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Department of Molecular & Clinical Endocrinology and Oncology (F.O., T.C., G.L., A.C.) and Institute of Internal Medicine and Metabolic Disease (B.D.S.), University "Federico II", 80131 Naples, Italy; Department of Obstetrics and Gynecology (S.P., T.R., F.Z.), University of Catanzaro "Magna Graecia", 88100 Catanzaro, Italy; and "MeriGen" Laboratory of Molecular Biology (S.D.B., D.L.), 80131 Naples, Italy
Address all correspondence and requests for reprints to: Francesco Orio, M.D., Department of Molecular & Clinical Endocrinology and Oncology, University "Federico II" of Naples, Via S. Pansini 5, 80131 Naples, Italy. E-mail: francescoorio{at}virgilio.it.
The aim of this study was to evaluate the presence of early vascular damage in young normal-weight women with polycystic ovary syndrome (PCOS).
Thirty young normal-weight women with PCOS, who had no additional metabolic or cardiovascular diseases, and 30 healthy women (controls) matched for age and body mass index were studied. A complete hormonal assay was performed in each subject. Serum insulin and glucose levels were measured at baseline and after the oral glucose tolerance test. Plasma endothelin-1 levels and serum lipid profile were also assessed. The endothelial function was studied by flow-mediated dilation on the brachial artery, and arterial structure was evaluated by intima-media thickness measurement using Doppler ultrasound of both common carotid arteries.
A significant (P < 0.05) difference in flow-mediated dilation (14.3 ± 1.9% vs. 18.1 ± 2.0% for PCOS patients and controls, respectively) and in intima-media thickness (0.53 ± 0.09 mm vs. 0.39 ± 0.08 mm for PCOS patients and controls, respectively) was found between PCOS and control subjects. Serum endothelin-1 levels were also significantly (P < 0.05) higher in PCOS patients compared with controls (1.1 ± 0.4 pmol/liter vs. 0.5 ± 0.2 pmol/liter for PCOS patients and controls, respectively).
In conclusion, our data show that young, normal-weight, nondyslipidemic, nonhypertensive women with PCOS have an early impairment of endothelial structure and function.
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