title: Comprehensive Assessment of the Hemostatic System in Polycystic Ovarian Syndrome.
abstract: Polycystic ovarian syndrome (PCOS) affects 12 to 19% of women and has reproductive and metabolic features (endothelial dysfunction, increased diabetes, and cardiovascular risk factors). It also appears to have altered coagulation and fibrinolysis with a prothrombotic state with epidemiological evidence of increased venous thromboembolism. We aimed to comprehensively assess hemostasis in women with PCOS versus control women. In an established case-control cohort of lean, overweight, and obese women with (n = 107) and without PCOS (n = 67), with existing measures of plasminogen activator inhibitor 1 (PAI-1), asymmetric dimethylarginine (ADMA), hormonal, and metabolic markers, we also assessed prothrombin fragments 1 and 2 (PF1 & 2), plasminogen, tissue plasminogen activator (tPA), and thrombin generation (TG). Higher levels of ADMA (0.70 vs. 0.39 µmol/L, p < 0.01), PAI-1 (4.80 vs. 3.66 U/mL, p < 0.01), and plasminogen (118.39 vs. 108.46%, p < 0.01) were seen in PCOS versus controls, and persisted after adjustment for age and body mass index (BMI). PF1 & 2 was marginally lower (180.0 vs. 236.0 pmol/L, p = 0.05), whereas tPA and TG were not different between groups, after adjustment for age and BMI. Significant relationships were observed between hormonal and metabolic factors with ADMA and PAI-1. We demonstrate impaired fibrinolysis in PCOS. In the context of abnormal endothelial function and known hormonal and metabolic abnormalities, this finding may underpin an increased risk of cardiovascular disease and venous thrombosis in PCOS.
authors.affiliation: School of Medical Sciences, RMIT University, Bundoora, Victoria, Australia.
authors.forename: Genia F
authors.initials: GF
authors.lastname: Burchall
authors.affiliation: School of Medical Sciences, RMIT University, Bundoora, Victoria, Australia.
authors.forename: Terrence J
authors.initials: TJ
authors.lastname: Piva
authors.affiliation: School of Pathology and Laboratory Medicine, University of Western Australia, Nedlands, Australia.
authors.forename: Matthew D
authors.initials: MD
authors.lastname: Linden
authors.affiliation: School of Public Health and Preventive Medicine, Monash University, Clayton, Victoria, Australia.
authors.forename: Melanie E
authors.initials: ME
authors.lastname: Gibson-Helm
authors.affiliation: School of Public Health and Preventive Medicine, Monash University, Clayton, Victoria, Australia.
authors.forename: Sanjeeva
authors.initials: S
authors.lastname: Ranasinha
authors.affiliation: School of Public Health and Preventive Medicine, Monash University, Clayton, Victoria, Australia.
authors.forename: Helena J
authors.initials: HJ
authors.lastname: Teede
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D001798:Blood Proteins / Q000378:metabolism*; D015992:Body Mass Index; D016022:Case-Control Studies; D005260:Female; D006487:Hemostasis; D006489:Hemostatic Techniques; D006801:Humans; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000150:complications / Q000628:therapy; D011085:Polycystic Ovary Syndrome / Q000097:blood* / Q000150:complications / Q000628:therapy*; D054556:Venous Thromboembolism / Q000097:blood* / Q000209:etiology / Q000517:prevention & control*
chemical_list: D001798:Blood Proteins