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Journal of Clinical Endocrinology & Metabolism, Vol 70, 1457-1461, Copyright © 1990 by Endocrine Society
ARTICLES |
A McElduff, D Lissner, M Wilkinson and S Posen
Department of Endocrinology, Royal North Shore Hospital, St. Leonards, New South Wales, Australia.
We performed 6-h human PTH-(1-34) infusions in 8 control subjects, 10 subjects with primary hyperparathyroidism, and 7 men with idiopathic hypercalciuria. We measured serum calcium, serum 1,25-dihydroxyvitamin D, urinary calcium, and fractional phosphate excretion. The PTH-induced rise in serum 1,25-dihydroxyvitamin-D was significantly smaller in the hyperparathyroid patients than in either the controls or the hypercalciuric patients. The rise in serum calcium was similar in all 3 groups. The hyperparathyroid subjects had higher basal fractional phosphate excretion than the other two groups. PTH failed to increase fractional phosphate excretion in the hyperparathyroid individuals, whereas there was a statistically significant increase in the other two groups. PTH was without significant effect on urinary calcium excretion in any of the three groups. There were no discernible differences between the responses of the hypercalciuric patients and those of the normal subjects. These findings suggest that while responses to PTH are normal in hypercalciuria, some hyperparathyroid patients are resistant to exogenous PTH. This resistance is limited to specific arms of the PTH response pathway and may not involve PTH receptors.
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