title: Polycystic ovary syndrome has no independent effect on vascular, inflammatory or thrombotic markers when matched for obesity.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
authors.affiliation: Academic Endocrinology, Diabetes and Metabolism, Hull York Medical School, Hull, UK. hassan.kahal@hyms.ac.uk
authors.forename: H
authors.initials: H
authors.lastname: Kahal
authors.forename: A
authors.initials: A
authors.lastname: Aburima
authors.forename: T
authors.initials: T
authors.lastname: Ungvari
authors.forename: A S
authors.initials: AS
authors.lastname: Rigby
authors.forename: A J
authors.initials: AJ
authors.lastname: Dawson
authors.forename: A M
authors.initials: AM
authors.lastname: Coady
authors.forename: R V
authors.initials: RV
authors.lastname: Vince
authors.forename: R A
authors.initials: RA
authors.lastname: Ajjan
authors.forename: E S
authors.initials: ES
authors.lastname: Kilpatrick
authors.forename: K M
authors.initials: KM
authors.lastname: Naseem
authors.forename: S L
authors.initials: SL
authors.lastname: Atkin
mesh_terms: D000328:Adult; D001792:Blood Platelets / Q000502:physiology*; D002318:Cardiovascular Diseases / Q000209:etiology; D059168:Carotid Intima-Media Thickness; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D028421:Isoprostanes / Q000652:urine; D009765:Obesity / Q000097:blood / Q000503:physiopathology*; D015539:Platelet Activation; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000503:physiopathology*; D012307:Risk Factors
chemical_list: D028421:Isoprostanes