Decidual Endovascular Trophoblast Invasion in Women with Polycystic Ovary Syndrome: An Experimental Case-Control Study

Context: Previous experimental and clinical data suggest impaired decidual trophoblast invasion in patients with polycystic ovarian syndrome (PCOS). Objective: 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. Design: This was an experimental case-control study. Setting: The study was conducted at the academic Departments of Obstetrics and Gynecology and the Unit of Pathology (Italy). Patients: 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. Intervention: Interventions included the collection of trophoblastic and decidual tissue at the 12th week of gestation. Main Outcome Measures: Clinical, ultrasonographic, and biochemical data as well as the histological analysis of decidual endovascular trophoblast invasion. Results: 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. Conclusions: 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. (J Clin Endocrinol Metab 97: 2441-2449, 2012)