Coagulation factor dysregulation in polycystic ovary syndrome is an epiphenomenon of obesity.

Abstract

Obese women with polycystic ovary syndrome (PCOS) exhibit a hypercoagulable state, with the suggestion that this may be obesity-driven rather than an intrinsic facet of PCOS; however, this has not yet been definitively determined since body mass index (BMI)is so highly correlated with PCOS. Therefore, only a study design where obesity, insulin resistance and inflammation are matched can answer this question. This was a cohort study. Patients Weight and aged-matched nonobese women with PCOS (n = 29) and control women (n = 29) were included. Measurements Plasma coagulation pathway protein levels were measured. Circulating levels of a panel of nine clotting proteins known to differ in obese women with PCOS were determined by Slow Off-rate Modified Aptamer (SOMA)-scan plasma protein measurement. Women with PCOS showed a higher free androgen index (FAI) and anti-Müllerian hormone, but measures of insulin resistance, and C reactive protein (as a marker of inflammation), did not differ between the nonobese women with PCOS and the control women. Seven pro-coagulation proteins (plasminogen activator inhibitor-1, fibrinogen, fibrinogen gamma chain, fibronectin, d-dimer, P-selectinand plasma kallikrein) and two anticoagulant proteins (vitamin K-dependent protein-S and heparin cofactor-II) known to be elevated in obese women with PCOS did not differ from controls in this cohort. This novel data showthat clotting system abnormalities do not contribute to the intrinsic mechanisms underlying PCOS in this nonobese noninsulin resistant population of women with PCOS matched for age and BMI, and without evidence of underlying inflammation, but rather the clotting factor changes are an epiphenomenon coincident with obesity; therefore, increased coagulability is unlikely in these nonobese PCOS women.