[Osteocalcin--a marker of bone metabolism and calcium regulating hormones in steroid osteoporosis].
L Ia Rozhinskaia, Kolesnikova Gs, Marova Ei, Konnova Ev
Abstract
L Ia Rozhinskaia, Kolesnikova Gs, Marova Ei, Konnova Ev
Abstract
Altogether 15 patients with Itsenko-Cushing disease with moderate osteoporosis and 10 healthy persons were investigated. Calcium metabolism, calcium regulating hormones and osteocalcin were studied. Endogenous hypercorticoidism was characterized by a higher secretion of parathyroid hormone against a background of hypercalcemia. Positive correlation of these indices was revealed. In patients with Itsenko-Cushing disease the blood level of vitamin D was decreased as compared to that in the controls. A significant decrease in the blood level of osteocalcin was observed in patients with endogenous hypercorticoidism, there being close negative correlation between the level of osteocalcin and cortisol, and between osteocalcin and 17-hydroxycorticosteroid excretion with urine. A conclusion has been made that the excess of glucocorticosteroids suppresses osteoblast function, slows, down osteogenesis, disturbs the secretion of calcium regulating hormones and calcium metabolism enhancing resorption; this combined action of glucocorticoids causes rapid development of osteoporosis in endogenous hypercorticoidism.
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Altogether 15 patients with Itsenko-Cushing disease with moderate osteoporosis and 10 healthy persons were investigated. Calcium metabolism, calcium regulating hormones and osteocalcin were studied. Endogenous hypercorticoidism was characterized by a higher secretion of parathyroid hormone against a background of hypercalcemia. Positive correlation of these indices was revealed. In patients with Itsenko-Cushing disease the blood level of vitamin D was decreased as compared to that in the controls. A significant decrease in the blood level of osteocalcin was observed in patients with endogenous hypercorticoidism, there being close negative correlation between the level of osteocalcin and cortisol, and between osteocalcin and 17-hydroxycorticosteroid excretion with urine. A conclusion has been made that the excess of glucocorticosteroids suppresses osteoblast function, slows, down osteogenesis, disturbs the secretion of calcium regulating hormones and calcium metabolism enhancing resorption; this combined action of glucocorticoids causes rapid development of osteoporosis in endogenous hypercorticoidism.
Key concepts: Osteocalcin, Internal medicine, Endocrinology, Bone remodeling, Osteoporosis, Calcium, Parathyroid hormone, Hormone