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Parathyroid Function in Patients with Pheochromocytoma

SAM S. MILLER, M.D.; GLEN W. SIZEMORE, M.D.; SHELDON G. SHEPS, M.D., F.A.C.P.; and GERTRUDE M. TYCE, Ph.D.
[+] Article and Author Information

Grant support: in part by Research Grant NS-9143 from the National Institute of Health, U.S. Public Health Service, and a grant from the Mayo Foundation.

Read in part at the 55th Annual Session of the American College of Physicians, 31 March through 5 April 1974, in New York, New York.

▸Requests for reprints should be addressed to Dr. S. S. Miller, in care of the Section of Publications, Mayo Clinic, 200 First Street SW, Rochester, MN 55901.


Rochester, Minnesota


Ann Intern Med. 1975;82(3):372-375. doi:10.7326/0003-4819-82-3-372
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Serum calcium, serum immunoreactive parathyroid hormone (PTH), and plasma immunoreactive calcitonin were measured in 12 patients with catecholamine-secreting tumors. Only two patients had high serum calcium and immunoreactive PTH concentrations (one also had high basal immunoreactive calcitonin); in both, the hypercalcemia persisted after removal of their pheochromocytomas but was corrected by removal of hyperplastic parathyroid glands and medullary thyroid carcinomas. Of the 10 patients with normal serum calcium and immunoreactive PTH concentrations, 2 had high immunoreactive calcitonin concentrations and medullary thyroid carcinomas alone were found. Our results suggest that [1] hypercalcemia occurs infrequently in patients with pheochromocytoma, [2] chronic circulating catecholamine excess does not cause increased immunoreactive PTH or immunoreactive calcitonin secretion in patients with pheochromocytoma, and [3] the parathyroid disease in patients with pheochromocytoma is a genetically determined component of multiple endocrine neoplasia.

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