A COMPARISON OF THE 17-KETOSTEROID EXCRETION IN CUSHING'S SYNDROME ASSOCIATED WITH ADRENAL TUMOR AND WITH ADRENAL HYPERPLASIA*

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Abstract
Ninety cases of Cushing''s syndrome (24 studied personally) have been collected in which the adrenals have been visualized and 17-ketosteroid assays made. These cases have been classified according to the adrenal pathologic changes into three groups (A) with benign tumor, (B) without tumor, (C) with malignant tumor. The avg. 17-ketosteroid excretion of the three groups was (A) 5.7, (B) 18.1, (C) 124.4. These differences are explained as follows: hyperfunction of both adrenals is the result of overstimulation by ACTH which leads to overproduction of both gluconeogenic and androgenic adrenal hormones, hence to an elevated 17-ketosteroid excretion. A benign adrenal tumor causing Cushing''s syndrome arises from gluconeogenic hormone-producing cells, and the gluconeogenic hormone increases the urinary 17-ketosteroids but slightly while inhibiting ACTH and hence the production of 17-ketosteroid precursors from the uninvolved adrenal tissue. This results in a low 17-ketosteroid excretion. Malignant adrenal tumors arise from undifferentiated cells and produce unpredictable kinds and amounts of hormone.

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