STEPHEN J. MARX, M.D.; DAVID POWELL, M.R.C.P.; PETER M. SHIMKIN, M.D.; SAMUEL A. WELLS, M.D.; ALFRED S. KETCHAM, M.D.; JAMES E. MCGUIGAN, M.D.; JOHN P. BILEZIKIAN, M.D.; G. D. AURBACH, M.D.
Parathyroid hormone and gastrin immunoassays were done at the Endocrine Unit, Massachusetts General Hospital, Boston, Massachusetts, and the Department of Medicine, University of Florida College of Medicine, Gainesville, Florida.
▸Requests for reprints should be addressed to G. D. Aurbach, M.D., Section on Mineral Metabolism, Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, MD 20014.
MARX S., POWELL D., SHIMKIN P., WELLS S., KETCHAM A., MCGUIGAN J., BILEZIKIAN J., AURBACH G.; Familial Hyperparathyroidism: Mild Hypercalcemia in at Least Nine Members of a Kindred. Ann Intern Med. 1973;78:371-377. doi: 10.7326/0003-4819-78-3-371
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Published: Ann Intern Med. 1973;78(3):371-377.
Nine members of a kindred were hypercalcemic. The hypercalcemia was mild in all. A diagnosis of hyperparathyroidism in many could not be definitely established by standard methods, but measurement of parathyroid hormone levels in samples obtained by selective venous catheterization confirmed the presence of overactive parathyroid tissue. Venous catheterization indicated bilateral parathyroid disease in four of five previously unexplored patients. Three of the hypercalcemic individuals had additional manifestations of multiple endocrine adenomatosis. There were no known cases of peptic disease in the entire kindred, and both basal and stimulated gastrin levels showed no abnormalities.
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Endocrine and Metabolism, Nephrology, Fluid and Electrolyte Disorders.
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