Effects of short term glucocorticoid administration in primary hyperparathyroidism: Comparison to sarcoidosis

N. A. Breslau, J. E. Zerwekh, M. J. Nicar, C. Y C Pak

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Abstract

The hypercalcemia of both sarcoidosis and primary hyperparathyroidism (PHPT) has been associated with increased serum 1,25-dihydroxycholecalciferol [1,25-(OH)2D] and enhanced intestinal absorption of Ca. The hypercalcemia of sarcoidosis responds to short term steroid treatment with an associated reduction in serum 1,25-(OH)2D and intestinal Ca absorption. To gain insight into the lack of suppression of the hypercalcemia of PHPT by steroids, 10 patients with PHPT were studied while kept on a constant diet for 15 days. Days 1-3 represented the equilibration period, days 4-7 constituted the control period, and days 8-15 made up the treatment period (prednisolone, 50 mg daily in 4 divided doses). In response to prednisolone, patients with PHPT had significant increases in serum Ca [11.5 ± 0.3 to 11.9 ± 0.4 (SEM) mg/dl], serum P (2.4 ± 0.2 to 3.1 ± 0.1 mg/dl), and urinary Ca (393 ± 55 to 529 ± 53 mg/day; P < 0.005 for each). The response of serum 1,25-(OH)2D to steroids in the patients with PHPT was variable, and therefore did not change significantly for the group as a whole (73 ± 9 to 66 ± 11 pg/ml; normal, < 50 pg/ml). Fractional intestinal Ca absorption was not reduced by steroid treatment (0.77 ± 0.04 to 0.74 ± 0.03; normal < 0.61). Bone resorption was enhanced by the glucocorticoids, as suggested by significant increases in urinary hydroxyproline (34 ± 5 to 41 ± 5; normal, < 36 mg/day) and fasting urinary Ca excretion (0.28 ± 0.05 to 0.41 ± 0.06 mg/100 glomerular filtrate; normal, < 0.11 mg/100 ml glomerular filtrate). The augmented bone resorption may have been mediated directly by the steroids or may have resulted from enhanced PTH secretion (80 ± 40 to 102 ± 46 μleq/ml; P < 0.025; normal, < 30 μleq/ml) induced by the steroids. These observations on the differences in response to glucocorticoids between patients with PHPT and those with sarcoidosis may partly explain the resistance to suppression of the hypercalcemia of PHPT.

Original languageEnglish (US)
Pages (from-to)824-830
Number of pages7
JournalJournal of Clinical Endocrinology and Metabolism
Volume54
Issue number4
StatePublished - 1982

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Primary Hyperparathyroidism
Sarcoidosis
Glucocorticoids
Steroids
Hypercalcemia
Intestinal Absorption
Serum
Prednisolone
Bone Resorption
Bone
Calcitriol
Hydroxyproline
Nutrition
Fasting
Therapeutics
Scanning electron microscopy
Diet

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Effects of short term glucocorticoid administration in primary hyperparathyroidism : Comparison to sarcoidosis. / Breslau, N. A.; Zerwekh, J. E.; Nicar, M. J.; Pak, C. Y C.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 54, No. 4, 1982, p. 824-830.

Research output: Contribution to journalArticle

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N2 - The hypercalcemia of both sarcoidosis and primary hyperparathyroidism (PHPT) has been associated with increased serum 1,25-dihydroxycholecalciferol [1,25-(OH)2D] and enhanced intestinal absorption of Ca. The hypercalcemia of sarcoidosis responds to short term steroid treatment with an associated reduction in serum 1,25-(OH)2D and intestinal Ca absorption. To gain insight into the lack of suppression of the hypercalcemia of PHPT by steroids, 10 patients with PHPT were studied while kept on a constant diet for 15 days. Days 1-3 represented the equilibration period, days 4-7 constituted the control period, and days 8-15 made up the treatment period (prednisolone, 50 mg daily in 4 divided doses). In response to prednisolone, patients with PHPT had significant increases in serum Ca [11.5 ± 0.3 to 11.9 ± 0.4 (SEM) mg/dl], serum P (2.4 ± 0.2 to 3.1 ± 0.1 mg/dl), and urinary Ca (393 ± 55 to 529 ± 53 mg/day; P < 0.005 for each). The response of serum 1,25-(OH)2D to steroids in the patients with PHPT was variable, and therefore did not change significantly for the group as a whole (73 ± 9 to 66 ± 11 pg/ml; normal, < 50 pg/ml). Fractional intestinal Ca absorption was not reduced by steroid treatment (0.77 ± 0.04 to 0.74 ± 0.03; normal < 0.61). Bone resorption was enhanced by the glucocorticoids, as suggested by significant increases in urinary hydroxyproline (34 ± 5 to 41 ± 5; normal, < 36 mg/day) and fasting urinary Ca excretion (0.28 ± 0.05 to 0.41 ± 0.06 mg/100 glomerular filtrate; normal, < 0.11 mg/100 ml glomerular filtrate). The augmented bone resorption may have been mediated directly by the steroids or may have resulted from enhanced PTH secretion (80 ± 40 to 102 ± 46 μleq/ml; P < 0.025; normal, < 30 μleq/ml) induced by the steroids. These observations on the differences in response to glucocorticoids between patients with PHPT and those with sarcoidosis may partly explain the resistance to suppression of the hypercalcemia of PHPT.

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