Desoxycorticosterone Secretion Rates in Hyperadrenocorticism1

Abstract

Twelve patients with hyperadrenocorticism have been presented, 3 with primary aldosteronism and 9 with Cushing's syndrome. Three patients (B.F., O.G., J.B.) had increased excretion rates of tetrahydrodesoxycorticosterone (THDOC) and an increased secretion rate of desoxycorticosterone (DOC). Patient B.F. had primary aldosteronism with hypertension and hypokalemic alkalosis. The administration of Aldactone-A resulted in correction of the hypertension, hypokalemic alkalosis, and partial correction of the high Nae: Ke 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 weU 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 (O.G.) 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 as the cause of the syndrome. Patient J.B. with Cushing's syndrome exhibited marked evidence of a defect in 11β-hydroxylation of steroids. She excreted large quantities of THDOC and THS under basal conditions and excreted more upon stimulation by ACTH. It is postulated that hypokalemic alkalosis found in patients with malignancies affecting the adrenal cortex may be caused by an excess of desoxycorticosterone.