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The effects of amino-glutethimide on adrenocortical function have been studied in 24 subjects, including 10 patients with Cushing's syndrome, 3 with primary aldosteronism and 1 with secondary hyperaldosteronism. Aminoglutethimide inhibited adrenal secretion of both cortisol and aldosterone. Inhibition of cortisol secretion was most clearly demonstrable in a patient with Cushing's syndrome caused by autonomous steroid secretion from an adrenal adenoma. In normal subjects, administration of large doses of amino-glutethimide was accompanied by consistent increases in plasma ACTH, and it is likely that these “compensatory” increases in ACTH were responsible for maintaining near-normal cortisol secretion rates and plasma 17-hydroxycorticosteroid (17-OHCS) concentrations in these subjects. Decreases in cortisol secretion occurred in 7 of 9 patients with Cushing's disease given amino-glutethimide, and this was of modest therapeutic value in 4 of these patients treated for several months. The most consistent effect of amino-glutethimide was a decrease in aldosterone secretion rate, which occurred in patients with primary aldosteronism as well as in normal subjects and patients with Cushing's syndrome. The fall in aldosterone secretion was accompanied by an increase in urinary sodium, a decrease in urinary potassium, a rise in plasma renin activity, and, in hypertensive patients, some lowering of the blood pressure. In addition to its effects as an inhibitor of adrenal steroid secretion, amino-glutethimide was also shown to alter the extra-adrenal metabolism of cortisol so that urinary 17-OHCS were disproportionately low relative to cortisol input or plasma 17-OHCS concentrations.
Fishman et al. (Sat,) studied this question.