ADRENOCORTICAL FUNCTION IN MYXEDEMA*†

Abstract

THERE has been a prevailing concept that adrenocortical function is decreased in myxedema. This concept has been based mainly upon the decreased urinary excretion of 17-ketosteroids (1–12) in almost all cases of myxedema, the decreased excretion of formaldehydogenic (13), 17-ketogenic (12), 11-oxy (8, 14, 15) and 17-hydroxy corticosteroids (11) in many, and the failure of adrenocorticotropin (ACTH) to produce a fall in circulating eosinophils (7, 10, 15) in at least some of the cases studied. However, the reported information is somewhat conflicting, both as to findings and to interpretation. Previous studies from our laboratory (16) have shown that in myxedema there is delayed diuretic response to a water load. This is not correctable by cortisone, but is corrected by thyroid therapy—indicating that this defect is not due to adrenal insufficiency. With the development of methods for studying adrenocortical function and functional capacity or reserve more specifically and directly, the following investigation was undertaken.