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Recognition of Partial Defects in Antidiuretic Hormone Secretion

MYRON MILLER, M.D., F.A.C.P.; THEODORE DALAKOS, M.D.; ARNOLD M. MOSES, M.D., F.A.C.P.; HERBERT FELLERMAN, M.D.; and DAVID H. P. STREETEN, M.B., F.A.C.P.
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Supported in part by research grant RR00229, Division of Research Facilities and Resources, U.S. Public Health Service, Washington, D.C., and grant AM05252, National Institute of Arthritis and Metabolic Disease, National Institutes of Health, Bethesda, Md.

Dr. Miller was supported by a Clinical Investigatorship from the Veterans Administration.

▸Requests for reprints should be addressed to Myron Miller, M.D., Veterans Administration Hospital, Irving Ave. & University Place, Syracuse, N.Y. 13210


Syracuse, New York


Ann Intern Med. 1970;73(5):721-729. doi:10.7326/0003-4819-73-5-721
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A dehydration procedure has been used to identify patients with partial antidiuretic hormone (ADH) deficiency. The test consists of water deprivation until the osmolality of hourly voided urines reaches a plateau and then relating the urine osmolality at which this occurs to the osmolality recorded after subsequent injection of ADH. In patients with normal neurohypophysial function and patients with primary polydipsia, urine osmolality at the end of such a period of deprivation was much greater than plasma osmolality and did not increase more than 5% after the injection of 5 units of aqueous vasopressin. In patients with severe ADH deficiency urine osmolality before ADH was much less than plasma osmolality; after ADH injection, however, it was increased by more than 50%. Thirteen patients in whom urine osmolality was greater than plasma osmolality after water deprivation and was further increased by 9% to 67% after ADH injection were considered to have partial ADH deficiency. Some patients with ADH deficiency apparently exhausted their limited neurohypophysial ADH stores during prolonged dehydration, with resultant change from partial to severe hormone deficiency.

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