Most patients with pituitary hypofunction have evidence of multiple target gland insufficiency arising from a destructive lesion in or near the sella turcica. Some patients with extensive pituitary destruction, however, exhibit hypogonadism as the only clinically evident defect; if the disease progresses, failure of thyroid and adrenal function later becomes apparent. Thus, it has been postulated and confirmed in animal experiments1 that a lesser degree of pituitary destruction is necessary to affect gonadal function than to affect the function of the thyroid gland and adrenal cortex.
Investigation of the functional consequences of pituitary lesions in man, however, has been handicapped by the lack of procedures to test the pituitary's reserve capacity to secrete its several hormones. Recently, a delicate test of adrenocorticotrophic hormone (corticotropin; ACTH) reserve has been described, employing 1,2-bis-(3 pyridyl)-2-methyl-1-propanone (SU-4885), an inhibitor of adrenal 11-β-hydroxylase.2 This drug blocks the formation of the adrenal end-products, especially
GREEN WL, INGBAR SH. Decreased Corticotropin Reserve as Isolated Pituitary Defect. Arch Intern Med. 1961;108(6):945–952. doi:10.1001/archinte.1961.03620120129018
Customize your JAMA Network experience by selecting one or more topics from the list below.
Create a personal account or sign in to: