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Suppression of Parathyroid Hormone Secretion with Oral Calcium in Normal Subjects and Patients with Primary Hyperparathyroidism^*

Departments of Medicine and Pharmacology, Columbia University College of Physicians and Surgeons New York, New York 10032
the Regional Bone Center, Helen Hayes Hospital West Haverstraw, New York 10993

Address requests for reprints to: Jack F. Tohme, M.D., Department of Medicine, 9–410 Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, New York 10032.

Exquisite sensitivity of normal parathyroid glands to small changes in ambient calcium concentrations and impaired sensitivity in primary hyperparathyroidism have been shown in vitro. Using an assay for PTH that detects rapid changes in PTH secretion (N-terminal-specific RIA; normal range, <3–33 pg/mL), we determined PTH suppressibility in response to a standardized dose of oral calcium in normal subjects and patients with primary hyperparathyroidism. Nine normal subjects were given oral calcium (25 mg/kg), and blood was analyzed half-hourly for 3 h for calcium and N-terminal PTH (N-PTH). Serum calcium rose by 0.34 ± 0.06 mg/dL (0.085 ± 0.015 mmol/L), and N-PTH levels declined rapidly from 15.3 ± 1.4 to 4.2 ± 1.1 pg/mL (–73 ± 6%; P < 0.01). In six subjects N-PTH concentrations became undetectable. Nine patients with primary hyperparathyroidism were tested in the same manner. Serum calcium rose by 0.53 ± 0.1 mg/dL (0.13 ± 0.025 mmol/L), and N-PTH levels declined less, from 66 ± 14 to 52 ± 12 pg/mL (–21 ± 4%; P < 0.05). In none of the patients was the PTH reduced to less than 20 pg/mL. These results illustrate in vivo that the PTH response to oral calcium in primary hyperpara-thyroidism is markedly different from that in normal subjects.

^* This work was supported in part by NIH Grants DK-32333, AR-39191, AR-36446, DK-01836, and RR00645.

Received March 20, 1989.