Obstetrics and Gynecology Unit, Department of Obstetrics, Gynecology and Pediatrics, Azienda Ospedaliera Arcispedale Santa Maria Nuova, Istituto di Ricovero e Cura a Carattere Scientifico, University of Modena and Reggio Emilia, Viale Risorgimento, 42123 Reggio Emilia, Italy.
J Clin Endocrinol Metab. 2012 Jul;97(7):2441-9. doi: 10.1210/jc.2012-1100. Epub 2012 Apr 16.
Previous experimental and clinical data suggest impaired decidual trophoblast invasion in patients with polycystic ovarian syndrome (PCOS).
The objective of the study was to test the hypothesis that decidual endovascular trophoblast invasion in pregnant patients with PCOS is impaired and to clarify the potential mechanisms involved.
This was an experimental case-control study.
The study was conducted at the academic Departments of Obstetrics and Gynecology and the Unit of Pathology (Italy).
Forty-five pregnant subjects screened from a wide population of women waiting for legal pregnancy termination were included in the final analysis. Specifically, 15 pregnant patients with PCOS were enrolled as cases and another 30 age- and body mass index (BMI)-matched healthy pregnant women without any feature of PCOS were enrolled as the controls.
Interventions included the collection of trophoblastic and decidual tissue at the 12th week of gestation.
Clinical, ultrasonographic, and biochemical data as well as the histological analysis of decidual endovascular trophoblast invasion.
The rate of implantation site vessels with endovascular trophoblast invasion (ratio between total number of implantation site vessels and total number of vessels with endovascular trophoblast invasion) and the extent of endovascular trophoblast invasion (proportion between immunoreactive areas to cytokeratin 7 and to CD34) were significantly lower in patients with PCOS compared with healthy non-PCOS controls. Endovascular trophoblast invasion data were significantly and indirectly related to the markers of insulin resistance and testosterone concentrations in PCOS patients.
Pregnant patients with PCOS patients have impaired decidual trophoblast invasion. Further studies are needed to evaluate the exact mechanisms through which insulin resistance and hyperandrogenemia exert this effect.
先前的实验和临床数据表明，多囊卵巢综合征（PCOS）患者的蜕膜滋养细胞浸润受损。
本研究旨在检验 PCOS 患者妊娠蜕膜血管内滋养细胞浸润受损的假设，并阐明潜在的相关机制。
这是一项实验性病例对照研究。
该研究在意大利的妇产科学术部门和病理学科进行。
从广泛的等待合法妊娠终止的女性人群中筛选出 45 名孕妇，最终纳入 45 名孕妇进行分析。具体而言，纳入了 15 名患有 PCOS 的妊娠患者作为病例组，另外纳入了 30 名年龄和体重指数（BMI）匹配且无任何 PCOS 特征的健康妊娠妇女作为对照组。
干预措施包括在妊娠第 12 周采集滋养层和蜕膜组织。
临床、超声和生化数据，以及蜕膜血管内滋养细胞浸润的组织学分析。
与健康非 PCOS 对照组相比，PCOS 患者的着床部位血管内滋养细胞浸润率（着床部位血管总数与血管内滋养细胞浸润总数的比值）和血管内滋养细胞浸润程度（细胞角蛋白 7 和 CD34 免疫反应面积的比例）显著降低。血管内滋养细胞浸润数据与 PCOS 患者的胰岛素抵抗和睾酮浓度标志物呈显著且间接相关。
患有 PCOS 的妊娠患者的蜕膜滋养细胞浸润受损。需要进一步研究以评估胰岛素抵抗和高雄激素血症产生这种影响的确切机制。
