title: Referral bias in defining the phenotype and prevalence of obesity in polycystic ovary syndrome.
abstract: BACKGROUND
  The described phenotype of the polycystic ovary syndrome (PCOS) has been primarily based on findings in a referred (self or otherwise) population. It is possible that the phenotype of PCOS would be different if the disorder were to be detected and studied in its natural (unbiased) state.
  
  
  OBJECTIVE
  Our objective was to compare the phenotype of PCOS detected in an unselected population with that identified in a referral population.
  
  
  METHODS
  Participants included 292 PCOS patients identified at a tertiary care outpatient facility (referral PCOS) and 64 PCOS women (unselected PCOS) identified through the screening of a population of 668 seeking a pre-employment physical. Among the women undergoing a pre-employment physical, 563 did not demonstrate features of the disorder (unselected controls). All PCOS subjects met the National Institutes of Health 1990 criteria for the disorder.
  
  
  METHODS
  We estimated prevalence of obesity and severity of disease burden.
  
  
  RESULTS
  Referral PCOS subjects had greater mean body mass index and hirsutism score and higher degrees of hyperandrogenemia, were more likely to be non-Hispanic White (83.90%), and demonstrated a more severe PCOS subphenotype than unselected PCOS or unselected controls. The prevalence of obesity and severe obesity in referral PCOS was 2.3 and 2.5 times greater than estimates of the same in unselected PCOS and 2.2 and 3.8 times greater than estimates in unselected controls, respectively. Alternatively, unselected PCOS subjects had a prevalence of obesity and severe obesity and a mean body mass index similar to those of the general population from which they were derived.
  
  
  CONCLUSIONS
  The phenotype of PCOS, including the racial/ethnic mix, severity of presentation, and rate of obesity, is affected significantly by whether the PCOS subject arises from a referral population or through unselected screening, likely reflecting the degree of patient concern and awareness and access to healthcare.
authors.affiliation: Department of Obstetrics and Gynecology, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA.
authors.forename: Uche
authors.initials: U
authors.lastname: Ezeh
authors.forename: Bulent O
authors.initials: BO
authors.lastname: Yildiz
authors.forename: Ricardo
authors.initials: R
authors.lastname: Azziz
mesh_terms: D000328:Adult; D015982:Bias; D015992:Body Mass Index; D005260:Female; D006801:Humans; D017588:Hyperandrogenism / Q000150:complications; D009765:Obesity / Q000453:epidemiology* / Q000208:ethnology; D010641:Phenotype; D011085:Polycystic Ovary Syndrome / Q000150:complications*; D015995:Prevalence; D012017:Referral and Consultation
references.citation: Hum Reprod Update. 2010 Jan-Feb;16(1):51-64
references.pmid: 19567450
references.citation: Fertil Steril. 2007 Sep;88(3):727-9
references.pmid: 17706215
references.citation: J Obstet Gynaecol Res. 2011 Aug;37(8):1020-6
references.pmid: 21481088
references.citation: Hum Reprod. 2008 Aug;23(8):1924-31
references.pmid: 18579512
references.citation: Fertil Steril. 2005 Jun;83(6):1717-23
references.pmid: 15950641
references.citation: BJOG. 2009 Nov;116(12):1633-9
references.pmid: 19781047
references.citation: J Clin Endocrinol Metab. 2006 Dec;91(12):4842-8
references.pmid: 17003085
references.citation: Fertil Steril. 1999 Nov;72(5):915-25
references.pmid: 10561000
references.citation: Fertil Steril. 2009 Feb;91(2):456-88
references.pmid: 18950759
references.citation: J Clin Endocrinol Metab. 2004 Feb;89(2):453-62
references.pmid: 14764747
references.citation: Eur J Endocrinol. 2010 Jun;162(6):1093-9
references.pmid: 20371657
references.citation: Fertil Steril. 1998 Feb;69(2):286-92
references.pmid: 9496343
references.citation: Obes Res. 2002 May;10(5):345-50
references.pmid: 12006633
references.citation: J Clin Endocrinol Metab. 1998 Sep;83(9):3078-82
references.pmid: 9745406
references.citation: Am J Obstet Gynecol. 1995 Apr;172(4 Pt 1):1251-6
references.pmid: 7726265
references.citation: Hum Reprod. 2012 Oct;27(10):3067-73
references.pmid: 22777527
references.citation: Reprod Sci. 2011 Dec;18(12):1230-6
references.pmid: 22096008
references.citation: Hum Reprod Update. 2008 Jan-Feb;14(1):15-25
references.pmid: 17905857
references.citation: J Clin Endocrinol Metab. 2004 Jun;89(6):2745-9
references.pmid: 15181052
references.citation: Fertil Steril. 2007 Nov;88(5):1389-95
references.pmid: 17462641
references.citation: Fertil Steril. 2010 Nov;94(6):2197-201
references.pmid: 20303485
references.citation: J Clin Endocrinol Metab. 2008 Jan;93(1):162-8
references.pmid: 17925334
references.citation: Eur J Obstet Gynecol Reprod Biol. 2005 Oct 1;122(2):206-12
references.pmid: 16219521
references.citation: Clin Endocrinol (Oxf). 1990 Feb;32(2):213-20
references.pmid: 2112067
references.citation: Reprod Biomed Online. 2010 Oct;21(4):572-80
references.pmid: 20800551
references.citation: Akush Ginekol (Sofiia). 2010;49(4):32-7
references.pmid: 20734639
references.citation: Clin Endocrinol (Oxf). 2007 Nov;67(5):735-42
references.pmid: 17760884
references.citation: J Res Med Sci. 2011 Jun;16(6):763-9
references.pmid: 22091305
references.citation: Hum Reprod. 2010 Feb;25(2):544-51
references.pmid: 19910321
references.citation: Reprod Biol Endocrinol. 2011 Mar 25;9:39
references.pmid: 21435276
references.citation: Exp Clin Endocrinol Diabetes. 2011 Sep;119(8):502-8
references.pmid: 21553368
references.citation: Fertil Steril. 2009 Aug;92(2):626-34
references.pmid: 18706545
references.citation: J Clin Endocrinol Metab. 2008 Apr;93(4):1276-84
references.pmid: 18182456
references.citation: World Health Organ Tech Rep Ser. 2000;894:i-xii, 1-253
references.pmid: 11234459
references.citation: J Clin Endocrinol Metab. 2005 Aug;90(8):4650-8
references.pmid: 15944216
references.citation: J Clin Endocrinol Metab. 2006 Oct;91(10):3922-7
references.pmid: 16849400