The role of the liver and the adrenal in producing elevated plasma 17-hydroxycorticosteroid levels in surgery.

In another paper of this series (1) it was demonstrated that most patients undergoing surgery developed increased plasma levels of 17-hydroxycorticosteroids. Evidence was presented that these rises are mediated in part by extra-adrenal factors. The concept that extra-adrenal factors may affect adrenal steroid levels is not a new one but little evidence to support such a concept has been presented. The liver is known to contain enzyme systems capable of modifying these compounds in vitro (2). The reduced effect of the diseased liver in estrogen metabolism has been advanced by many authors as the explanation of the clinical evidence suggestive of estrogenic overactivity in patients with cirrhosis of the liver (3). That liver disease results in profound alteration of adrenocortical steroid metabolism also, has been demonstrated in current studies by Brown, Willardson, Samuels, and Tyler (4). Thus it seemed logical to study the relation of hepatic function to the magnitude of the rise in 17hydroxycorticosteroids after surgery. In addition, it was hoped that by the determination of free and conjugated steroids of this type in the urine an estimate of the total adrenal output of these substances would be obtained. By the correlation of the data it was expected that the influence of increased adrenal secretion and of impaired steriod disappearance resulting from hepatic dysfunction could be evaluated at least on a qualitative basis. In this report data dealing with these aspects of the effect of surgery on adrenal steroid