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Effects of Short Term Glucocorticoid Administration in Primary Hyperparathyroidism: Comparison to Sarcoidosis^*

Mineral Metabolism Section, Department of Internal Medicine, Southwestern Medical School, University of Texas Health Science Center at Dallas Dallas, Texas 75235

Address requests for reprints to: Dr. Neil Breslau, Mineral Metabolism Section, Department of Internal Medicine, Southwestern Medical School, University of Texas Health Science Center at Dallas, 5323 Harry Hines Boulevard, Dallas, Texas 75235.

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 ml 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 leq/ml; P < 0.025; normal, <30 leq/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.

^* Presented in part at the National Meeting of the American Federation for Clinical Research, San Francisco, CA, April 1981. This work was supported by NIH Grants 1-R01-AM-26253-01A1 and M01-RR- 00633.

Received July 16, 1981.

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