title: Insulin resistance, obesity, hypofibrinolysis, hyperandrogenism, and coronary heart disease risk factors in 25 pre-perimenarchal girls age < or =14 years, 13 with precocious puberty, 23 with a first-degree relative with polycystic ovary syndrome.
abstract: Pre-peri-menarchal diagnosis of polycystic ovary syndrome (PCOS) is important, because intervention with metformin-diet may prevent progression to full blown PCOS.
  
  
  
  In 25 girls age < or =14 years with probable familial PCOS, 10 pre-, 15 post-menarchal, 13 with precocious puberty, 23 with a first-degree relative with PCOS, we hypothesized that reversible coronary heart disease (CHD) risk factors, insulin resistance, clinical and biochemical hyperandrogenism, and hypofibrinolysis were already established.
  
  
  
  Fasting measures: insulin, glucose, total, LDL- (LDL-C), and HDL-cholesterol (HDL-C), triglycerides (TG), systolic and diastolic blood pressure (SBP, DBP), plasminogen activator inhibitor activity (PAI-Fx), total (T) and free testosterone (FT), androstenedione, and DHEAS.
  
  
  
  Clinical and/or biochemical hyperandrogenism was present in all 25 girls, with elevations of T or FT, or androstenedione in seven of ten pre-menarchal girls and in all 15 post-menarche. PAI-Fx was high in 28% of the 25 girls vs 6.5% in age-gender-race matched controls (p = 0.013). Categorized by race-age-specific distributions in 870 schoolgirls, the 25 girls with probable familial PCOS were more likely to have top decile body mass index (BMI), insulin, HOMA-insulin resistance (HOMA-IR), SBP, DBP, and TG, and bottom decile HDL-C. By analysis of variance, adjusting for race, age and BMI, PCOS girls had higher FT and waist circumference than controls, but did not differ for SBP, DBP, HDL-C, or TG (p>0.05).
  
  
  
  Pre-peri-menarchal acquisition of centripetal obesity amplifies CHD risk factors and hypofibrinolysis in hyperandrogenemic girls with probable familial PCOS and precocious puberty. When schoolgirls become as obese as girls with probable familial PCOS, they acquire the same CHD risk factors, and differ only by lower free T and less centripetal obesity.
authors.affiliation: Cholesterol Center, Jewish Hospital of Cincinnati, Cincinnati, OH 45229, USA. glueckch@healthall.com
authors.forename: Charles J
authors.initials: CJ
authors.lastname: Glueck
authors.forename: John A
authors.initials: JA
authors.lastname: Morrison
authors.forename: Ping
authors.initials: P
authors.lastname: Wang
mesh_terms: D000293:Adolescent; D000735:Androstenedione / Q000097:blood; D025861:Blood Coagulation Disorders, Inherited / Q000150:complications* / Q000235:genetics; D002648:Child; D003327:Coronary Disease / Q000209:etiology* / Q000235:genetics; D005192:Family Health; D005260:Female; D005342:Fibrinolysis / Q000502:physiology; D020022:Genetic Predisposition to Disease; D006801:Humans; D017588:Hyperandrogenism / Q000150:complications* / Q000175:diagnosis / Q000235:genetics; D007333:Insulin Resistance; D009765:Obesity / Q000150:complications*; D015849:Plasminogen Inactivators / Q000097:blood; D011085:Polycystic Ovary Syndrome / Q000150:complications* / Q000175:diagnosis / Q000235:genetics; D011629:Puberty, Precocious / Q000150:complications* / Q000175:diagnosis / Q000235:genetics; D012307:Risk Factors
chemical_list: D015849:Plasminogen Inactivators; D000735:Androstenedione