[In vivo and in vitro studies on 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone in normal subjects and in those with various adrenocortical disorders (author's transl)].
Simultaneous measurement of 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) and 18-hydroxycorticosterone (18-OH-B) in the peripheral plasma was carried out on normal subjects and in patients with adrenocortical disorders. The mean plasma levels of 18-OH-DOC at 0800h in normal males and in the follicular and luteal phases of normal females were 8.2 +/- 3.9 ng/100 ml (Mean +/- SD), 7.8 +/- 2.6 ng/100ml and 11.5 +/- 2.8 ng/100ml, respectively. The corresponding levels of 18-OH-B in normal males and in the follicular and luteal phases of normal females were 10.3 +/- 4.2 ng/100ml, 12.4 +/- 4.5 ng/100ml and 13.8 +/- 4.1 ng/100ml, respectively. No differences between the sexes nor the phases of the menstrual cycle were confirmed. ACTH stimulation increased plasma concentrations of 18-OH-DOC and 18-OH-B by 5.1 and 4.4 times respectively, while dexamethasone markedly decreased these 2 steroids. An upright posture increased these steroids significantly. In patients with Cushing syndrome, plasma levels of these 2 steroids were rarely high in cases with adrenocortical hyperplasia and adrenocortical carcinoma, while they were usually within the normal range in adrenocortical adenoma. These 2 steroid levels were increased in primary aldosteronism, idiopathic hyperaldosteronism and congenital 17 alpha-hydroxylase deficiency. They were decreased in Addison's disease and the salt-loosing type of congenital 21 alpha-hydroxylase deficiency. Patients with congenital 21 alpha-hydroxylase deficiency (simple form) showed elevated levels of 18-OH-DOC and normal levels of 18-OH-B. In vitro production of 18-OH-DOC and 18-OH-B was studied by tissue slices of the normal adrenal cortex, adrenocortical carcinoma causing Cushing syndrome, aldosteronoma and nodular hyperplasia with hyperaldosteronism. In the normal adrenal cortex, the mean production rates of 18-OH-DOC and 18-OH-B were 31 and 26 ng/g tissue/hr, respectively. ACTH and angiotensin II significantly increased the production of both 18-OH-DOC and 18-OH-B. In adrenocortical carcinoma, the production of these steroids was markedly diminished and not stimulated with either ACTH or angiotensin II. Aldosteronoma tissue produced these 2 steroids 20 to 40 times that of the normal adrenal tissue and was significantly increased with the addition of ACTH and angiotensin II. Nodular hyperplasia with hyperaldosteronism produced much 18-OH-DOC and 18-OH-B, but did not respond to ACTH and angiotensin II.
D015069:18-Hydroxycorticosterone / Q000378:metabolism*; D000303:Adrenal Cortex Diseases / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone; D000328:Adult; D003345:Corticosterone / Q000031:analogs & derivatives*; D003480:Cushing Syndrome / Q000378:metabolism; D003907:Dexamethasone; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D006899:Mixed Function Oxygenases / Q000172:deficiency
D015069:18-Hydroxycorticosterone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D006899:Mixed Function Oxygenases; D003345:Corticosterone