Abstract

ABSTRACT Cardiovascular illness is more frequent in women with polycystic ovary syndrome (PCOS), even young women. Recent findings have linked endothelial dysfunction and chronic, low-grade inflammation—as evidenced by elevated serum C-reactive protein (CRP) levels—with developing atherosclerosis. This study compared endothelial dysfunction and high-sensitivity CRP (hs-CRP) levels in 37 women with PCOS and 25 control subjects matched with the cases for age and body mass index. A majority of women with PCOS had oligomenorrhea or amenorrhea. High-resolution ultrasonography was used to estimate arterial endothelium and smooth muscle function by recording changes in brachial artery diameter at baseline, during reactive hyperemia (flow-mediated dilation [FMD]), and after sublingual administration of 0.4 mg nitroglycerin. Reactive hyperemia was induced by inflating a cuff on the upper arm to a suprasystolic level and then deflating the cuff. Women diagnosed as having PCOS had significantly higher serum levels of luteinizing hormone, testosterone, and androstenedione than control women and significantly lower levels of sex hormone-binding globulin. Fasting insulin levels were higher in the PCOS group, but there were no group differences in fasting glucose levels. Women with PCOS were more insulin-resistant than control women, and they had higher concentrations of hs-CRP (Fig. 1). CRP levels correlated with body mass index, insulin sensitivity, and FMD. Endothelium-dependent vasodilation correlated with hs-CRP levels and insulin resistance. No correlation was found between endothelium-independent vascular responses and either metabolic or hormonal parameters. These results are the first evidence that nonobese women with PCOS have elevated hs-CRP levels as well as endothelial dysfunction. Endothelium-dependent dysfunction seems to be associated with both insulin resistance and chronic low-grade inflammation. Measures lowering insulin resistance may prove to be cardioprotective in these women.

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