Desoxycorticosterone Secretion Rates in Hyperadrenocorticism1

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Abstract
Twelve patients with hyperadrenocorticism were presented 3 with primary aldosteronism and 9 with Cuahing''s syndrome. Three patients had increased excretion rates of tetrahydrodesoxycorticosterone (THDOC) and an increased secretion rate of desoxycorticosterone (DOC). One had primary aldosteronism with hypertension and hypokalemic alkalosis. The administration of Aldactone-A resulted in correction of the hypertension hypokalemic alkalosis partial correction of the high Nat:Kt ratio. The urinary excretion rates of 17-ketosteroids and the measured glucocorticoids were normal. There was an increase in the excretion rate of aldosterone as well as of THDOC and THS. The secretion of both aldosterone and desoxycorticosterone was increased significantly. The cause of the defect in this patient was found to be a primary adrenocortical carcinoma. Removal of the carcinoma resulted in only partial correction of the excessive secretion rate of DOC. One patient with Cushing''s syndrome had a marked increase in the rate of formation of glucocorticoids as indicated by the excessive urinary excretion rate of cortisol tetrahydrocortisol tetrahydrocortisone and 17-ketogenic steroids. The secretion rate of DOC and the excretion rate of THDOC and THS were significantly increased. The patient was found to have a bronchogenic carcinoma causing the syndrome. The patient with Cushing''s syndrome exhibited marked evidence of a defect in 11[beta] -hydroxylation of steroids. She excreted large quantities of THDOC and THS under basal conditions and excreted more upon stimulation by ACTH [adenocorticotropic hormone]. It is postulated that hypokalemic alkalosis ound in patients with malignancies affecting the adrenal cortex may be caused by an excess of desoxycorticosterone.