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The Constant Plasma 18-Hydroxycorticosterone to Aldosterone Ratio: An Expression of the Efficacy of Corticosterone Methyloxidase Type II Activity in Disorders with Variable Aldosterone Production^*

C. E. KATER, E. G. BIGLIERI, C. R. ROST, M. SCHAMBELAN, J. HIRAI, B. C. F. CHANG and N. BRUST

Medical Service, San Francisco General Hospital Medical Center, and the Department of University of California San Francisco, California
The Division of Endocrinology, Escola de Medicina Sao Paulo, S.P., Brasil

Address requests for reprints to: Edward G. Biglieri, M.D., Clinical Study Center, Building 100, Room 321, San Francisco General Hospital, 1001 Potrero Avenue, San Francisco, California 94110.

Aldosterone and 18–hydroxycorticosterone (18–OHB) are produced by the adrenocortical zona glomerulosa. Under normal conditions, plasma 18–OHB levels parallel and are influenced by the same trophic factors that regulate aldoste-rone production. To evaluate corticosterone-methyl-oxidase II activity, the final step of aldosterone biosynthesis, in conditions associated with chronic derangements of the pituitary-adrenal and/or renal-adrenal axis, we measured the plasma 18–OHB to aldosterone ratio, cortisol, PRA or plasma renin concentration, and potassium (K) in 104 such patients and 15 normal subjects. The 18-OHB to aldosterone ratios in the pituitary-adrenal group were not significantly different from normal regardless of elevated or reduced ACTH and/or cortisol levels [patients with Cushing's syndrome, 3.55 ± 0.68 (±SE); ACTH deficiency, 2.03 ± 0.34; 21-hydroxylase deficiency, 3.09 ± 0.23; normal subjects, 2.50 ± 0.15]. The renal-adrenal group also had normal ratios regardless of plasma renin concentration and K levels [patients with aldosterone-producing adenomas, 2.85 ± 0.15; idiopathic hyperaldosteronism, 2.14 ± 0.19; salt-losing nephropathy, 3.06 ± 0.54; Bartter's syndrome, 2.89 ± 0.20; isolated (hyporeninemic) hypoaldosteronism, 3.20 ± 0.39]. Only in patients with 17a-hydroxylase deficiency (230.1 ± 118.6) was the ratio abnormally high. Chronic perturbations of aldosterone production by ACTH, the renin-angiotensin system, and/or K did not alter this last step of aldosterone biosynthesis (corticosterone-methyl-oxidase II), as defined by their plasma concentrations. Any influence of these trophic factors must be proximal to the site of 18-OHB production.

^* This work was supported in part by USPHS Grants HL-11046 from the NHLBI and AM-06415 from the NIAMDD. The studies were carried out in the General Clinical Research Center at San Francisco General Hospital Medical Center (RR–00083) with support by the Division of Research Resources, NIH.

Establishe d investigator of CNPq-Conselho National De Desen-volvimento Cientifico E Tecnologico, Brasil, under Contract 30.0449/ 81.

Received October 11, 1983.

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