The Response of Urinary 17-hydroxy- Corticoids to Corticotrophin Zinc As

An increased interest in the study of the adrenal cortex, together with the ready availability of corticotrophin (A.C.T.H.), have, in recent years, led to the development of improved methods for the assessment of adrenal cortical function. The first of such methods was devised by Thorn, Forsham, Prunty, and Hills (1948) and depended upon the fall in blood eosinop'lils after injection of a single dose of corticotrophin. It was subsequently realized, however, that this test was by no means specific, since a fall in eosinophils could be produced by the injection of adrenaline, for example, without any effect on the adrenal steroids (Nelson, Sandberg, Palmer, and Glenn, 1952). Moreover, there is a considerable spontaneous variation in the eosinophil count and results may be difficult to interpret when the initial count is low. The urinary 17-ketosteroid excretion after corticotiophin provides a more valuable indication of adrenal cortical function and many of the current tests rely on this estimation. In males, however, the 17-ketosteroids are only partly derived from the adrenal cortex, and sometimes a clearly defined rise after corticotrophin is not obtained even in normal individuals. Jenkins, Forsham, Laidlaw, Reddy, and Thorn (1955) find that 14% of normal controls showed a rise of less than 2 mg. in 24 hours. Recently, relatively simple methods have been devised for the estimation of urinary 17-hydroxycorticoids, and it seems that these methods provide a more direct measure of adrenal cortical function since the 17-hydroxycorticoids represent that fraction of the adrenal steroids known as the glucocorticoids, of which hydrocortisone and its urinary metabolites are the most important. It is now recognized that for an adequate assessment of its function a prolonged stimulation of the adrenal cortex is necessary. Jenkins et al. (1955) describe