An Adrenocortical Tumor Secreting Weak Mineralocorticoids

Abstract

An adrenocortical carcinoma (15.5g) secreting excessive amounts of steroids with weak mineralocorticoid activity in a25-year-old woman was studied with particular reference to its in vivo and in vitro secretions of steroids. Severe hypertension, occasional low serum potassium and suppressed PRA were the major clinical findings, and were improved with removal of the tumor. In the preoperative stage, plasma levels of 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone, corticosterone and 18-hydroxycorticosterone were all increased. However, the plasma level of aldosterone was repeatedly normal. Although plasma levels of pregnenolone, 17-hydroxypregnenolone, progesterone and 17-hydroxyprogesterone were very high, those of other late step steroids, i.e. 11-deoxycortisol, cortisol, dehydroepiandrosterone, androstenedione and testosterone were almost normal. From these findings, a major etiological role of weak mineralocorticoids such as 11-deoxycorticosterone, 18-hydroxycorticosterone and corticosterone in her hypertension was suggested.

Close examination of steroidogenesis disorders in a DOC- and progesterone-producing adrenocortical carcinoma

“…This finding is consistent with earlier reports indicating that plasma DOC levels are under the control of ACTH in benign DOC-producing tumors, but not in malignant tumors [3,4,[15][16][17]. Dexamethasone suppresses adrenal steroidogenesis by suppressing ACTH secretion from the pituitary gland.…”