Chetkowski R J, Chang R J, DeFazio J, Meldrum D R, Judd H L
Obstet Gynecol. 1984 Jul;64(1):27-31.
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.
多囊卵巢疾病女性体内循环类固醇激素过多的腺源性，一直难以通过先前描述的干扰技术来确定。最近有研究表明，每日注射一种强效促性腺激素释放激素激动剂可实现对卵巢类固醇分泌的完全且可逆的抑制。为了研究C-21类固醇激素的来源，在多囊卵巢疾病患者和正常对照受试者中，于注射该激动剂前后测量了循环水平。在注射地塞米松、促肾上腺皮质激素（ACTH）以及双侧卵巢切除术后，也测定了这些激素的血清水平。与正常对照受试者相比，多囊卵巢疾病患者的血清孕烯醇酮、17α-羟孕烯醇酮和17α-羟孕酮水平显著升高。孕烯醇酮和17α-羟孕烯醇酮过量水平的腺源性更难确定，且似乎与17α-羟孕酮的腺源性不同。
