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

In this article we describe a clinical case of primary hyperparathyroidism, gout tophus and diabetes mellitus type 2. The relationship between hyperuricemia and hypercalcemia linked to primary hyperparathyroidism is discussed.

Научно-исследовательский институт акушерства, гинекологии и репродуктологии имени Д.О. Отта, Россия,

Multiple endocrine neoplasia type 1 (MEN1) is the most common cause of hereditary primary hyperparathyroidism (PHPT). Bone disorders are considered one of the key symptoms in PHPT present with the significant reduction in bone mineral density and low-energy fractures. Previously, these bone disorders were believed to be caused solely by the increase in the level of parathyroid hormone and its subsequent effect on bone resorption. The current paradigm, however, states that the mutations in the menin gene, which cause the development of MEN1, can also affect the metabolism of the cells of the osteoid lineage. This review analyzes both the proven and the potential intracellular mechanisms through which menin can affect bone metabolism.

Osteomalacia is a systemic bone disease, characterized by an excessive accumulation of non-mineralized osteoid and an imbalance in the organic matrix formation and mineralization. A rare cause of disease is tumor-induced osteomalacia, most often due to phosphaturic mesenchymal tumors (PMT). Usually there are benign small tumors, affecting the soft tissues and bones of any location. The basic pathogenesis of underlying oncogenic osteomalacia is a decreased renal tubular reabsorption of phosphate consequent to hyperproduction of fibroblast growth factor 23 in PMT. Clinical features are nonspecific, the average period from the symptoms onset to diagnosis reaches 3 years and at least 5 years before surgical treatment. Finding the tumour is crucial, as complete removal is curative. We present a clinical case of tumor-induced osteomalacia due to PMT required the complex differential diagnosis with other rare diseases.

2006 г. в связи с высокой распространенностью нарушений фосфорно-кальциевого обмена и костной патологии у пациентов с ХБП, в KDIGO (Kidney Disease: Improving Global Outcomes-Инициатива по улучшению глобальных исходов заболеваний почек) минеральные нарушения вместе с нарушением метаболизма костной ткани и развитием кальцификации сосудов или других мягких тканей были объединены в понятие МКН при ХБП [1]. В настоящее время МКН при ХБП составляют значительную проблему для мирового здравоохранения. Данные нарушения, по разным источникам, в 70-80% случаев сопровождают СД, что, несомненно, повышает риск развития инвалидизирующих состояний у данной когорты пациентов [2]. СД и ХБП-два хронических неинфекционных заболевания, которые по темпам роста распространенности за последние 20 лет превысили эпидемические пороги во всех странах мира. Это явилось основанием для проведения многочисленных исследований, касающихся механизмов их развития. Согласно данным Международной федерации диабета от 2015 г., распространенность СД на планете колеблется от 4 до 11,5%, в среднем составляя 8,8%. Распространенность ХБП (по совокупности всех стадий) несколько превышает таковую для СД и составляет в среднем 15% [2].

No abstract

Adrenal insufficiency (AI) is a syndrome caused by disturbance in the synthesis and secretion of hormones of the adrenal cortex, which ensure the vital activity, energy and water-salt homeostasis. The widest hormonal deficiency is observed in primary hypocorticism, when the synthesis of not only glucocorticoids (GC) and adrenal androgens, but also mineralocorticoids is disrupted. Lifelong replacement therapy with GCs for this pathology may be associated with a risk of bone loss and osteoporosis. However, at present, there are no clear guidelines for diagnosis of bone condition, including and bone mineral density (BMD) monitoring during treatment with GCs in patients with AI. This review summarizes collected data on the key pathogenetic links of glucocorticoid-induced osteoporosis, incidence of decreased BMD and fractures in patients with AI. In this review factors that influence bone metabolism in this cohort of patients are considered: the type and the dose of prescribed GCs, the type (primary, secondary, HH in congenital adrenal cortex dysfunction) and the duration of AI, age, gender, and the presence of concomitant endocrine disorders (hypogonadism, growth hormone (GH) deficiency). In addition, the review presents data on the effect of adrenal androgen replacement therapy and recombinant GH therapy on bone metabolism in secondary AI.