Prevalence of polycystic ovaries in women with self-reported symptoms of oligomenorrhoea and/or hirsutism: Northern Finland Birth Cohort 1966 Study

Taponen, Saara; Ahonkallio, S.; Martikainen, Hannu; Koivunen, Riitta; Ruokonen, Aimo; Sovio, Ulla; Al, Hartikainen; Pouta, Anneli; Laitinen, Jaana; King, Vanessa; Franks, Stephen; McCarthy, Mark I.; Järvelin, Marjo‐Riitta

doi:10.1093/humrep/deh214

Cited by 84 publications

(84 citation statements)

References 18 publications

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“…We also examined the relationship between FTO genotype and androgen levels (as a continuous trait relevant to PCOS status) in 324 of the UK cases and in 1,000 women from the population-based Northern Finland Birth Cohort of 1966 (NFBC1966, described previously [6,[19][20][21]), in whom there were available measures of both testosterone and FTO genotype. None of these women was on oral hypoglycaemic agents (including metformin) or hormonal therapy, and none was pregnant at the time of study.…”

Section: Methodsmentioning

confidence: 99%

Association of variants in the fat mass and obesity associated (FTO) gene with polycystic ovary syndrome

et al. 2008

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Aims/hypothesis Variants in the fat-mass and obesityassociated gene (FTO) influence susceptibility to type 2 diabetes via an effect on adiposity/obesity. Given the important role of obesity in the aetiology of both polycystic ovary syndrome (PCOS) and type 2 diabetes mellitus, our aim was to establish whether FTO variants are also implicated in PCOS susceptibility. MethodsWe performed a genetic association study of FTO variant rs9939609 using case-control analyses, conducted in 463 PCOS patients (geometric mean BMI 27.5 kg/m 2 ) and 1,336 female controls (geometric mean BMI 25.3 kg/ m 2 ) of UK British/Irish origin. We also sought evidence for associations between FTO variation and circulating testosterone levels in 324 UK PCOS patients and 1,000 women from the Northern Finland Birth Cohort of 1966. Outcome Diabetologia (2008) [adjusted]). This association was most evident in obese PCOS patients (PCOS patients below median BMI vs UK controls, p=0.11; above median BMI vs controls, p=2.9× 10 −4 ). No relationship between FTO genotype and androgen levels was seen. Conclusions/interpretation We provide the first evidence that variants that predispose to common obesity also result in altered susceptibility to PCOS, confirming the mechanistic link between these conditions. The predominant effect of FTO variants on PCOS susceptibility is probably mediated through adiposity.

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Section: Methodsmentioning

confidence: 99%

Association of variants in the fat mass and obesity associated (FTO) gene with polycystic ovary syndrome

et al. 2008

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“…The former group ('symptomatic cases') have biochemical features -as a group -consistent with PCOS. 24,25 Because these cases do not reach the 2003 Rotterdam consensus definition of PCOS 20 (though as a group they have an increased prevalence of ultrasound-confirmed PCO morphology compared with controls), 26 we label these as 'symptomatic cases'. Available phenotypic data include BMI, serum testosterone and SHBG.…”

Section: Finnish Birth Cohortmentioning

confidence: 99%

Relationship between E23K (an established type II diabetes-susceptibility variant within KCNJ11), polycystic ovary syndrome and androgen levels

et al. 2007

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Polycystic ovary syndrome (PCOS) is strongly associated with hyperinsulinaemia and type II diabetes (T2D). Sequence variation within KCNJ11 (encoding Kir6.2, the beta-cell inwardly rectifying potassium channel) is implicated in the pathogenesis of neonatal diabetes, hyperinsulinaemia of infancy and multifactorial T2D. Comprehensive tagging studies have demonstrated that the KCNJ11 E23K variant (or ABCC8 A1369S in LD40.9) is responsible for the known association between KCNJ11 and T2D. Given the phenotypic overlap between PCOS and T2D, we investigated whether E23K is involved in susceptibility to PCOS and related traits. Case -control analyses for the KCNJ11 E23K variant were performed in (a) 374 PCOS cases and 2574 controls of UK British/Irish origin, and (b) 550 women with PCOS symptoms and 1114 controls from a Finnish birth cohort. The relationship between E23K genotype and androgen levels (a key intermediate phenotype relevant to PCOS) in 1380 samples was studied. The UK case-control analysis revealed no association between E23K genotypes and PCOS status (P ¼ 0.49; Cochran -Armitage test), and no significant relationship between E23K genotype and androgen measures in the samples for which these phenotypes were available (P ¼ 0.19). Similarly, the Finnish case-control analysis showed no association between E23K genotypes and PCOS status (P ¼ 0.75; Cochran -Armitage test), and no significant relationship between E23K genotype and androgen measures in the samples for which these phenotypes were available (Finnish controls, P ¼ 0.25; Finnish cases, P ¼ 0.08). In conclusion, these data (involving 44600 subjects) provide no evidence that common variants of the KCNJ11 E23K polymorphism have a major influence on PCOS susceptibility, though modest effect sizes (ORo1.25) cannot be excluded.

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“…Metabolic and hormonal parameters before and after sibutramine and placebo treatment. Triglycerides, mmol/L [33,148] and white women in the U.S. [31]. However, the prevalence rate for the Swedish population was lower than reported for Southern European women [30,32], black American women [31] and Australian women [40], where prevalence rates for PCOS, according to NIH criteria, varies between 6.5 -8.7%.…”

Section: Paper Imentioning

confidence: 81%

“…In Sri Lanka, more than 90% of women with self-reported symptoms of oligo/amenorrhea and/or hirsutism were later shown to have PCOS [150]. A Finnish study reports polycystic ovaries were later detected in 18% of women reporting only hirsutism, in 48% of women reporting only oligomenorrhea, and in 70% of women reporting both symptoms [148]. As indicated in the Australian prevalence study it is difficult to include the transvaginal ultrasound in prevalence studies of PCOS as less than half of women are willing to undergo the examination [40].…”

Section: Paper Imentioning

confidence: 99%

Metabolic Aspects of Polycystic Ovary Syndrome

2015

Postgraduate Obstetrics & Gynecology

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Prevalence of polycystic ovaries in women with self-reported symptoms of oligomenorrhoea and/or hirsutism: Northern Finland Birth Cohort 1966 Study

Cited by 84 publications

References 18 publications

Association of variants in the fat mass and obesity associated (FTO) gene with polycystic ovary syndrome

Association of variants in the fat mass and obesity associated (FTO) gene with polycystic ovary syndrome

Relationship between E23K (an established type II diabetes-susceptibility variant within KCNJ11), polycystic ovary syndrome and androgen levels

Metabolic Aspects of Polycystic Ovary Syndrome

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