Adrenal Response to Acth in Various Clinical Conditions

IN MAN, stimulation of the adrenal cortex by ACTH results in secretion of 11-oxygenated steroids in which compound F predominates. This in turn produces an increase in the urinary excretion of metabolites of these adrenal steroids, causing an increased titer of 17-ketosteroids, formaldehydogenic corticoids and glycogenic corticoids in the urine. The urinary titer of steroids can thus be employed as a measure of the ability of the adrenal to respond to ACTH stimulation (1). It has been reported that certain adrenocortical hormones cause peripheral blood eosinopenia and an increased urinary uric acid/creatinine (U/C) ratio (1). Therefore, these changes, when measured, may be used as additional indices of adrenal function. Various other means of determining the presence or absence of adrenal function have been suggested. These include epinephrine stimulation of the Irypothalamic-anterior pituitary-adrenocortical axis, using the fourhour total blood eosinophil response as the end point (2, 3), and the more specific ACTH stimulation of the adrenal cortex with the 4-hour eosinophil and U/C changes noted (4). A 48-hour ACTH test was introduced by Thorn and Forsham (1), in which measurements of eosinophils, U/C and urinary 17-ketosteroids were used as a means of more accurately estimating adrenal response during continued ACTH stimulation. We have utilized a modification of this test in an attempt to evaluate its usefulness in determining adrenal function in a group of patients exhibiting a variety of diseases. Some of the data have already been reported (5).