Clinical studies on ACTH in the blood. I. Blood ACTH levels in normal subjects and in various endocrine diseases; effect of various steroids

Abstract

ACTH was assayed by the measurement of corticosterone in the adrenal venous plasma after the intravenous administration of test materials into the hypophysectomized rats whose right adrenal glands had been extirpated one week before. This method gave linearity of response to log doses of ACTH ranging from 0.03 to 1.0 milliunits (mU), with precision index (λ) of 0.32, enabling to detect 0.6 mU per 100 ml of plasma ACTH when a dose of 5 ml of plasma was injected.1) Plasma from 5 normal subjects was found to contain ACTH in levels less than 0.6 mU per 100 ml. The oxycellulose technic was applied to extract ACTH from about 100 ml blood from 5 normal subjects in preparation for a biological assay, which revealed a mean ACTH level of 0.04 mU per 100 ml of blood. (96% fiducial range, 0.023-0.063 mU/100 ml of blood.) Four patients with Cushing's syndrome due to adrenal cortical hyperplasia and 2 patients with the same syndrome due to adrenal cortical adenoma failed to show elevated plasma ACTH levels. Similarly, no ACTH was detected in 7 patients with abnormal pigmentation and 9 of 10 patients with hyperthyroidism. Seven patients with adrenogenital syndrome had elevated ACTH levels ranging from 0.6 to 5.7 mU per 100 ml of plasma (mean±standard error (S.E.), 1.6±0.8 mU/100 ml of plasma.) In 10 patients with Addison's disease, plasma ACTH ranged from 0.9 to 93.8 mU per 100 ml (mean±S.E., 13.8±9.5 mU/100 ml of plasma.) 2) The elevated level of ACTH found in patients with adrenogenital syndrome and Addison's disease was significantly reduced by the oral administration of glucocorticoids, whereas aldosterone and desoxycorticosterone had no significant suppresive effect. One of the anabolic steroids, i.e. 2-hydroxymethylene-17α-methyl dihydrotestosterone (HMD), and testosterone had no effect on plasma ACTH levels, either.