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Synthetic Human Parathyroid Hormone- (1–34) for the Study of Pseudohypoparathyroidism^*

LAWRENCE E. MALLETTE, JOHN L. KIRKLAND, ROBERT F. GAGEL, WILLIAM M. LAW, JR and HUNTER HEATH, III

Divisions of Endocrinology and Metabolism, Departments of Internal Medicine and Pediatrics, Baylor College of Medicine, and Medicine and Research Services, Veterans Administration Medical Center Houston, Texas 77030
the Endocrine Research Unit, Division of Endocrinology and Metabolism, Department of Medicine, Mayo Clinic, Mayo Research Foundation, and Mayo Medical School Rochester, Minnesota 55905

Address requests for reprints to: Dr. Mallette, Medical Service 111E, Veterans Administration Medical Center, 2002 Holcombe Boulevard, Houston, Texas 77030.

The synthetic amino-terminal fragment of PTH, PTH-(1–34), was recently released for clinical testing of PTH responsiveness. We measured the urinary cAMP and phosphaturic responses to infusion of PTH-(1–34) [3U/kg BW (200 U maximum), iv in 10 min] in patients with pseudohypoparathyroidism and idiopathic hypoparathyroidism, as well as normal subjects. The protocol used data from 5 30-min urine collections and 4 blood samples. Based on the results in 7 patients with pseudohypoparathyroidism (hypocalcemia with increased serum immunoreactive PTH concentrations), 2 patients with suspected pseudohypoparathyroidism, 9 patients with surgical hypoparathyroidism, and 10 normal subjects, this testing protocol differentiated well among these conditions. The patients with pseudohypoparathyroidism had blunted cAMP and phosphaturic responses to PTH-(1–34) administration compared to those of either normal or hypoparathyroid subjects. Induced hypercalcemia failed to restore a normal cAMP response to PTH-(1–34) infusion in 2 patients with pseudohypoparathyroidism. Calculation of the cAMP response to PTH-(1–34) as nanomoles per dL glomerular filtrate during the first 30 min after infusion provided better differentiation among groups than other parameters of cAMP metabolism. Calculating the phosphaturic response as the percent fall in tubular maximum for phosphate reabsorption during the first hour after infusion gave the best degree of statistical separation among groups. We conclude that this new diagnostic agent is effective for the study of renal responsiveness to PTH, and that the protocol described here reliably differentiates patients with pseudohypoparathyroidism from those with hypocalcemia due to other causes.

^* This work was supported by the VA, a grant from the Armour Pharmaceutical Co., and NIH Grants AM-31307, RR-585, RR-188, and RR-350.

Present address: Suite 303, U. T. Physicians Office Building, 1928 Alcoa Highway, Knoxville, Tennessee 37920.

Received December 4, 1987.