17-HYDR0XYC0RTIC0STER0IDS AND 17-KETOSTEROIDS IN URINE OF HUMAN SUBJECTS: CLINICAL APPLICATION OF A METHOD EMPLOYING β-GLUCURONIDASE HYDROLYSIS*

Abstract

NUMEROUS methods for measurement of urinary steroids have been devised in an attempt to estimate the level of adrenal cortical function. Of these, the methods oldest in point of time and those most widely used and accepted have been procedures for the measurement of 17-ketosteroids after acid hydrolysis (1, 2). Because of obvious clinical and physiologic discrepancies, such as the low values obtained in certain patients with Cushing's syndrome, a number of other techniques have been devised. These methods depend on the measurement of neutral reducing lipid substances (3), or of formaldehydogenic substances after periodic acid oxidation (4, 5) or involve the reduction of copper (6–8), or biologic assays (9–11). However, all of the techniques by which any large proportion of the interfering nonsteroidal substances present in urine have been eliminated, yield values which represent only a small fraction of the presumed normal secretion of the adrenal cortex (3–13). In addition, all of these methods have a relatively high “biologic blank”; that is, significant levels are found in the urines of patients with severe adrenal insufficiency and following total adrenalectomy. In a preceding paper a method was described for the determination of the concentrations of 17-hydroxycorticosteroids and 17-ketosteroids in the urine after glucuronidase hydrolysis (14). The term “17-hydroxycorticosteroids” is used to include those steroids with a 17,21-dihydroxy-20-keto side chain.