THYROID-ADRENOCORTICAL INTERRELATIONS: FAILURE TO DEMONSTRATE ANTAGONISM BETWEEN TRIIODO- THYRONINE AND HYDROCORTISONE IN MAN 1

It is generally accepted that acute injury re-sults in an outpouring of adrenocortical hormones 5 (1, 2), and that these hormones play an important role in the response of the total organism to such injury. The marked increase in urinary nitrogen excretion which characteristically occurs immedi-ately following acute injury is usually considered to result from the catabolic action of the adreno-cortical hormones on protein metabolism (3). Supporting this concept are recent studies corre-lating the negative nitrogen balance following surgical trauma in man with the rise in 17-hy-droxysteroid excretion (4). The participation of the thyroid gland in the response to acute injury in man is less well deline-ated. Certain observations have suggested that there may be an increase in circulating thyroid hormone in man following trauma (5,6); other in-vestigators have been unable to confirm this finding (7, 8). The role of the thyroid is particularly difficult to evaluate following injury because the increased output of adrenocortical hormones may affect some of the methods used to assay thyroid function (9-11), and may also tend to inhibit thyroid activity (9, 11-14). Goldenberg, Lutwak, Rosenbaum, and Hayes (15) have recently proposed that the catabolic response to injury is due primarily to excess thy-roid hormone rather than adrenocortical hormones