Studies on the Mechanism of Hyponatremia and Impaired Water Excretion in Myxedema
Authors: MARTIN GOLDBERG
Journal: Annals of Internal Medicine (1962)

Case Reports1 January 1962Studies on the Mechanism of Hyponatremia and Impaired Water Excretion in MyxedemaMARTIN GOLDBERG, M.D., MARTIN REIVICH, M.D.MARTIN GOLDBERG, M.D.Search for more papers by this author, MARTIN REIVICH, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-56-1-120 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptAmong the endocrine disorders impaired water excretion is a well-documented characteristic of adrenal and pituitary insufficiency (1). An inability to normally excrete a water load in primary myxedema has been described (2-4), but there appears to be disagreement as to both the frequency of its occurrence and the magnitude of the defect. The underlying mechanism for this abnormal antidiuresis has not been clearly delineated. Vogt (3) attributed the cause to defective adrenocorticotropic hormone production in response to a water load, but Crispell, Parson, and Sprinkle (2) could not correct the defect in water excretion in four patients with myxedema by...References1. GARRODBURSTON ORA: The diuretic response to ingested water in Addison's disease and panhypopituitarism and the effect of cortisone thereon. Clin. Sci. 11: 113, 1952. MedlineGoogle Scholar2. CRISPELLPARSONSPRINKLE KRWP: A cortisone-resistant abnormality in diuretic response to ingested water in primary myxedema. J. Clin. Endocr. 14: 640, 1954. CrossrefGoogle Scholar3. VOGT JH: Impaired water excretion capacity in primary myxedema improved by corticosteroids, corticotrophin and thyroid substitution. Acta Endocr. 35: 277, 1960. MedlineGoogle Scholar4. BLEIFERBELSKYSAXONPAPPER KHJLLS: The diuretic response to administered water in patients with primary myxedema. Clin. Res. 7: 245, 1959. Google Scholar5. 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Author, Article, and Disclosure InformationAuthors: MARTIN GOLDBERG, M.D.; MARTIN REIVICH, M.D.Affiliations: Philadelphia, PennsylvaniaFrom the Chemical Section of the Department of Medicine and the Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania.This study was supported in part by funds from Grant H-340, National Heart Institute, National Institutes of Health, United States Public Health Service, from OG-16, Division of General Sciences, National Institutes of Health, and from the C. Mahlon Kline Fund for the Development of the Department of Medicine.Requests for reprints should be addressed to Martin Goldberg, M. D., Chemical Section, Department of Medicine, 860 Gates Pavilion, University of Pennsylvania, 3400 Spruce Street, Philadelphia 4, Pennsylvania. 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