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*

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Abstract
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.