METABOLISM OF FREE AND CONJUGATED 17-HYDROXYCORTICOSTEROIDS IN SUBJECTS WITH LIVER DISEASE*

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Abstract
INTRODUCTION APREVIOUS report from this laboratory (1) demonstrated a delay in the removal of cortisol but not of tetrahydrocortisone (Tetra E) from the plasma of subjects with liver disease. Since Tetra E glucuronide is one of the principal end-products of cortisol metabolism (2), it was felt that the impaired removal of cortisol in subjects with liver disease was attributable to a block in the degradation of cortisol to its reduction products rather than to an impairment of conjugation of the reduced 17-hydroxycorticosteroids (17-OHCS). With the development of methods for the measurement of 17-OHCS conjugated with glucuronic acid in body fluids (3, 4), subnormal levels of conjugated 17-OHCS in the plasma of subjects with liver disease after the ingestion of cortisone were noted in other laboratories. These findings were thought to be a result of a diminished capacity to conjugate 17-OHCS in subjects with hepatic disorders (5, 6).