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Pathophysiology of Deoxycorticosterone-Secreting Adrenal Tumors^*

Medical Service, San Francisco General Hospital Medical Center, and the Department of Medicine, University of California San Francisco, California 94110

Address all correspondence and requests for reprints to: E. G. Biglieri, M.D., Building 100, Room 321, San Francisco General Hospital Medical Center, 1001 Potrero Avenue, San Francisco, California 94110.

Two patients with hypermineralocorticoidism due to deoxycorticosterone (DOC) excess are described. The plasma 17-deoxysteroids of the zona fasciculata (ZF), namely DOC, corticosterone, 18-hydroxydeoxycorticosterone, and 18-hydroxycorticosterone, were elevated. Plasma androgen concentrations were normal, and plasma aldosterone and renin levels were low. One patient, who had benign adrenocortical adenoma, had normal plasma cortisol levels. The other patient, who had metastatic adrenocortical carcinoma, had low plasma cortisol, presumably due to elevated plasma corticosterone levels. While tumors producing only 17-deoxysteroids are rare, they have provided new insights into the regulation of 17-deoxysteroid secretion by the ZF. Presumptive suppression of a non-ACTH factor by adenoma-produced DOC transiently impaired the early postoperative responses to ACTH of the ZF 17-deoxysteroids of the contralateral adrenal. The dissociation of 17-deoxysteroids from cortisol in normal subjects given either dexamethasone or DOC acetate provides additional evidence for such a factor.

^* This work was supported by USPHS Research Grant AM-06415 from the NIDDK. The studies were carried out in the General Clinical Research Center at San Francisco General Hospital (RR-00083), supported by the Division of Research Resources, NIH.

Received February 12, 1987.

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