. Type 3 APS is characterized by the combination of autoimmune thyroid diseases with other endocrine and non-endocrine autoimmune pathologies in the absence of adrenal cortical dysfunction and hypoparathyriodism. Type 4 APS is presented by the combinations of autoimmune diseases other than the aforementioned ones. The above syndromes usually manifest themselves at the age between 20 and 60 years; they are of the polygenic type and associated with the genetic markers, such as HLAII-complex haplotypes, CTLA-4, PTPN22, FOXP3 genes, etc. In addition, the latent forms of APS have been described that occur in the populations much more frequently than the manifest disorders. These latent diseases can exert strong influence on the compensation and risk of complications of the underlying pathology. Of great importance in this context is the timely identification of the groups of patients at risk of developing clinical forms of APS among the subjects presenting with a single endocrine pathology.

Vitiligo is a common polygenic autoimmune disease in which the foci of depigmentation are formed on the skin and/or mucous membranes as a result of the death of melanocytes. There are several hypotheses for the pathogenesis of the disease, the leading role among them is played the autoimmune hypothesis. This review summarizes the available literature data on the prevalence and structure of comorbid endocrine autoimmune pathology in vitiligo patients. In most studies conducted in Europe, America and Asia the prevalence of autoimmune thyroid diseases (including autoimmune thyroiditis and Graves disease), diabetes mellitus and autoimmune adrenal insufficiency was higher in vitiligo patients than in the general population. The results of some studies indicate a frequent association of vitiligo with autoimmune polyglandular syndromes. In the structure of comorbid pathology the highest prevalence was in autoimmune thyroid diseases. A number of studies have established a higher prevalence of autoimmune endocrine diseases in women, as well as in nonsegmental vitiligo patients and in cases of family history of vitiligo and/or other autoimmune diseases. In addition, it was shown that the prevalence of endocrine diseases increases with increasing area of depigmentation. The data obtained justify the advisability of conducting a timely examination of vitiligo patients with the aim of early detection of comorbid diseases and the appointment of appropriate treatment. Further studies are needed to investigate the effect of the identified associations on the course of vitiligo and comorbid endocrinopathies, as well as the effectiveness of therapy and the quality of life of patients.

On September 30, 2022, a meeting of the interdisciplinary expert council “Prevention and treatment of obesity. How to Achieve a Healthy Metabolic Balance. To reduce the social and economic burden of obesity and its consequences in the Russian Federation, it is necessary to introduce socially significant initiatives to prevent obesity and increase its detection rate, as well as to update modern approaches to the treatment of this chronic disease, taking into account its multifactorial pathogenesis, comorbidity, risk of complications and patient disability. Based on the results of the scientific reports and discussions held during the expert council, the experts made decisions on a further plan within the framework of socially significant initiatives for the prevention of obesity

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Гипогликемический синдром-это симптомокомплекс, развивающийся вследствие снижения уровня глюкозы крови. В практике эндокринолога основной причиной гипогликемии у больных без сахарного диабета является инсулинпродуцирующая опухоль поджелудочной железы-инсулинома. В ткани инсулиномы происходят различные молекулярно-генетические нарушения, которые приводят к изменению секреции инсулина и его предшественников. Нередко возникает ситуация, в которой не удается установить причину снижения уровня глюкозы крови. В таких случаях развитие гипогликемии может быть результатом различных генетически детерминированных ферментных, аутоиммунных и рецепторных нарушений, которые обусловливают изменение метаболизма глюкозы или синтеза/биоактивности инсулина. При мягком течении таких врожденных заболеваний гипогликемические состояния могут впервые проявляться во взрослом возрасте. В представленном обзоре описаны различные генетические предикторы (мутации), играющие решающую роль в возникновении ферментных, аутоиммунных, рецепторных и пролиферативных нарушений и, как следствие, гипогликемии.