Gonzalez F, Chang L, Horab T, Stanczyk F Z, Crickard K, Lobo R A
Department of Gynecology and Obstetrics, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, USA.
Fertil Steril. 1999 Mar;71(3):439-44. doi: 10.1016/s0015-0282(98)00469-5.
To test the hypothesis that in women with polycystic ovary syndrome (PCOS), adrenal cytochrome P450c 17alpha activity is different after physiologic vs. pharmacologic ACTH stimulation and that ovarian activity promotes adrenal hyperactivity that is different after physiologic vs. pharmacologic ACTH stimulation.
Prospective controlled pilot study.
Reproductive endocrinology unit of an academic medical center.
PATIENT(S): Six women with PCOS who had adrenal hyperandrogenism were compared with four women with normal ovulation.
INTERVENTION(S): Adrenal dynamic blood sampling was performed before and after 6 months of GnRH agonist administration.
MAIN OUTCOME MEASURE(S): Comparison of physiologic and pharmacologic ACTH-stimulated levels of progesterone, 17-hydroxyprogesterone, and androgens before and after ovarian steroid modulation.
RESULT(S): In women with PCOS, exaggerated responses of androstenedione and 11beta-hydroxyandrostenedione as well as elevated ratios of 17-hydroxyprogesterone to progesterone and of androstenedione to 17-hydroxyprogesterone after physiologic ACTH stimulation did not persist after GnRH-agonist administration. Three of the six women with PCOS had an increased response of androstenedione and a ratio of androstenedione to 17-hydroxyprogesterone that were >2 SD above the mean of those in the women with normal ovulation after pharmacologic ACTH stimulation; this finding persisted after GnRH-agonist administration.
CONCLUSION(S): In women with PCOS, increases in adrenal androgen sensitivity after physiologic ACTH stimulation reflected in both arms of cytochrome P450c 17alpha activity may be influenced by ovarian activity. However, 17,20-lyase hyperactivity in a subset after pharmacologic ACTH stimulation may be an intrinsic adrenal disorder.
检验以下假设：在多囊卵巢综合征（PCOS）女性中，生理性与药物性促肾上腺皮质激素（ACTH）刺激后肾上腺细胞色素P450c 17α活性不同，且卵巢活性促进肾上腺功能亢进，而生理性与药物性ACTH刺激后的肾上腺功能亢进也不同。
前瞻性对照试验研究。
一所学术医疗中心的生殖内分泌科。
6名患有肾上腺雄激素过多症的PCOS女性与4名排卵正常的女性进行比较。
在给予促性腺激素释放激素（GnRH）激动剂6个月前后进行肾上腺动态采血。
比较卵巢类固醇调节前后生理性和药物性ACTH刺激的孕酮、17-羟孕酮和雄激素水平。
在PCOS女性中，生理性ACTH刺激后雄烯二酮和11β-羟雄烯二酮的过度反应以及17-羟孕酮与孕酮的比率和雄烯二酮与17-羟孕酮的比率升高，在给予GnRH激动剂后未持续存在。6名PCOS女性中有3名在药物性ACTH刺激后雄烯二酮反应增加，且雄烯二酮与17-羟孕酮的比率高于排卵正常女性平均值2个标准差以上；这一发现在给予GnRH激动剂后持续存在。
在PCOS女性中，生理性ACTH刺激后肾上腺雄激素敏感性增加反映在细胞色素P450c 17α活性的两个方面，可能受卵巢活性影响。然而，药物性ACTH刺激后一部分患者的17,20-裂解酶活性亢进可能是一种内在的肾上腺疾病。
