RESISTANCE OF GONADOTROPIN-RELEASING-HORMONE DRIVE TO SEX STEROID-INDUCED SUPPRESSION IN HYPERANDROGENIC ANOVULATION

Citation
Tl. Daniels et Sl. Berga, RESISTANCE OF GONADOTROPIN-RELEASING-HORMONE DRIVE TO SEX STEROID-INDUCED SUPPRESSION IN HYPERANDROGENIC ANOVULATION, The Journal of clinical endocrinology and metabolism, 82(12), 1997, pp. 4179-4183
Citations number
32
ISSN journal
0021972X
Volume
82
Issue
12
Year of publication
1997
Pages
4179 - 4183
Database
ISI
SICI code
0021-972X(1997)82:12<4179:ROGDTS>2.0.ZU;2-S
Abstract
Women with hyperandrogenic anovulation (HAA) exhibit increased GnRH dr ive, as evidenced by a faster LH pulse frequency that slows in respons e to progestin-induced opioidergic tone. To determine whether increase d GnRH-LH drive in HAA reflects altered sex steroid exposure caused by chronic anovulation or is an intrinsic hypothalamic attribute, we com pared the pulsatile LH response to oral contraceptive (OC)-induced sup pression in seven women with HAA, with that of seven eumenorrheic wome n (EW). LH levels were determined at 10-min intervals for 12 h after 1 9-21 days of OC use and 5-7 days after cessation. Testosterone, andros tenedione, estradiol, FSH, and LH levels were determined at weekly int ervals before, during, and after OC use. LH pulse number/12 h was high er (P < 0.001) in HAA during and after OCs, when compared with that of EW. Mean LH was increased in HAA before, during, and after OCs. Testo sterone, androstenedione, and estradiol levels were higher in HAA befo re OCs, but they decreased to similar levels during OC use in both gro ups. FSH concentrations were similar before and during OCs but rose mo re after cessation of OCs in EW. These findings indicate that GnRH dri ve in HAA is resistant to OC-induced suppression and, therefore, could be an intrinsic hypothalamic attribute.