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

• Published in: The journal of clinical endocrinology and metabolism Vol. 60; no. 2; p. 225
• Main Authors: Kater, C E, Biglieri, E G, Rost, C R, Schambelan, M, Hirai, J, Chang, B C, Brust, N
• Format: Journal Article
• Language: English
• Published: United States 01.02.1985
• Subjects: 18-Hydroxycorticosterone - blood; Adenoma - metabolism; Adolescent; Adrenal Gland Diseases - metabolism; Adrenal Gland Neoplasms - metabolism; Adrenocorticotropic Hormone - deficiency; Adult; Aged; Aldosterone - biosynthesis; Aldosterone - blood; Child; Child, Preschool; Corticosterone - analogs & derivatives; Cushing Syndrome - metabolism; Cytochrome P-450 CYP11B2; Female; Humans; Hydrocortisone - blood; Infant; Kidney Diseases - metabolism; Male; Middle Aged; Mixed Function Oxygenases - metabolism; Pituitary Diseases - metabolism; Pituitary Neoplasms - metabolism; Potassium - blood; Renin - blood; Renin-Angiotensin System
• ISSN: 0021-972X; 1945-7197
• DOI: 10.1210/jcem-60-2-225

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 aldosterone 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 17 alpha-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-methyloxidase II), as defined by their plasma concentrations. Any influence of these trophic factors must be proximal to the site of 18-OHB production.