17-HYDROXYPROGESTERONE RESPONSES TO GONADOTROPIN-RELEASING-HORMONE AGONIST BUSERELIN AND ADRENOCORTICOTROPIN IN POLYCYSTIC-OVARY-SYNDROME -INVESTIGATION OF ADRENAL AND OVARIAN CYTOCHROME P450C17-ALPHA DYSREGULATION

Abnormal regulation of cytochrome P450c17 alpha causes the exaggerated secretion of ovarian androgens in polycystic ovary syndrome (PCOS). T his enzyme is active in both the ovaries and adrenal glands. We examin ed whether there is an abnormal regulation of cytochrome P450c17 alpha in the adrenal gland by investigating the relationship of 17-hydroxyp rogesterone (17-OH progesterone) hyperresponsiveness to the gonadotrop hin releasing hormone (GnRH) agonist, buserelin, testing with 17-OH pr ogesterone response to adrenocorticotrophic hormone (ACTH) in PCOS, In all, 68 women with PCOS and 24 normal women were included in the stud y, Ultrasound, clinical and hormonal parameters were used to define PC OS, 17-OH progesterone response to ACTH was measured in all the women. In 52 of the 68 women with PCOS, 17-OH progesterone response to buser elin was measured, The mean basal 17-OH progesterone concentrations we re similar in both PCOS and control groups, PCOS n omen had significan tly higher net increment in 17-OH progesterone after ACTH administrati on (P<0.02). No significant correlations were found between the peak 1 7-OH progesterone values, the net increments in 17-OH progesterone and the area under the 17-OH progesterone-response curves after ACTH stim ulation and buserelin test, Although 17-OH progesterone response to AC TH was significantly higher in the patients with PCOS than in the cont rol subjects, the lack of relationship between 17-OH progesterone resp onse to GnRH agonist buserelin and 17-OH progesterone response to ACTH stimulation suggests that the dysregulation of the cytochrome P450c17 alpha enzyme may not play a role in adrenal androgen excess seen in P COS.