Origin of serum progestins in polycystic ovarian disease.
The glandular origin of excess circulating steroid hormones in women with polycystic ovarian disease has been difficult to establish with previously described perturbation techniques. Recently it was demonstrated that daily administration of a potent gonadotropin-releasing hormone agonist achieves complete and reversible suppression of ovarian steroid secretion. To examine the source of C-21 steroid hormones, circulating levels were measured before and after administration of the same agonist in polycystic ovarian disease subjects and normal control subjects. Serum levels of these hormones were also determined after administration of dexamethasone and adrenocorticotropic hormone (ACTH) as well as bilateral oophorectomy. Subjects with polycystic ovarian disease exhibited significant elevations of serum pregnenolone, 17OH -pregnenolone, and 17OH -progesterone by comparison with normal control subjects. The glandular origins of the excess levels of pregnenolone and 17OH -pregnenolone were more difficult to determine and appear to be different from that of 17OH -progesterone.
D006907:17-alpha-Hydroxypregnenolone / Q000097:blood; D019326:17-alpha-Hydroxyprogesterone; D000324:Adrenocorticotropic Hormone; D003907:Dexamethasone; D005260:Female; D006801:Humans; D006908:Hydroxyprogesterones / Q000097:blood; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000378:metabolism*; D011372:Progestins / Q000378:metabolism*
D006908:Hydroxyprogesterones; D011372:Progestins; D006907:17-alpha-Hydroxypregnenolone; D019326:17-alpha-Hydroxyprogesterone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone