Abstract
ACTH in urine, extracted by benzoic acid adsorption and assayed by adrenal ascorbic acid depletion in hypophysectomized rats, showed a definite elevation upon administration of an 11-β-hydroxylase inhibitor, SU-8874 (2-methyl-1,2-bispyridyl-1-propanone hydrochloride), in 3 normal subjects and in 3 patients with intact pituitaries, whereas 4 patients with hypopituitarism failed to show an elevation. Elevated urinary ACTH levels were found in 4 cases of adrenogenital syndrome and in 3 cases of Cushing's syndrome due to bilateral adrenal hyperplasia. While increased urinary ACTH was suppressed by oral administration of 20 mg or less of hydrocortisone in 3 cases of Addison's disease and in one case of carcinoma of the prostate after bilateral adrenalectomy, more than 30 mg was required to suppress the increased urinary ACTH in Cushing's syndrome owing to bilateral adrenal hyperplasia.
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