Second Department of Obstetrics and Gynecology, Athens University Medical School, Aretaieion Hospital, Athens 11528, Greece.
J Clin Endocrinol Metab. 2011 Mar;96(3):623-31. doi: 10.1210/jc.2010-0130. Epub 2010 Dec 22.
Ovarian and adrenal hyperandrogenism characterize premenopausal women with polycystic ovary syndrome (PCOS). Androgens decline with age in healthy and PCOS women.
The objective of the study was to investigate hyperandrogenism in PCOS after menopause.
This was a case-control, cross-sectional study.
The study was conducted at a university hospital endocrinology unit.
Twenty postmenopausal women with PCOS and 20 age- and body mass index-matched controls participated in the study.
Serum cortisol, 17-hydroxyprogesterone (17-OHP), Δ(4)-androstenedione (Δ(4)A), dehydroepiandrosterone sulfate (DHEAS), total testosterone (T), and free androgen index (FAI) levels were measured at baseline, after ACTH stimulation, and after 3-d dexamethasone suppression. The ACTH and cortisol levels were measured during the CRH test.
Androgen profile at baseline, after ACTH stimulation, and 3-d dexamethasone suppression tests were the main outcome measures.
Postmenopausal PCOS women had higher 17-OHP, Δ(4)A, DHEAS, total T, FAI (P < 0.05) and lower SHBG (P < 0.05) baseline levels than control women. ACTH and cortisol responses during the CRH test were similar in the two groups. After ACTH stimulation, Δ(4)A, DHEAS, and total T levels were equally increased in both groups. After dexamethasone suppression, LH levels did not change in either group; 17-OHP-, Δ(4)A-, and FAI-suppressed levels remained higher in PCOS than in control women (P < 0.05), whereas total T and DHEAS levels were suppressed to similar values in both groups.
In postmenopausal PCOS women, ACTH and cortisol responses to CRH are normal. Androgen levels at baseline are higher in PCOS than control women and remain increased after ACTH stimulation. The dexamethasone suppression results in postmenopausal PCOS women suggest that DHEAS and total T are partially of adrenal origin. Although the ovarian contribution was not fully assessed, increased Δ(4)A production suggests that the ovary also contributes to hyperandrogenism in postmenopausal PCOS women. In conclusion, postmenopausal PCOS women are exposed to higher adrenal and ovarian androgen levels than non-PCOS women.
卵巢和肾上腺雄激素过多症是绝经前多囊卵巢综合征（PCOS）妇女的特征。在健康和 PCOS 女性中，雄激素随年龄增长而下降。
本研究旨在探讨绝经后 PCOS 中的高雄激素血症。
这是一项病例对照、横断面研究。
该研究在一所大学医院内分泌科进行。
20 名绝经后 PCOS 妇女和 20 名年龄和体重指数匹配的对照组参加了研究。
在基础状态、ACTH 刺激后和 3 天地塞米松抑制后测量血清皮质醇、17-羟孕酮（17-OHP）、Δ（4）-雄烯二酮（Δ（4）A）、脱氢表雄酮硫酸酯（DHEAS）、总睾酮（T）和游离雄激素指数（FAI）水平。在 CRH 试验期间测量 ACTH 和皮质醇水平。
基础状态、ACTH 刺激后和 3 天地塞米松抑制试验中的雄激素谱是主要观察指标。
绝经后 PCOS 妇女的基础状态 17-OHP、Δ（4）A、DHEAS、总 T、FAI 水平较高（P <0.05），SHBG 水平较低（P <0.05）。两组 CRH 试验期间的 ACTH 和皮质醇反应相似。ACTH 刺激后，两组的 Δ（4）A、DHEAS 和总 T 水平均同等增加。地塞米松抑制后，两组 LH 水平均无变化；PCOS 组的 17-OHP、Δ（4）A-和 FAI-抑制水平仍高于对照组（P <0.05），而总 T 和 DHEAS 水平在两组中均被抑制到相似水平。
在绝经后 PCOS 妇女中，CRH 对 ACTH 和皮质醇的反应正常。PCOS 妇女的基础雄激素水平高于对照组妇女，ACTH 刺激后仍保持升高。地塞米松抑制后，PCOS 绝经后妇女的结果表明 DHEAS 和总 T 部分来自肾上腺。尽管未完全评估卵巢的贡献，但增加的 Δ（4）A 产生表明卵巢也会导致绝经后 PCOS 妇女的高雄激素血症。总之，绝经后 PCOS 妇女的肾上腺和卵巢雄激素水平高于非 PCOS 妇女。
