The Excretion of Individual 17-Oxosteroids in Cushing's Syndrome

Abstract

The urinary excretion levels of individual 17-oxosteroids in eight patients with Cushing's syndrome have been determined quantitatively. Using these values approximate secretion rates of cortisol and 11\g=b\-hydroxyandrostenedione were calculated and found to be elevated above the normal range. The excretion values for 11-deoxy-17-oxosteroids were highly variable, being below normal, normal or elevated in different patients. The excretion patterns in adrenocortical hyperplasia and carcinoma showed no characteristic differences; however, the patients with adrenal adenoma showed steroid excretions which suggested that these tumours secreted cortisol almost exclusively, together with small quantities of 11\g=b\-hydroxyandrostenedione, and minimal amounts of 11-deoxy-C19-steroids. The majority of patients excreted aetiocholanolone and androsterone in an abnormally high ratio; this also occurred after administration of androst-4-ene-3:17\x=req-\ dione, and it is suggested that in Cushing's syndrome the hepatic enzymes preferentially reduce adrenal androgen to metabolites with the 5\g=b\ configuration.

C19and C215β/5αMetabolite Ratios in Subjects Treated with the 5α-Reductase Inhibitor Finasteride: Comparison of Male Pseudohermaphrodites with Inherited 5α-Reductase Deficiency*

“…In hypothyroidism, anorexia nervosa, Cushing's syndrome, and other low T 3 syndromes, such as chronic illness, the deficiency of 5a-reductase activity appears to involve mainly hepatic 5«-reductase activity (21)(22)(23)(24)(25)(26). The defect is reversible, as demonstrated by MauvaisJarvis et al in studies of hypothyroid subjects (21).…”

Oral and Intravenous Suppression Tests in the Diagnosis of Cushing's Syndrome

“…Androgen metabolism is altered (James, 1961), and it has been shown that the proportion of secreted cortisol con¬ verted to urinary 17-OHCS is decreased as the secretion rate increases (James & Caie, 1964). The continued administration of dexamethasone to normal subjects also causes increased formation of 5ß metabolites relative to 5a compounds (Wilson & Schenker, 1964).…”