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Edward G. Biglieri, MD; Jan R. Stockigt, MD; Morris Schambelan, MD

Arch Intern Med. 1970;126(6):1004-1007.

Abstract
Oral administration of 400µg of fludrocortisone acetate for three days suppresses aldosterone production in normal subjects with minimal effect on the excretion of Porter-Silber chromogens. Administration of fludrocortisone acetate to hypertensive patients with hyperaldosteronism suppressed aldosterone production into the normal range in all patients with essential hypertension and in one patient with adrenal nodular hyperplasia, but failed to do so in the patients with aldosterone-producing adenoma or nodular hyperplasia, confirmed subsequently. Administration of fludrocortisone acetate to hypertensive outpatients with hyperaldosteronism is an effective screening procedure for further evaluation of primary adrenal disease.

Author Affiliations
San Francisco

From the Medical Services, San Francisco General Hospital and the Department of Medicine, University of California School of Medicine, San Francisco.

Footnotes
Received for publication March 11, 1970; accepted August 10.

Reprint requests to Editorial Office, San Francisco General Hospital, 1001 Potrero Ave, San Francisco 94110 (Dr. Biglieri).

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