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PCOS

Soluble platelet/endothelial cell adhesion molecule (sPECAM)-1 is increased in polycystic ovary syndrome and related to endothelial dysfunction

Pages 370-374 | Received 08 May 2011, Accepted 10 Oct 2011, Published online: 29 Mar 2012
 

Abstract

Striking evidence indicates endothelial impairment in polycystic ovary syndrome (PCOS) but the mechanisms linking PCOS status to cardiovascular risk remain elusive. Platelet/endothelial cell adhesion molecule (PECAM)-1 is a soluble (s) signaling molecule involved in inflammation and angiogenesis with predictive value for endothelial dysfunction in patients at risk. In a prospective, controlled study, sPECAM-1 levels and the relationships to metabolic, inflammatory and vascular PCOS traits were evaluated in 26 patients and 29-age- and body mass index-matched controls. To assess endothelial injury, carotid artery intimae-media thickness (CIMT) and brachial artery flow-mediated vasodilatation (FMD) were employed. Of the 26 women with PCOS, 25 completed a six-month metformin combined with ethinylestradiol 0.3 mg/drospirenone 3 mg therapy. Soluble PECAM-1 levels were increased in PCOS (p = 0.018 vs. Controls) and significantly decreased at follow-up (p = 0.0002). Smoking and weight had no effect on sPECAM-1 dynamics. In both univariate and multivariate analysis, basal sPECAM-1 was inversely related to FMD (r = −0.311, p = 0.021) but not CIMT. To conclude, sPECAM-1 is increased in PCOS, an effect reversed by combined metformin and anti-androgenic contraceptive therapy. Elevated sPECAM-1 contributes to endothelial dysfunction however further studies are inquired to assess its relevance as biomarker and potential therapeutic target in PCOS.

Acknowledgements

The excellent contribution of I. Marian, M.D. is acknowledged.

Declaration of interest: This work was supported by the Ministry of Education and Research grant CNCSIS 552/2007-2008.

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