title: Excess Metabolic and Cardiovascular Risk is not Manifested in all Phenotypes of Polycystic Ovary Syndrome: Implications for Diagnosis and Treatment.
abstract: OBJECTIVE
  To assess the potential differences in the metabolic and cardiovascular disease (CVD) risk between the distinct phenotypes of the Polycystic Ovary Syndrome (PCOS) according to the Rotterdam definition regardless of body mass index (BMI).
  
  
  METHODS
  The study included 300 women; 240 women with PCOS, according to the Rotterdam criteria and 60 controls without PCOS. All women were further subdivided, according to their BMI, into normal-weight and overweight/obese and PCOS women were furthermore subdivided to the 4 phenotypes of the syndrome. A complete hormonal and metabolic profile as well as the levels of high sensitivity C reactive protein (hsCRP) and lipoprotein-associated phospholipase A2 (Lp-PLA2) were measured.
  
  
  RESULTS
  Levels of surrogate markers of subclinical atherosclerosis (hsCRP and Lp-PLA2), levels of evaluated CVD risk score using risk engines, and several correlations of CVD risk factors.
  
  
  RESULTS
  hsCRP levels were higher but not significantly so in PCOS women compared with controls. In lean PCOS patients, Lp-PLA2 levels were significantly higher, compared with lean controls, mainly in the 2 classic phenotypes. Overweight/obese patients in all 4 phenotypes had significantly higher Lp-PLA2 levels compared with overweight/obese controls. Evaluated CVD risk according to 4 risk engines was not different among phenotypes and between PCOS patients and controls. There were several correlations of risk factors with metabolic syndrome and non-alcoholic fatty liver disease requiring appropriate treatment.
  
  
  CONCLUSIONS
  Only 2 of 4 Rotterdam phenotypes, identical with those of the classic PCOS definition, have excess cardiometabolic risk. These need to be treated to prevent CVD events.
authors.forename: Georgios
authors.initials: G
authors.lastname: Daskalopoulos
authors.forename: Artemis
authors.initials: A
authors.lastname: Karkanaki
authors.forename: Athanasia
authors.initials: A
authors.lastname: Piouka
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Prapas
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Panidis
authors.forename: Paraschos
authors.initials: P
authors.lastname: Gkeleris
authors.affiliation: Second Propedeutic Department of Internal Medicine, Medical School, Aristotle University of Thessaloniki, Hippocration Hospital, 15 Marmara St, 55132, Thessaloniki, Greece. vathyros@gmail.com.
authors.forename: Vasilios G
authors.initials: VG
authors.lastname: Athyros
mesh_terms: D000328:Adult; D050197:Atherosclerosis / Q000453:epidemiology / Q000209:etiology; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism*; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000209:etiology*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D024821:Metabolic Syndrome / Q000453:epidemiology / Q000209:etiology*; D065626:Non-alcoholic Fatty Liver Disease / Q000453:epidemiology; D009765:Obesity / Q000150:complications / Q000503:physiopathology; D050177:Overweight / Q000150:complications / Q000503:physiopathology; D010641:Phenotype; D011085:Polycystic Ovary Syndrome / Q000150:complications / Q000503:physiopathology*; D012307:Risk Factors; D055815:Young Adult
chemical_list: D002097:C-Reactive Protein