Measurements of levels of 17α-OHP are useful in the evaluation of patients with suspected congenital adrenal hyperplasia as the typical enzymes that are defective, namely 21-hydroxylase and 11β-hydroxylase , lead to a build-up of 17α-OHP. In contrast, the rare patient with 17α-hydroxylase deficiency will have very low or undetectable levels of 17α-OHP. 17α-OHP levels can also be used to measure contribution of progestational activity of the corpus luteum during pregnancy as progesterone but not 17α-OHP is also contributed by the placenta .
In an adult with a virilizing adrenocortical adenoma and in six similar published instances, the high levels of urinary 17-ketosteroids usually present were associated with normal excretion of 17(OH)corticosteroids or Porter-Silber chromogens. Urinary estrogens were high in 1 of 3 patients. In 5 of 9 adult patients assembled from the literature virilization in association with an adrenal cancer was characterized by increased levels of urinary 17(OH)corticosteroids; also, urinary estrogens were high in each of the 4 patients in whom they were measured. The above data point to a variety of enzyme patterns of steroidogenesis in association with virilizing adrenal tumors in adults. Thus, in those with an adenoma, desmolase activity is increased with high androgen production from 17(OH)steroids and normal or high estrogen formation from androgens without an increase in 17(OH)corticosteroid excretion. In those with an adrenal cancer, 17(OH)corticosteroid output is increased in about one half, androgen synthesis is of course always high, and, judging from the cases cited, estrogen production is invariably high. The basal levels of urinary 17-ketosteroids appear to be of no aid in the identification of virilization in adults due to an adrenal adenoma and that resulting from an adrenal cancer. The data indicate that cancer is more likely if in addition to high urinary 17-ketosteroids, the levels of 17(OH)corticosteroids and of estrogens are abnormally elevated in urine.