The effect of cortisone on the urinary excretion of 17-ketosteroids in patients with Cushing's syndrome.

The administration of cortisone to patients with virilism associated with adrenal hyperplasia results in a marked decrease in urinary 17-ketosteroid excretion (1-3) whereas no significant fall occurs in those patients whose virilism is due to an adrenal tumor (4, 5). The administration of cortisone inhibits pituitary adrenocorticotropin secretion causing secondary atrophy of the adrenals (6, 7); hence a decrease in 17-ketosteroid excretion ensues in those patients in whom the normal pituitary-adrenal interrelationship is preserved. The data obtained in patients with adrenogenital syndrome (4) as a result of the injection of cortisone stimulated a similar investigation of patients suffering from an allied disease, Cushing's syndrome. It is generally agreed that the manifestations of Cushing's syndrome are due to excessive 11-oxygenated corticosteroid secretion by the adrenal cortex, although the pituitary (8) and the hypothalamus (9) as well as the adrenal (10) have been postulated as the site primarily involved. If either an adrenal or pituitary tumor is present, it seems reasonable that the source of excessive secretion responsible for the disease picture lies in the neoplastic tissue and in such patients because of the autonomous nature of the tumor no fall in 17-ketosteroids would be anticipated following the injection of exogenous cortisone. On the other hand if no tumor exists, the bilateral adrenal hyperplasia may arise de novo and be independent of pituitary control, or the normal pituitary-adrenal interrelationships may still be operating. If the latter obtains, then the administration