CALCIUM HOMEOSTASIS IN IMMOBILIZATION - AN EXAMPLE OF RESORPTIVE HYPERCALCIURIA
CALCIUM HOMEOSTASIS IN IMMOBILIZATION - AN EXAMPLE OF RESORPTIVE HYPERCALCIURIA
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DOI:
10.1056/nejm198205133061903
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发表时间:
1982-01-01
影响因子:
158.5
通讯作者:
BROADUS, AE
中科院分区:
文献类型:
--
作者:
STEWART, AF;ADLER, M;BROADUS, AE
Prolonged immobilization may result in hypercalcemia, hypercalciuria, and osteoporosis. Although bone resorption is central to this syndrome, the mechanism of resorption is uncertain. In particular, the role of systemic Ca-regulating hormones remains unclear. In 14 immobilized subjects fasting Ca excretion, 24-h urinary Ca excretion during restricted Ca intake, the renal P threshold, plasma 1,25-dihydroxyvitamin D, nephrogenous cAMP, and immunoreactive parathyroid hormone were measured. Mean serum Ca levels were normal, but fasting and 24-h Ca excretion were markedly elevated (0.28 mg/dl of glomerular filtrate and 314 mg/24 h, respectively). The mean levels of serum P (4.8 mg/dl) and the renal P threshold (4.3 mg/dl) were elevated. Mean plasma 1,25-dihydroxyvitamin D was strikingly reduced (9.9 pg/ml), as were nephrogenous cAMP (0.64 nmol/dl of glomerular filtrate) and immunoreactive parathyroid hormone in both assays. The parathyroid-1,25-dihydroxyvitamin D axis is suppressed in patients with immobilization-induced hypercalciuria, as would be predicted by a model of resorptive hypercalciuria.