Endothelial cell dysfunction is reported to occur in polycystic ovary syndrome (PCOS) but it is unclear if this is due to obesity or inherent to PCOS. We hypothesized that in body mass index (BMI)-matched women with obesity, with and without PCOS, endothelial cell dysfunction protein markers would differ due to the inherent pathophysiology of PCOS. 92 women with PCOS and 19 control subjects were identified from a PCOS and control biobank and matched for obesity (BMI ≥ 30 kg/m2). Endothelial dysfunction markers were determined by the Slow Off-rate Modified Aptamer (SOMA)-scan proteomics method. Intercellular adhesion molecule-1 (ICAM1; p < 0.05), tissue plasminogen activator (tPA; p < 0.05), plasminogen activator inhibitor-1 (PAI-1; p < 0.05) and D-dimer (p < 0.003) were significantly elevated in PCOS but did not correlate with either insulin resistance (IR) or hyperandrogenemia. BMI, C-reactive protein (CRP) and sex hormone binding protein (SHBG) did not differ between subjects, but IR and testosterone were increased (p < 0.01) in PCOS, as expected. Endothelial dysfunction is an inherent feature of the pathophysiology found in PCOS, with markers of both endothelial activation/dysfunction (ICAM1 elevation) and coagulation and fibrinolysis (tPA, PAI-1 and D-Dimer elevation) in obese PCOS compared to matched controls. These circulatory proteins are of direct relevance to potential development of cardiovascular disease in PCOS.
Borde et al. (Mon,) studied this question.