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.
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.
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].
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