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

• Published in: Clinical endocrinology (Oxford) Vol. 79; no. 2; pp. 252 - 258
• Main Authors: Kahal, H., Aburima, A., Ungvari, T., Rigby, A. S., Dawson, A. J., Coady, A. M., Vince, R. V., Ajjan, R. A., Kilpatrick, E. S., Naseem, K. M., Atkin, S. L.
• Format: Journal Article
• Language: English
• Published: Oxford Blackwell Publishing Ltd 01.08.2013; Blackwell; Wiley Subscription Services, Inc
• Subjects: Adult; Biological and medical sciences; Blood Platelets - physiology; Cardiovascular Diseases - etiology; Carotid Intima-Media Thickness; Endocrinopathies; Endothelium, Vascular - physiopathology; Female; Female genital diseases; Fundamental and applied biological sciences. Psychology; Gynecology. Andrology. Obstetrics; Humans; Insulin Resistance; Isoprostanes - urine; Medical sciences; Non tumoral diseases; Obesity - blood; Obesity - physiopathology; Platelet Activation; Polycystic Ovary Syndrome - blood; Polycystic Ovary Syndrome - physiopathology; Risk Factors; Vertebrates: endocrinology; Obesity; Nutrition disorder; Biological marker; Cardiovascular disease; Female sterility; Inflammation; Polycystic ovary; Thrombosis; Female genital diseases; Vascular disease; Ovarian diseases; Blood vessel; Cyst; Circulatory system; Benign neoplasm; Endocrinology; Nutritional status
• ISSN: 0300-0664; 1365-2265
• DOI: 10.1111/cen.12137

Summary 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 case–control 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 hyperaemia. 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 regulation 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‐5′‐diphosphate or inhibition with prostacyclin, clot structure and fibrinolytic efficiency ex vivo, endothelial reactive hyperaemic 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.