Cedars M I, Steingold K A, de Ziegler D, Lapolt P S, Chang R J, Judd H L
Department of Obstetrics and Gynecology, University of California Los Angeles Center.
Fertil Steril. 1992 Mar;57(3):495-500. doi: 10.1016/s0015-0282(16)54890-0.
To examine the possible impact of abnormal adrenal steroidogenesis on the ovarian dysfunction seen in polycystic ovarian disease (PCOD).
Prospective analysis of blood sampling monthly for 6 months, then three times weekly for 90 days.
Tertiary institutional outpatient care.
Six anovulatory women with a diagnosis of PCOD.
Six-month suppression with gonadotropin-releasing hormone agonist (GnRH-a) followed by suppression with dexamethasone (DEX) for 90 days.
Serum levels of testosterone (T), androstenedione (A), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), cortisol, estradiol (E2), progesterone (P), follicle-stimulating hormone (FSH), luteinizing hormone (LH) and bioactive LH.
Gonadotropin-releasing hormone agonist administration suppressed greater than 60% of the circulating levels of T and A, suggesting an ovarian origin. Minimal changes of DHEA, DHEAS, and cortisol were seen. With the addition of DEX, there was greater than 90% suppression of the total circulating A, T, DHEA, DHEAS, and cortisol, supporting the adrenal origin of the non-GnRH-a suppressible androgens. Excessive ovarian T and A secretion returned during the 90-day recovery study period in spite of rises of FSH concentrations that changed the ratio of FSH to LH in all subjects. Four of the six women failed to ovulate. In comparison of the women who did and did not ovulate during recovery, no differences in absolute levels or changes in concentrations of steroids or gonadotropins could be detected.
Using sequential and simultaneous administration of GnRH-a and DEX, we were able to delineate the contributions of the ovaries and adrenals to the abnormal steroidogenesis seen in PCOD. Despite prolonged suppression of ovarian and then adrenal steroidogenesis, ovarian dysfunction, evidenced by abnormal androgen production, returned with cessation of agonist administration.
研究肾上腺类固醇生成异常对多囊卵巢疾病（PCOD）中所见卵巢功能障碍的可能影响。
前瞻性分析，每月采血1次，共6个月，然后每周采血3次，共90天。
三级医疗机构门诊。
6名诊断为PCOD的无排卵女性。
先用促性腺激素释放激素激动剂（GnRH-a）抑制6个月，然后用地塞米松（DEX）抑制90天。
血清睾酮（T）、雄烯二酮（A）、脱氢表雄酮（DHEA）、硫酸脱氢表雄酮（DHEAS）、皮质醇、雌二醇（E2）、孕酮（P）、促卵泡激素（FSH）、促黄体生成素（LH）和生物活性LH的水平。
给予GnRH-a后，循环中T和A水平的抑制率大于60%，提示其来源于卵巢。DHEA、DHEAS和皮质醇的变化极小。加用DEX后，循环中总A、T、DHEA、DHEAS和皮质醇的抑制率大于90%，支持非GnRH-a可抑制雄激素的肾上腺来源。在90天的恢复研究期内，尽管所有受试者的FSH浓度升高，改变了FSH与LH的比值，但卵巢过度分泌T和A的情况仍出现。6名女性中有4名未排卵。在比较恢复期间排卵和未排卵的女性时，未检测到类固醇或促性腺激素的绝对水平或浓度变化存在差异。
通过序贯和同时给予GnRH-a和DEX，我们能够明确卵巢和肾上腺对PCOD中异常类固醇生成的作用。尽管卵巢和肾上腺类固醇生成受到长期抑制，但随着激动剂给药的停止，以雄激素产生异常为证据的卵巢功能障碍又复发了。
