title: Phenotypic spectrum of polycystic ovary syndrome: clinical and biochemical characterization of the three major clinical subgroups.
abstract: OBJECTIVE
  We tested the hypothesis that the three clinical phenotypes of polycystic ovary syndrome (PCOS) represent forms of the same metabolic disorder.
  
  
  METHODS
  Prospective cohort analysis.
  
  
  METHODS
  University-based tertiary care.
  
  
  METHODS
  Three-hundred sixteen untreated consecutive women diagnosed as having PCOS.
  
  
  METHODS
  None.
  
  
  METHODS
  Each subject underwent an evaluation of ovulatory function, body habitus, acne, and hirsutism; serum free and total testosterone (T), 17-hydroxyprogesterone (17-HP), and DHEAS; and fasting plasma glucose and insulin levels. Insulin resistance and beta-cell function were assessed using the homeostatic assessment model equation (HOMA-IR and HOMA-beta-cell, respectively).
  
  
  RESULTS
  The Oligo+HA+Hirsutism phenotype was present in 48% of subjects, Oligo+HA in 29%, and Oligo+Hirsutism in 23%. The three phenotypes did not differ in mean body mass index, waist-to-hip ratio, racial composition, degree of oligo-ovulation, prevalence of acne, or family history of hyperandrogenic symptomatology. However, subjects demonstrating the Oligo+HA+Hirsutism phenotype were the youngest and had the greatest degrees of hyperandrogenemia, hyperinsulinemia, and beta-cell function; patients with the Oligo+Hirsutism phenotype where the oldest and had the mildest degrees of hyperandrogenemia, hyperinsulinemia, and beta-cell function. Subjects with the Oligo+HA phenotype demonstrated intermediate degrees of hyperandrogenemia and metabolic dysfunction.
  
  
  CONCLUSIONS
  We conclude that the three clinical phenotypes of PCOS do not represent forms of the same metabolic disorder and may be the result of varying degrees of metabolic dysfunction; greater degrees of beta-cell function and circulating insulin levels favored the development of hirsutism and frank hyperandrogenemia.
authors.affiliation: Department of Obstetrics and Gynecology, David Geffen School of Medicine, University of California at Los Angeles, California, USA.
authors.forename: Wendy Y
authors.initials: WY
authors.lastname: Chang
authors.forename: Eric S
authors.initials: ES
authors.lastname: Knochenhauer
authors.forename: Alfred A
authors.initials: AA
authors.lastname: Bartolucci
authors.forename: Ricardo
authors.initials: R
authors.lastname: Azziz
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D015992:Body Mass Index; D016009:Chi-Square Distribution; D005260:Female; D006628:Hirsutism / Q000097:blood / Q000145:classification / Q000235:genetics; D006801:Humans; D010641:Phenotype; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000145:classification* / Q000235:genetics*; D011446:Prospective Studies