Gonzalez F, Hatala D A, Speroff L
Department of Reproductive Biology, School of Medicine, Case Western Reserve University, Cleveland, Ohio.
Am J Obstet Gynecol. 1991 Sep;165(3):535-45. doi: 10.1016/0002-9378(91)90280-5.
It has been postulated that in polycystic ovary syndrome ovarian steroids can influence adrenal steroidogenesis. To test this hypothesis, basal and dexamethasone-suppressed-corticotropin-stimulated steroid hormone responses were compared among three groups of women before, during, and after gonadotropin-releasing hormone agonist treatment for 3 months. The groups were characterized as follows: (1) women with polycystic ovary syndrome with high dehydroepiandrosterone sulfate levels (greater than 400 micrograms/dl), (2) women with polycystic ovary syndrome with normal dehydroepiandrosterone sulfate levels (less than 300 micrograms/dl), and (3) normal ovulatory women. In response to gonadotropin-releasing hormone agonist, basal serum luteinizing hormone, follicle-stimulating hormone, estradiol, estrone, 17-hydroxyprogesterone, androstenedione, and testosterone in all three groups were suppressed to similar levels. Basal serum dehydroepiandrosterone sulfate levels in the group with high levels declined, but they did not reach the normal, unaltered concentrations in the other two groups. Two subjects with polycystic ovary syndrome in this group with high levels, who showed the greatest declines in basal serum dehydroepiandrosterone sulfate levels (34%, 40%), also had evidence of 3 beta-hydroxysteroid dehydrogenase deficiency before treatment, which was resolved by the end of treatment. In both groups with polycystic ovary syndrome, the increase in maximum incremental rise of dehydroepiandrosterone and dehydroepiandrosterone sulfate levels in response to a pharmacologic dose of corticotropin from a dexamethasone-suppressed baseline (adrenal androgen capacity) remained unaltered during gonadotropin-releasing hormone agonist administration. We conclude that ovarian steroids may promote excessive adrenal androgen secretion in women with polycystic ovary syndrome, may induce 3 beta-hydroxysteroid dehydrogenase deficiency as a mechanism for adrenal involvement in some women with polycystic ovary syndrome, and do not influence adrenal androgen capacity.
据推测，在多囊卵巢综合征中，卵巢类固醇可影响肾上腺类固醇生成。为验证这一假设，在三组女性中比较了促性腺激素释放激素激动剂治疗3个月之前、期间及之后基础状态以及地塞米松抑制促肾上腺皮质激素刺激后的类固醇激素反应。这些组的特征如下：（1）硫酸脱氢表雄酮水平高（大于400微克/分升）的多囊卵巢综合征女性；（2）硫酸脱氢表雄酮水平正常（小于300微克/分升）的多囊卵巢综合征女性；（3）正常排卵女性。对促性腺激素释放激素激动剂的反应是，所有三组中的基础血清促黄体生成素、促卵泡生成素、雌二醇、雌酮、17-羟孕酮、雄烯二酮和睾酮均被抑制至相似水平。硫酸脱氢表雄酮水平高的组中基础血清硫酸脱氢表雄酮水平下降，但未降至其他两组未改变的正常浓度。该硫酸脱氢表雄酮水平高的组中有两名多囊卵巢综合征患者，其基础血清硫酸脱氢表雄酮水平下降幅度最大（34%，40%），治疗前也有3β-羟类固醇脱氢酶缺乏的证据，治疗结束时该情况得到缓解。在两组多囊卵巢综合征患者中，从地塞米松抑制的基线（肾上腺雄激素能力）开始，给予药理剂量促肾上腺皮质激素后，脱氢表雄酮和硫酸脱氢表雄酮水平的最大增量升高在促性腺激素释放激素激动剂给药期间保持不变。我们得出结论，卵巢类固醇可能促进多囊卵巢综合征女性肾上腺雄激素分泌过多，可能诱导3β-羟类固醇脱氢酶缺乏作为肾上腺参与某些多囊卵巢综合征女性发病的一种机制，且不影响肾上腺雄激素能力。
