Problemy endokrinologii最新文献

Worldwide, the number of patients with diabetes has quadrupled over the past three decades. Every eleventh adult is currently diagnosed with diabetes mellitus, 90% of which are type 2 diabetes mellitus (DM2). Generally recognized complications of chronic hyperglycemia include micro- and macrovascular changes, damage to peripheral and/or autonomous nerve fibers. Scientists have also long discussed the relationship between an increase in the number of certain cancers and the presence of DM2. Based on the presence of common risk factors such as age, ethnicity, dietary habits and physical activity, many epidemiological and experimental studies are being conducted, which gradually contribute to understanding the relationship between these diseases. Taking into account the results of numerous studies, hyperglycemia, hyperinsulinemia and chronic inflammation, which are observed in DM 2, have a positive association with an increased risk of certain types of malignancies. In this article, the authors consider pathological changes in DM2 that potentiate the development of oncological diseases and epidemiological data reflecting the correlation between DM2 and the occurrence of malignant tumors.

Background: Autoimmune diseases such as Graves' disease are complex pathologies that often require intensive and long-term treatment. However, the mechanisms contributing to the development and maintenance of this pathology are still not fully understood. Understanding the role of the innate immune response, especially in the context of monocytes, in the development of Graves' disease remains a poorly understood aspect.

Aim: To study the level of ROS production in monocytes in patients with Graves' disease after RAI to identify the level of activation of the macrophage-monocyte system.

Materials and methods: The hormonal status and monocyte activity were analyzed before and 1, 3 and 6 months after RAI. The level of ROS was determined using spontaneous and luminol- and luceginin-derived chemiluminescence.

Results: The study included 48 patients with Graves' disease, aged from 18 to 65 years. In patients with Graves' disease, a decrease in the intensity of free radical processes in monocytes was detected compared to the control group. These changes were observed both before and after RAI. It has been shown that changes in ROS production are independent of thyroid function and antibody levels. The changes indicate the potential immunosuppressive effects of radionuclide treatment and its effect on monocyte NADPH oxidase activity. A decrease in the production of secondary ROS in monocytes was also noted, which may indicate a decrease in the activation of monocytes during antigenic stimulation and inhibition of autoimmune processes.

Conclusion: Reduced metabolic activity of monocytes and low levels of ROS synthesis correlate with inhibition of the autoimmune process and decreased activation of the macrophage-monocyte system. The study confirms the importance of the role of monocytes in the ROS production system and their influence on the autoimmune process in Graves' disease. These results may have clinical significance and contribute to the development of new immunotropic strategies for the treatment of this disease.

Primary hyperparathyroidism (PHPT) is a common endocrine disorder characterized by autonomous secretion of parathyroid hormone by altered parathyroid glands. In most cases PHPT is a sporadic disease, 5-10% of observations are genetically determined syndromal and non-syndromal forms. Studies of families with hereditary forms of PHPT have led to the discovery of key oncosuppressor genes and proto-oncogenes whose somatic mutations underlie the development of many sporadic parathyroid tumors. Another interest in the pathogenesis of primary hyperparathyroidism is studying mechanisms of epigenetic regulation in tumor tissue. In the first part of this review, we will discuss the classification, morphology, and etiology of PHPT. In the second part, we will present a summary of the most important studies using genetic analysis, classified according to the method used.

Modern pediatric endocrinology represents the dawn of a new era in diagnosis and treatment, based on scientific research in molecular genetics and the development of advanced diagnostic and therapeutic tools. At the Pediatric Clinic of the En docrinology Research Centre (ERC), later the Institute of Pediatric Endocrinology, molecular genetic research began in 1990 in collaboration with the N.P. Bochkov Research Centre for Medical Genetics and the Institute of Immunology. The ERC's Laboratory of Molecular Genetics has been operational since 2001, conducting research in partnership with foreign clinics and institutions.

Congenital adrenal hyperplasia (CAH) encompasses a group of autosomal recessive disorders characterized by defects in enzymes critical for steroidogenesis, with 21-hydroxylase deficiency due to mutations in the CYP21A2 gene being the most prevalent form.Since the introduction of replacement therapy and neonatal screening programs in the 1950s, there has been a significant increase in survival rates among newborns diagnosed with CAH. However, despite these advancements, mortality associated with this condition remains disproportionately high. Achieving optimal therapeutic compensation through medication remains a complex challenge, contributing to a range of long-term complications. These complications stem from both the underlying disease and its treatment, impacting key physiological functions, including metabolism, growth and development, cardiovascular health, and fertility. These multifaceted outcomes underscore the need for ongoing research and the refinement of therapeutic approaches to better manage this intricate condition. This article presents a series of four clinical cases of CAH characterized by the absence of sustained compensation for glucoand mineralocorticoid deficiencies. These cases were further complicated by the development of large adrenal masses and ectopic testicular adrenal rest tissue (TART), emphasizing the challenges in achieving long-term disease management.

Hepatogenic diabetes (HepD) is a form of diabetes where the primary pathogenesis is a liver disease, usually cirrhosis, complicated by the development of portal hypertension with the formation of porto-caval shunts. In the development of HepD, in addition to traditional risk factors for carbohydrate metabolism disorders, the pathogenetic features of liver diseases play a significant role. However, the exact mechanism of HepD development remains unclear, and several questions are still open for discussion. Despite having distinct pathophysiological and clinical features, hepatogenic diabetes is currently not considered as an independent disease. This is likely due to the difficulties in differentiating between types of diabetes due to the bidirectional relationship between glucose metabolism disorders and chronic liver diseases. It is known that diabetes negatively affects the development and progression of chronic liver diseases of various etiologies, and their combination is associated with worse clinical outcomes in terms of mortality, the occurrence of liver decompensation, and the development of hepatocellular carcinoma (HCC). Unfortunately, early diagnosis and the selection of optimal therapeutic strategies for diabetes may be challenging due to the lack of established clinical guidelines and the presence of comorbidities in patients with HepD.

The obesity epidemic is a major public health problem nowadays. The pathophysiology of obesity, which underlies its chronic, progressive, self-sustaining course, determines the difficulties in developing effective and safe methods for body weight control. The article is dedicated to the consideration of the evolution of conservative treatment of obesity, in particular, the history of pharmacotherapy of this disease, characterized by many ups and downs, is presented. The paper discusses, in chronological order, the emergence, efficacy, mechanisms of action, and described side effects of drugs that were investigated and used for weight loss at one time or another, as well as the reasons why many of them were subsequently withdrawn from the market. Until recently, long-term effective and safe pharmacotherapy of obesity remained an insurmountable challenge. Only in the last two decades has the understanding of the molecular mechanisms of appetite control reached a level that allows for a more productive search and development of promising drugs aimed at the pathogenetic treatment of obesity. This article discusses the status of currently available drugs for weight loss, as well as the prospects for drug treatment of obesity. The results of clinical trials of advanced therapeutic molecules, including gastrointestinal hormone receptor agonists, reinforce the belief that a breakthrough in the drug treatment of obesity is possible.

On September 27, 2024, a discussion-based working meeting on the issue of vitamin D deficiency in patients with overweight and obesity was held in Vladikavkaz.The meeting aimed to evaluate the relationship between vitamin D deficiency, overweight, and associated comorbidities, as well as to explore modern strategies and practical approaches for managing such patients in endocrinology practice. The resolution of the meeting was developed by its participants, comprising leading endocrinologists.

Background: Functional hypothalamic amenorrhea (FHA) and polycystic ovary syndrome (PCOS) are pathologies most common in women of reproductive age. Menstrual irregularities (oligo/amenorrhea) are the most common symptom of these diseases. FHA develops against the background of stress or excessive physical exertion, and is characterized by inhibition of neuroendocrine regulation of the hypothalamic-pituitary-ovarian axis with a subsequent decrease in the production of sex steroids. For PCOS, the most important pathogenetic links are insulin resistance and hyperandrogenism. The pathology of neuroendocrine regulation in ovarian hyperandrogenism is accompanied by excessive pulsatile secretion of gonadotropin-releasing hormone (GnRH), promoting increased production of luteinizing hormone (LH). Both FHA and PCOS lead to multiple complications from other organs and systems: cardiovascular pathology, decreased bone mineral density with prolonged amenorrhea and contribute to the development of infertility.

Objective: To analyze the works studying the problems of differential diagnosis of FHA and PCOS.

Methods: Using PubMed, eLibrary, CyberLeninka.ru, a systematic search was conducted for articles published over the past 6 years that met the following criteria: the research that describe methods and develop criteria for the differential diagnosis of FHA and PCOS. Selected impactive publications within 1998-2018 were also included in the review.

Results: This review highlights the differential diagnostic criteria for FHA and PCOS. The features of clinical, laboratory and instrumental studies are also described. Publications describing the coexistence of these pathologies in women are analyzed, and methods that allow differentiating these nosologies are described in detail.

Conclusion: A correct and timely diagnosis facilitates the prescription of appropriate treatment regimens, reduces the incidence of complications and improves the quality of life of women. In light of recent advances in the description of the mechanisms of neuroendocrine regulation of the reproductive system, it is necessary to further conduct research to study the role of neuropeptides in the development of FHA and PCOS, which may serve to create more accurate diagnostic markers of diseases.

Calcium is the most abundant mineral in the human body. About 99% of calcium is deposited in the bones in the form of hydroxyapatite and only 1% is located in the intracellular and extracellular fluid. Ionized calcium, which makes up about 50% of the total amount of circulating calcium, is biologically active; the remaining percentage is bound to plasma proteins (40%, of which albumin accounts for 90%, and globulins for 10%), or is in complex with anions (10%) such as citrate, lactate, bicarbonate, phosphate. Hypo- and hypercalcemia are common conditions treated by physicians of various specialities. Primary hyperparathyroidism and malignant tumors are the most common causes of hypercalcemia, whereas hypocalcemia is most often caused by hypoparathyroidism, malabsorption, vitamin D deficiency or chronic kidney disease. The interpretation of blood calcium concentration results affects the correct diagnosis, the need for further examination, and the choice of treatment. Concentration of ionized calcium is considered a more accurate indicator of the true status of calcemia compared to the concentration of total calcium, but its measurement is difficult due to strict preanalytical and analytical requirements. In the mid-1970s, calcium adjustment equations appeared, which are widely used today. However, some studies have expressed doubts about the sufficient reliability and sensitivity of the corresponding adjustment formulas. The diagnostic accuracy of widely used correction formulas in some clinical situations is lower than the diagnostic accuracy of uncorrected total calcium. The review discusses the history of the formulas for correcting total calcium for albumin, the factors influencing the result of correction, as well as its suitability in various conditions.