Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2013) 31 P207 | DOI: 10.1530/endoabs.31.P207

SFEBES2013 Poster Presentations Obesity, diabetes, metabolism and cardiovascular (67 abstracts)

Polycystic ovary syndrome has no independent effect on vascular, inflammatory or thrombotic markers when matched for obesity

Hassan Kahal 1 , Ahmed Aburima 1 , Tamas Ungvari 2 , Alan Rigby 1 , Alison Dawson 1 , Anne-Marie Coady 2 , Rebecca Vince 3 , Ramzi Ajjan 4 , Eric Kilpatrick 2 , Khalid Naseem 1 & Stephen Atkin 1


1Hull York Medical School, Hull, UK; 2Hull and East Yorkshire NHS Trust, Hull, UK; 3University of Hull, Hull, UK; 4Leeds Institute for Genetics, Health and Therapeutics, University of Leeds, Leeds, UK.


Introduction: Previous studies investigating cardiovascular (CV) risk in obese women with polycystic ovary syndrome (PCOS) have been potentially confounded by not adequately accounting for body weight.

Objective: To assess if PCOS increases CV risk independently in young obese women by examining carotid intima-media wall thickness (cIMT) and platelet function.

Design: A cross-sectional study comparing women with PCOS (n=21) to age (32.8±7.2 vs 33.5±6.7 years), and weight (100.9±16.7 vs 99.3±14.7 kg) matched controls (n=19). Platelet function was examined by flow cytometry, clot structure and fibrinolysis by turbidimetric assays and endothelial function by ELISA and post-ischaemic reactive hyperemia.

Results: The PCOS group had higher testosterone 1.2±0.3 vs 0.9±0.3 nmol/l (P=0.01), HOMA-IR 2.5±1.7 vs 1.7±1.0 (P=0.08), impaired glucose tolerance 33.3% vs 5.3% (P=0.02), and urinary isoprostane 16.0±4.4 vs 11.8±7.1 ng/ml (P=0.04) compared to controls. Mean cIMT 0.5±0.05 vs 0.48±0.06 mm (P=0.36), and basal platelet surface expression (percentage of positive cells) of P-selectin 0.52±0.3 vs 0.43±0.23 (P=0.40) and fibrinogen binding 0.97±0.4 vs 0.83±0.3 (P=0.48) did not significantly differ between the PCOS and control groups, respectively. Furthermore, platelets sensitivity to stimulation with adenosine-five’-diphosphate or inhibition with prostacyclin, clot structure and fibrinolytic efficiency ex vivo, endothelial reactive hyperemic index (RHI), inflammation (hsCRP) and adhesion markers (sE-selectin, sP-selectin, sVCAM-1 and sICAM-1) were not significantly different between the two groups.

Conclusions: PCOS appeared not to independently increase atherothrombotic risk when matched for obesity. It is likely that any excess CV risk in young obese women with PCOS can either be attributed to obesity or is not yet apparent at this early stage of the condition.

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