URINARY ESTROGENS (MEASURED FLUOROMETRICALLY AND BIOLOGICALLY) IN HYPERADRENOCORTICISM: INFLUENCE OF CORTISONE, COMPOUND F, COMPOUND B AND ACTH*

Abstract

WHEREAS the role of the adrenal cortex in promoting urinary excretion of 17-ketosteroids and reducing corticoids in man has been established, the participation of the adrenals in the production of urinary estrogens has not been well investigated. That the adrenal glands are involved in estrogen metabolism is indicated by the fact that estrone has been extracted from ox adrenal glands (1). Adrenocortical tumors causing either virilization, Cushing's syndrome or feminization with gynecomastia, sometimes produce an increased excretion of estrogens, but this is not always so. In congenital adrenal hyperplasia, there is usually an increase of the urinary excretion of fluorometrically measured estrogens (2). It has recently been shown that cortisone therapy reduces the urinary 17-ketosteroid excretion to a normal level in patients with congenital adrenal hyperplasia (2–5), but usually does not decrease the 17-ketosteroid output in cases of adrenal tumor (6, 7). It has been suggested that this response of 17-ketosteroids to cortisone therapy may be used as a test to differentiate congenital adrenal hyperplasia from adrenal tumors with elevated 17-ketosteroid excretion (7).