Previous studies have provided indirect evidence for impaired decidual trophoblast invasion in patients with polycystic ovarian syndrome (PCOS). Defects in decidual trophoblast invasion in pregnant patients with PCOS have been suggested by studies showing that there is decreased secretion of markers of insulin resistance and that uterine artery Doppler indices are more commonly altered in pregnant PCOS patients than in control subjects. There are no specific and direct data in the literature evaluating decidual trophoblast invasion in women with PCOS.
The aim of this experimental case-control study was to provide direct evidence that decidual endovascular trophoblast invasion in pregnant patients with PCOS is impaired and to evaluate the potential mechanisms involved. A wide population of pregnant women waiting for legal pregnancy termination for nonmedical reasons was screened for PCOS. Among these women, 45 pregnant women were included in the final analysis; 15 were patients with PCOS (cases), and 30 were age- and body mass index–matched healthy pregnant women without any feature of PCOS (control subjects). All legal pregnancy terminations were performed at the 12th week of gestation. At that time, histological samples of trophoblastic and decidual tissue were taken for evaluation of trophoblast invasion, and each participant underwent a clinical evaluation and an ultrasonographic assessment and had a venous blood sample taken for biochemical analysis. Serum levels of markers of insulin resistance and androgens (testosterone) were assayed. The percentage of implantation site vessels showing signs of endovascular trophoblast invasion and endovascular extension of endovascular trophoblast invasion was calculated.
Compared with healthy non-PCOS control subjects, the incidence of implantation site vessels showing signs of endovascular trophoblast invasion (ratio between total implantation site vessels and implantation site vessels with endovascular trophoblast invasion) and endovascular trophoblast invasion extension (ratio between the immunoreactive areas to cytokeratin 7 and to CD34) was significantly lower in patients with PCOS. A significant and indirect relationship among women with PCOS was found between the endovascular trophoblast invasion data and both markers of insulin resistance and testosterone concentrations.
These findings indicate that pregnant patients with PCOS have impaired decidual trophoblast invasion that appears to be mediated through insulin resistance and hyperandrogenism.