title: The inflammatory gene pathway is not a major contributor to polycystic ovary snydrome.
abstract: BACKGROUND
  Although inflammation is clearly associated with obesity, diabetes, and insulin resistance, the role of chronic inflammation in the etiology of polycystic ovary syndrome (PCOS) is unclear.
  
  
  OBJECTIVE
  To determine whether chronic inflammation plays a causal role in the etiology of PCOS, we tested for an association between PCOS and genetic markers mapping to 80 members of the inflammatory pathway.
  
  
  METHODS
  This was a case-control association study.
  
  
  METHODS
  The setting was an academic medical center.
  
  
  METHODS
  A total of 905 index case patients with PCOS and 955 control women (108 intensively phenotyped subjects with normal androgen levels and regular menses and 847 minimally phenotyped subjects with regular menses and no history of PCOS).
  
  
  METHODS
  Subjects were genotyped at single nucleotide polymorphisms mapping to 80 inflammatory genes. Logistic regression was used to test for an association between 822 single nucleotide polymorphisms and PCOS after adjustment for population stratification, body mass index, and/or age. In the index patients, we also tested for association with 11 quantitative traits (body mass index and testosterone, fasting insulin, fasting glucose, 2-hour postchallenge glucose, LH, FSH, total cholesterol, high-density lipoprotein, low-density lipoprotein, and triglyceride levels).
  
  
  METHODS
  The evidence for an association with PCOS and with 11 quantitative traits was investigated.
  
  
  RESULTS
  Nominally significant evidence for an association was observed with MAP3K7, IKBKG, TNFRS11A, AKT2, IL6R, and IRF1, but no results remained statistically significant after adjustment for multiple testing.
  
  
  CONCLUSIONS
  Genetic variation in the inflammatory pathway is not a major contributor to the etiology of PCOS or related quantitative traits in women with PCOS.
authors.affiliation: Division of Endocrinology, Metabolism, and Molecular Medicine (S.B., P.M., O.A.G., A.D., M.U.) and Center for Genetic Medicine (N.J.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; and Department of Obstetrics and Gynecology (R.S.L.), Pennsylvania State University, College of Medicine, Hershey, Pennsylvania 17033.
authors.forename: Surabhi
authors.initials: S
authors.lastname: Bhatt
authors.forename: Priscilla
authors.initials: P
authors.lastname: Mutharasan
authors.forename: Obed A
authors.initials: OA
authors.lastname: Garcia
authors.forename: Nadereh
authors.initials: N
authors.lastname: Jafari
authors.forename: Richard S
authors.initials: RS
authors.lastname: Legro
authors.forename: Andrea
authors.initials: A
authors.lastname: Dunaif
authors.forename: Margrit
authors.initials: M
authors.lastname: Urbanek
mesh_terms: D016022:Case-Control Studies; D008076:Cholesterol, HDL / Q000235:genetics; D019332:Endothelin-1 / Q000235:genetics; D005260:Female; D005787:Gene Frequency; D005951:Glucose Tolerance Test; D006801:Humans; D007249:Inflammation / Q000235:genetics*; D011085:Polycystic Ovary Syndrome / Q000453:epidemiology / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide; D040641:Quantitative Trait Loci; D015398:Signal Transduction / Q000235:genetics
chemical_list: D008076:Cholesterol, HDL; D019332:Endothelin-1