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This research describes a clinical case of treatment of a patient with thyrotoxicosis with concomitant hematological pathology – carriage of unstable hemoglobin Hasharon. A patient diagnosed with «Diffuse toxic nodular goiter. Thyrotoxicosis of medium severity. Drug-induced hypothyroidism» was admitted to the Department of radionuclide therapy for the purpose of treatment with radioactive iodine. Onset of disease - summer 2018 (thyroid-stimulating hormone (TSH) – 0 mIU/ml). The instrumental studies (ultrasound, scintillation scanning of the thyroid gland) were performed at the pre-radioiodine therapy (RIT) diagnostic stage. The history of the disease indicates, that in 2000 the patient was suspected of having abnormal hemoglobin, since then no examinations have been conducted and anemia has never been detected. find more The diagnosis of ancestral hemoglobinopathy with the presence (17%) of unstable Hasharon-Sinai-Sealy hemoglobin in a heterozygous form was verified during the preparation to RIT. The radionuclide therapy I131 with activity of 400 MBq was performed on 02.07.2019. The monthly monitoring of laboratory and instrumental indicants was carried out during the post-therapeutic period the state of hypothyroidism was reached by the end of 2 months after RT, no episodes of significant increase in bilirubin levels were observed during the observation period; no side effects from RT were stated. It becomes possible based on the example of the above observation, to judge the safety of conducting RT for treatment of thyrotoxicosis in patients with similar hemoglobinopathy, without excluding, however, the need for an individual approach in each case.The article focuses on the clinical case of Graves’ disease in a patient with HIV infection who is receiving antiretroviral therapy. The number of HIV-infected patients has increased significantly in recent decades all over the world. The currently used highly active antiretroviral therapy can significantly improve the prognosis for these patients. However, its use is associated with a number of complications, in particular the development of immune reconstitution syndrome, under which the development of such autoimmune diseases as Graves’ disease, polymyositis and Guillain-Barre syndrome may occur. Therefore, we would like to draw the attention of doctors to the possibility of such a complication in patients receiving antiretroviral therapy. Timely diagnosis and treatment of thyroid disorders will help to avoid the complications associated with an excess or deficit of thyroid hormones.Currently, cabergoline therapy is the main method of treatment with prolactin. The use of the drug in most cases leads to tumor regression, normalization of prolactin levels and restoration of gonadotropic function. The mechanism of its impact on tumor cells in vivo, which is dynamically traced in the same human tumor, is the case of considerable interest. We observed a 30-year-old patient who was operated on twice for a giant prolactinoma before and on treatment by cabergoline. The morphological study after the first surgery (before introducing of cabergoline therapy) revealed a prolactin-positive pituitary tumor with a Ki-67 labeling index of 8% and with strong expression of dopamine type 2 receptors (D2R), CD31 and CD34. After 4 months, during which the patient received cabergoline at a dose starting from 0.5 mg to 1.5 mg per week, a second transsphenoidal surgery was performed with subtotal removal of residual tumor tissue. During the morphological study of the second biopsy sample, the tumor retained a pronounced immunopositivity to prolactin and D2R, with a decrease in the labeling index Ki-67 to 2%, as well as a decrease in the expression of CD31 and CD34. Subsequent cabergoline therapyresulted in persistent normoprolactinemia, restoration of androgen (and reproductive) status, and no tumor recurrence over a 10-year period on cabergoline treatment. Thus, one of the mechanisms of effect of cabergoline that leads to tumor regression is a decrease in the proliferative index and angiogenesis of the tumor.Cardiovascular diseases remain the leading cause of death all over the world. Thyroid hormones play a significant role in the regulation of cardiac function. According to a number of researches, patients with cardiovascular diseases usually have a decrease in the concentration of thyroid hormones in the blood serum, which may be associated with a poor prognosis. Today it still remains unclear whether the change in the bioavailability of thyroid hormones in the myocardium is a favorable physiological mechanism or a replication of an adaptation disorder. Experimental researches suggest that thyroid hormone therapy may be applied in clinical cardiology. link2 This review describes the results of researches examining the use of thyroid hormones in patients with cardiovascular diseases, as well as experiment data on animal models. link3 The available data on the use of thyroid hormones in patients with acute myocardial infarction and heart failure allow us to suggest that normalization of thyroid hormone levels is a safe and potentially effective treatment method in the group of patients with cardiovascular disease. At the same time, the data on the use of thyroid hormones in patients who have undergone an open-heart surgery or heart transplantation are limited. However, at present, it is difficult to draw unambiguous conclusions about the benefits, as well as about the possible risk of using thyroid hormones in the described conditions. Large-scale clinical researches are required to confirm the safety and evaluate the effectiveness of such therapy. Moreover, it is necessary to set parameters for evaluating the safety and effectiveness and understand which hormone (thyroxine or triiodothyronine), what dosage and at what stage of the disease should be applied. Until we do not have answers for these questions, thyroid hormone therapy in patients with cardiovascular diseases should remain within the research field.Currently, among the priority tasks of the health care system is to improve the quality of medical care provided to the population and the accessibility of services. Incomplete staffing is a serious slowdown to the provision of quality care. The shortage of medical personnel is widespread in medicine, which is especially pronounced in primary health care, and endocrinology is no exception. The shortage of personnel is directly related to the problems of accessibility and quality of medical care. Reorganizing the system of professional training, retraining and continuing medical education in a volume that allows eliminating quantitative and qualitative defects in providing care for people with endocrine diseases, as well as analyzing staffing needs and planning based on the real needs of the population, will help to achieve the solution to the set tasks of the healthcare system.One of the reasons for the development of hypoglycemia is the synthesis of autoimmune antibodies to insulin or its receptor – insulin autoimmune syndrome (IAS). The largest number of cases of this syndrome is described in the Japanese population. The antibodies to insulin are most often polyclonal immunoglobulins. In monoclonal gammopathy of undetermined significance and multiple myeloma secreted pathological monoclonal immunoglobulin may have an affinity for human insulin, which induces the development of IAS. The prolonged persistence of episodes of hypoglycemia of unknown origin requires the exclusion of the monoclonal nature of secreted antibodies to insulin. Often the presence of pathological secretion for a long time is not recognized due to the absence of other manifestations of the disease. The manifestation of gammopathy is represented by a wide range of symptoms and syndromes requiring the collaboration of doctors of various specialties. This review summarizes the literature on IAS in patients with monoclonal gammopathy, whose disease debuted from episodes of spontaneous hypoglycemia. When hemoblastosis remission is achieved (when the secretion of the pathological protein is minimal or not determined), the glucose, insulin, and antibodies levels of insulin normalize, and when multiple myeloma recurs, episodes of hypoglycemia resume. The onset of the disease from the IAS can be considered as a new criterion for symptomatic multiple myeloma, dictating the need for the initiation of specific therapy.Primary adrenal insufficiency is manifested by a deficiency of adrenal cortex hormones and can lead to a life-threatening condition. Early diagnosis is key to patient survival. Auto-antibodies to one of the adrenal steroidogenesis enzymes, 21-hydroxylase, are an immunological marker of autoimmune adrenal insufficiency. On the one hand, the study of antibodies to 21-hydroxylase is a method that helps establish the etiology of the disease – the autoimmune genesis of adrenal gland damage. On the other hand, the determination of autoantibodies to 21-hydroxylase is the only prognostic factor of the risk of adrenal insufficiency, which makes it possible to prevent the development of acute adrenal crisis. The article provides a brief literature review on autoantibodies to 21-hydroxylase and the pathogenesis of autoimmune adrenal insufficiency, and a series of clinical cases that illustrates the significant role of autoantibodies to 21-hydroxylase in diagnosis of adrenal insufficiency.The specific relationship between the endocrine and immune systems is represented by a numerous number of factors and mechanisms that form the structure and ensure the function of each of the two systems. For example, immunocompetent cells can produce immunologically active substances, as well as some hormones. On the other hand, immune cells are available to the effects of endogenous hormones. Currently, the so-called cross-regulation of endocrine and immune mechanisms in an equilibrium of pro-and anti-inflammatory responses has not been sufficiently studied. Among other autoimmune lesions, autoimmune thyreopathy occupies a significant place. The development of an autoimmune lesion of the thyroid gland is a complex process, which is the result of the interaction of infiltrating lymphocyte and thyrocyte tissue that can express a wide range of molecules involved in the immune response. Immunological and immunogenetic factors play a major role in the pathogenesis of autoimmune thyroid diseases, such as autoimmune thyroiditis and Graves disease. Despite the fact that more than 100 years have passed since the first description of autoimmune thyroiditis and Graves disease has been known for many centuries, the mechanisms of these pathologies are still not fully understood.A large number of socially significant diseases is accompanied with oxidative stress and carry with tissue damage. Free radicals play a crucial role in the development of these diseases. Similar processes occur under the influence of ionizing radiation and bacterial infections. Recently, was indicated the significant role of oxidative stress in the development of autoimmune thyroiditis. It is assumed that the synthesis of thyroid hormones depends on the concentration of H2O2, which, due to its high toxicity, must be in strict accordance with the activity of antioxidant systems. Many biochemically negative processes occur on the apical membrane of the thyrocyte, which allows limiting the effect of free radicals and avoid cell destruction. However, in pathological conditions, enzymatic systems are disturbed and their components become abnormally activated in the cytoplasm, and it is leads to functional and morphological disorders. A deeper understanding of oxidative stress and its role in the development of autoimmune thyroiditis can contribute to the identification of new methods for its assessment, the expansion of therapeutic ranges for this disease.