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21-Deoxyaldosterone Excretion in Patients with Primary Aldosteronism and 21-Hydroxylase Deficiency^*

Department of Pharmacology, University of Heidelberg 6900 Heidelberg
Department of Pediatrics, University of Heidelberg 6900 Heidelberg
Deutsche Klinik für Diagnostik 6200 Wiesbaden, West Germany
St. Luke’s-Roosevelt Hospital Center New York, New York 10025

Address requests for reprints to: Dr. Sabina Lewicka, Department of Pharmacology, University of Heidelberg, IM Neuenheimer Feld 366, Heidelberg 6900, West Germany.

21-Deoxyaldosterone appears in urine in free and conjugated forms. Total excretion is best determined after acid hydrolysis (pH 1) of urine, followed by extraction, repeated chromatographic purification, and quantitation of the steroid by RIA. 21-Deoxyaldosterone excretion was normal in 70% of patients with essential hypertension (n = 18), while 30% (n = 8) had more or less elevated values. In patients with primary aldosteronism (n = 21) elevated as well as normal values of urinary 21-deoxyaldosterone were found, indicating that in some patients aldosterone may be formed not only from corticosterone but also from the 21-deoxy compound. In patients with 21-hydroxylase deficiency (n = 21) urinary 21-deoxyaldosterone was invariably elevated, whether the patients had the virilizing or salt-losing form of the disease. Although the clinical manifestations of the salt-losing form seem unrelated to the inability to convert 21-deoxyaldosterone to aldosterone, the determination of 21-deoxyaldosterone adds insight into the biosynthesis of aldosterone in primary aldosteronism and 21-hydroxylase deficiency.

^* This work was supported in part by Grant Le 570/1–1 from the Deutsche Forschungsgemeinschaft.

Received May 12, 1986.