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Effect of DL-2(p-Aminophenyl)-2-phenylethylamine on Adrenocortical Function in Cushing's Syndrome Due to Nontumorous Adrenocortical Hyperfunction¹

Endocrine Research Laboratory and Clinic of the Department of Medicine, The Mount Sinai Hospital and the Institute for Steroid Research, Montefiore Hospital New York, New York 10029

DL-2 (p-Aminophenyl)-2-phenylethylamine (SK&F-12185), a new adrenocortical blocking agent, was given to 3 patients with Cushing's syndrome due to nontumorous adrenocortical hyperfunction. The drug caused a rise in the urinary titer of neutral 17-ketosteroids, testosterone and 17-hydroxycorticoids. It induced a fall in the adrenal secretory rate of cortisol and in urinary tetrahydrocortisol and a rise in the adrenal secretory rate of 11-deoxycortisol and of the urinary excretion of tetrahydro S. Presumably one of the sites of action of the drug is interference with 11β-hydroxylation. In one subject treated with SK&F-12185 the urinary aldosterone titer failed to rise when he was placed on a low salt diet, suggestive of interference by the drug with aldosterone production. In one subject marked clinical improvement was noted. In a second only modest amelioration was observed. Drug fever prevented prolonged observation in the third subject, although a decrease in the urinary titers of tetrahydrocortisol suggested the effectiveness of the drug in decreasing cortisol production.

Aided by a grant-in-aid from Smith, Kline and French and by Grants FR-71 and CA-07304 from the NIH and by a grant from the American Cancer Society.

¹ A preliminary report on these patients was read by title at the 1966 Annual Meeting of The Endocrine Society.

Received March 27, 1967.

Accepted July 18, 1967.