Differences in metabolic properties among cortisol, prednisolone, and dexamethasone in liver and renal diseases: accelerated metabolism of dexamethasone in renal failure.

Since previous reports concerning the altered metabolism of various glucocorticoids in liver or renal diseases were inconsistent, this study was undertaken to reexamine the metabolism of cortisol, prednisolone, and dexamethasone in patients with these diseases. One milligram each of these glucocorticoids was given iv simultaneously to patients with chronic liver disease, patients with chronic renal failure, and normal subjects after 1 mg betamethasone was administered on the previous night to suppress endogenous cortisol secretion. Plasma steroid levels in periodically collected blood samples were assayed by respective RIA after separation by paper chromatography. Prolongation of the t1/2 of cortisol was found in both patients with liver disease and those with renal failure, and prolonged t1/2 and reduced MCR of prednisolone were found in renal failure but not in liver disease. In contrast, while prolonged t1/2 and reduced MCR of dexamethasone were found in liver disease, shortened t1/2 and increased MCR were found in renal failure. These results suggest that different glucocorticoids are metabolized differently in patients with liver disease and those with renal failure, and that these differences may be important when these agents are used for therapeutic purposes or for study of hypothalamic-pituitary-adrenocortical function in patients with liver and renal diseases.