Мінеральна щільність та метаболізм кісткової тканини у разі тиреотоксикозу

Abstract

Introduction. Hyperthyroidism is a pathological condition of the body due to increased of thyroid hormones in blood. The prevalence of this pathology increases with age. In the age period from 40 to 60 years it is 0.45%, and after 60 years the risk of the disease increases and is 1.4%. Aim is to analyze the condition of bone tissue in the conditions of thyrotoxicosis on the basis of literature data. Materials and methods are content analysis of the literature on studies of mineral density and bone metabolism in patients with thyrotoxicosis syndrome. Results. Thyroid hormones at physiological concentrations have an important role in skeletal development, reaching peak bone mass and maintaining bone mass during adulthood. It is proved that the effect of thyroid hormone on bone cells is carried out by hormone-receptor interactions. Receptors for thyroid hormones and TSH are found on osteoblasts and osteoclasts, which testifies to their direct action on the cell. The presence of calcium in the skeleton is mainly determined the bone mineral density. Hyperthyroidism is associated with negative calcium balance. When thyrotoxicosis decrease the bone density is observed in 10–20% of patients. This is due to a violation of bone remodeling by increasing metabolism with a disproportionate increase in bone resorption and increased bone formation, but the activation of bone formation cannot fully compensate for the loss of bone mass in the background enhanced resorption. With increasing severity of hyperthyroidism concentration in serum alkaline phosphatase, osteocalcin, and osteoprotegerin growth factor FGF-23 of fibroblasts, indicating increased bone metabolism accompanied by activation of bone resorption. When reducing subclinical hyperthyroidism TSH with normal T3 and T4, or elevated levels of thyroid hormones in the suppression of TSH. It is associated with decreased bone mineral density, increased fragility of bones with a high risk of fractures. Conclusions. Skeletal development and maintenance is regulated by a normal balance of thyroid hormones. Hyperthyroidism is associated with a prolonged cycle of bone remodeling, increased resorption and bone formation. However, the activation of bone formation observed in thyrotoxicosis is not able to fully compensate for the loss of bone mass against the background of increased resorption, which leads to osteoporosis and increased risk of fractures.