Journal of Clinical Endocrinology & Metabolism, Vol 59, 1022-1024, Copyright © 1984 by Endocrine Society

ARTICLES

Elevated urinary excretion of 18-oxocortisol in glucocorticoid- suppressible aldosteronism

CE Gomez-Sanchez, M Montgomery, A Ganguly, OB Holland, EP Gomez-Sanchez, CE Grim and MH Weinberger

A radioimmunoassay procedure for the measurement of urinary 18- oxocortisol was developed. The antibody was raised against 18- oxocortisol 3-carboxymethyloxime-BSA and had relatively high specificity, except for aldosterone (26.3%). The RIA required a preliminary HPLC purification using a Lichrosorb diol column eluted with toluene:acetonitrile:isopropanol:acetic acid (83:11.9:5.1:0.01). The eluate portion corresponding to 18-oxocortisol was evaporated and subjected to RIA. The RIA procedure had an intraassay variability of 11% when using a pool containing 10.8 micrograms/24 hr (n = 6) and 17% with a pool containing 3.28 micrograms/24 hr. The interassay variability was 11% (n = 4). The recovery of added 18-oxocortisol was 90 +/- 10%. The urinary excretion of 18-oxocortisol in 22 white normal subjects was 3.26 +/- 1.98 (SD) micrograms/24 hr (range 0.8 to 7.1 micrograms/24 hr). The mean excretion of 18-oxocortisol in 4 patients with glucocorticoid-suppressible aldosteronism (GSA) was 38.6 micrograms/24 hr (range 25.5 to 54.6 micrograms/24 hr). The excretion of 18-oxocortisol in 3 patients with adenomas producing primary aldosteronism (APA) varied between 11.1 to 17.3 micrograms/24 hr and in 3 patients with idiopathic aldosteronism (IA) varied between 2.5 to 10.6 micrograms/24 hr. 18-Oxocortisol excretion is increased markedly in the urine of patients with GSA: what role this relatively weak mineralocorticoid plays in the pathogenesis of their hypertension is unknown. Its elevation is probably a reflection of a postulated lack of involution of the 18-methyloxidase in the inner layers of the adrenal.

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