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S. RICHARDSON HILL, Jr., M.D.; JOHN F. NICKERSON, B.A.; SIDNEY B. CHENAULT, M.D.; JEAN H. McNEIL, M.D.; WILLARD R. STARNES, M.S.; MATTIE C. GAUTNEY, B.S.

AMA Arch Intern Med. 1959;104(6):982-994.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Introduction

The classification of clinical disorders associated with an abnormal secretion of aldosterone was clearly outlined by Conn.¹ Primary hyperaldosteronism had been previously described by Conn² and secondary hyperaldosteronism in patients with nephrosis, congestive heart failure, and cirrhosis by Deming, Luetscher, and Curtis.^3,4 Although the syndrome of primary hypoaldosteronism had not been described, it was anticipated by Conn,¹ and subsequently two patients have been reported as representing examples of this syndrome.^5,6 The exact pathophysiology of primary hypoaldosteronism is still in doubt.⁷

Although increased aldosterone secretion is not necessarily the primary cause of sodium and water retention in patients with edema, it is, in general, one constant finding in the chain of events leading to edema formation. Two groups of substances have been used to modify this aspect of edema; inhibitors of adrenal cortical activity⁸ and peripheral antagonists of aldosterone.⁹ The therapeutic usefulness of the adrenal inhibitor used most extensively, . . . [Full Text PDF of this Article]

Author Affiliations
Birmingham, Ala.

From the Department of Medicine and University Hospital, the University of Alabama Medical Center, and the Medical Service Veterans Administration Hospital.; Trainee, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health (Drs. Chenault and McNeill), and Student Fellow, National Institutes of Health (Mr. Nickerson), Bethesda, Md.

Footnotes
Submitted for publication June 11, 1959.

Read before the Section on Internal Medicine at the 108th Annual Meeting of the American Medical Association, Atlantic City, June 11, 1959.

Supported in part by grants from the National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Md., The Upjohn Company, The Eli Lilly Company, and Wyeth Laboratories.

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