Abstract
I131-labeled albumin turnover studies were carried out in 4 patients with Cushing''s syndrome due to adrenal cortical hyperplasia and in control subjects. In active Cushing''s syndrome there was a short biologic half-time of the tracer, signifying accelerated turnover. This abnormality was reversed after therapy and remission. Cushing''s syndrome due to the administration of cortisone also revealed accelerated albumin turnover, more pronounced with a larger dose. The total exchangeable albumin pool was reduced in Cushing''s syndrome, and was smallest in the two subjects with the shortest half-times and with the most severe clinical manifestations. Excess glucocorticoids were considered to have produced accelerated albumin catabolism, partly compensated for by increased synthesis.