The Depot-Form of Glucocorticoid Decreases Cortisol but not ACTH and Beta-Endorphin Levels in Human Plasma

Although the inhibitory effect of exogenous glucocorticoids on the hypothalamus-pituitary-adrenal axis has been long known, the site and mechanism of this effect has not been definitely established. There are many evidences from in vivo and in vitro animal studies indicating that synthetic corticosteroids, such as dexamethasone, suppress ACTH synthesis or release from the pituitary gland. The studies on this topic in human subjects are still scant (Fang, Tricon, Robertson and Meltzer 1981 ; Fehm, Voigt, Kummer, Lang and Pfeiffer 1979). Our study was undertaken to determine the influence of the depot-form of glucocorticoid administered intramuscularly in a common­ ly used dose on plasma Cortisol, ACTH and beta-endorphin (B-EP) levels. We examined 12 asthmatic patients of both sexes without any hormonal and metabolic disorders. 60 mg of acetonide triamcinolone (Kenalog 40®, E.R. Squibb & S.) was injected i.m. The blood samples were collected immediately before and on the 3-rd, 7-th, 14-th, 21-st and 35-th day after Kenalog injection, always between 8.00 and 10.00 a.m. All the investigated substances were determined radioimmunologically using commercial kits (Cortisol and ACTH - Amersham, B-EP - New England Nuclear). Our findings (see Fig. 1) suggest that one dose of the depot-form of triamcinolone has not effect on ACTH plasma level and are different from the results described by Clement-Jones, Lowry, Ress and Besser (1980) who have observed a decrease of plasma ACTH after 2 mg dexamethasone given to 7 normal subjects at