POMC and congenital adrenal hyperplasia: Suppressed DHEAS at presentation may be ascribed to low circulating ACTH, but persistent suppressed DHEAS despite normal ACTH during treatment could be a direct effect of ketoconazole (suppression of 17α-hydroxylase) or the result of intrinsic changes within the adrenal nodules, similar to those of testicular adrenal rest tissue in patients with congenital adrenal hyperplasia (increased 3β-hydroxysteroid dehydrogenase activity) (20).