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SHORT‐TERM EFFECT OF PREDNISONE ON SERUM 1,25‐DIHYDROXYVITAMIN D IN NORMAL INDIVIDUALS AND IN HYPER‐AND HYPOPARATHYROIDISM
Author(s) -
BRAUN J. J.,
JUTTMANN J. R.,
VISSER T. J.,
BIRKENHAGER J. C.
Publication year - 1982
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1982.tb02630.x
Subject(s) - prednisone , medicine , endocrinology , hypoparathyroidism , parathyroid hormone , vitamin d and neurology , basal (medicine) , oral administration , hyperparathyroidism , calcium , cholecalciferol , diabetes mellitus
Oral administration of prednisone (30 mg/day for 9 days) to six normal individuals induced a significant rise in the concentration of serum 1,25-dihydroxyvitamin D [1,25-(OH)2D] within 2 days. In four patients with primary hyperparathyroidism a larger increase of 1,25-(OH)-2D was observed within 3 days. In these patients the 1,25-(OH)-2D concentration remained elevated during the whole period of prednisone administration (10 days) whereas in the control group it had returned to basal levels or below after 9 days of prednisone administration. This response appeared dependent upon parathyroid hormone (PTH) as we found no change in the (basally low) 1,25-(OH)2D concentrations in five patients with hypoparathyroidism during 3-4 days of prednisone administration (30 mg/day). In these patients vitamin D medication had been interrupted 3-5 days before the administration of prednisone, whereafter serum calcium was kept between 2.10 and 2.30 mmol/1 by means of calcium infusion. The response of 1,25-(OH)2D to prednisone is best explained by a stimulatory action of glucocorticoids upon PTH secretion or by the induction of increased PTH sensitivity.