Summary. This report describes studies of calcium kinetics in ten normal young men. Serum, urinary, And fecal radioactivity was measured from 1 minute to 20 days after intravenous tracer 47Ca injection, and these results were analyzed jointly with data obtained from a simultaneous metabolic balance study, using digital computer techniques. Surface radioactivity' measurements were also obtained to gain further insight into the anatomic correlates of the tracer distribution. The data were satisfied by a model with four exchanging compartments. Series, branching, and mammillary models were analyzed. Several parameters of physiologic interest were independent of the model, but two were dependent on the duration of the study. Individual and mean values for these kinetic analyses are presented with their statistical uncertainties. These studies present detailed analyses in a healthy, normal population and provide a reference for future studies of skeletal metabolism and serum calcium homeostasis.

The effect of transdermal 17 beta-estradiol replacement on ionized calcium and PTH levels was examined in 15 postmenopausal women. After baseline studies in the fasting state, the effect of a calcium infusion on PTH levels was studied. Estrogen replacement resulted in a fall in fasting resting ionized calcium and a rise in PTH levels. After calcium infusion there was no change in the shape of the relationship between plasma calcium and PTH. The level of nonsuppressible PTH secretion was not altered. Transdermal estrogen did not alter basal vitamin D-binding protein levels, 25-hydroxyvitamin D levels, or calcitriol levels. We conclude that the effect of transdermal estrogen replacement on PTH secretion is completely explained by the lowering of ionized calcium, causing a rise in PTH secretion. Thus, with this route of estrogen replacement, there is no necessity to postulate a direct effect of 17 beta-estradiol on the parathyroid gland.

A B S T R A C T Since studies in animals and humans have shown that parathyroid hormone can stimulate bone formation and increase trabecular bone, and patients with primary and secondary hyperparathyroidism may exhibit osteosclerosis, we evaluated the effect of short-term administration of human parathyroid hormone, hPTH-(1-34), in patients with osteoporosis.Six patients with osteoporosis underwent detailed studies including blood and urinary measurements of calcium, phosphate, and magnesium; 47Ca kinetic studies; and 18-d balance studies before and during the short-term administration (3-4 wk) of a daily subcutaneous injection of hPTH fragment 1-34 given as 450 or 750 U/dose.The mean fasting plasma calcium values rose slightly after hPTH-(1-34) administration, primarily in the high-dose group. There was no difference in the mean fasting plasma inorganic phosphate levels. The mean daily urinary excretion of calcium and phosphate was significantly increased in patients given the higher dose.In patients given 450 U, net intestinal calcium absorption increased, phosphate absorption increased, calcium balance improved, and phosphate balance improved. In patients given 750 U, calcium balance and phosphate balance worsened.47Ca kinetic studies showed a minimal increase in bone accretion rate, a decrease in the mean transit time of calcium in the exchangeable pools, and a decrease in the exchangeable-pool size. In all six patients there was an increased renal clearance of 47Ca as a result of hPTH-(1-34) administration.These studies indicate that low doses of parathyroid

It has been hypothesized that estrogen may have a direct effect to reduce the set-point for PTH secretion which may be implicated in its hypocalcemic action. If this is so, estrogen receptors should be demonstrable within parathyroid tissue. Seven human parathyroid adenomas and five samples of normal bovine parathyroid tissue were examined using classical hormone-binding techniques. In no case was there evidence of displaceable estrogen binding of high affinity and low capacity. To exclude the presence of receptors within a small subset of the cells, five of the human adenomas were further studied by immunohistochemistry using a monoclonal antibody to the human estrogen receptor. In no case was there evidence of estrogen receptors. We conclude that the hypocalcemic action of estrogen replacement is unlikely to be mediated via a classical estrogen receptor within the parathyroid, although normal parathyroid tissue was not studied.