1

Definitions, prevalence and symptoms

of polycystic ovaries and polycystic

ovary syndrome

Roger Hart* MD, FRANZCOG, MRCOG

Senior Lecturer in Obstetrics and Gynaecology

Martha Hickey MD, FRANZCOG, MRCOG

Associate Professor of Obstetrics and Gynaecology

UWA School of Women’s and Infants’ Health, King Edward Memorial Hospital,

University of Western Australia, 375 Bagot Road, WA 6008 Subiaco, Perth, Australia

Stephen Franks MD, FRCP, Hon MD, FRCOG(ad eundem), F Med Sci

Professor of Reproductive Endocrinology

Institute of Reproductive and Developmental Biology, Imperial College London,

Hammersmith Hospital, London W12 0NN, UK

Polycystic ovarian morphology is seen on ultrasound in approximately 22% of women. Polycysticovary syndrome (PCOS) is a common and perplexing endocrine disorder of women in theirreproductive years, with a prevalence of up to 10%. Clinical expression of the syndrome variesbut commonly includes menstrual cycle disturbance, hyperandrogenism, insulin resistance andobesity. Recently, the European Society for Human Reproduction and Embryology and theAmerican Society for Reproductive Medicine (ESHRE/ASRM) achieved a new consensusregarding the definition of PCOS. This is now defined as the presence of any two of the followingthree criteria: (i) polycystic ovaries; (ii) oligo-/anovulation; and/or (iii) clinical or biochemicalevidence of hyperandrogenism. This revised definition provides an international framework forthe clinical assessment of PCOS and for future research and collaboration.

Key words: fetal origins; hirsutism; insulin resistance; polycystic ovaries; polycystic ovarysyndrome; prevalence; weight.

Polycystic ovary syndrome (PCOS) is a syndrome of ovarian dysfunction that isfrequently associated with the systemic condition of insulin resistance. Its cardinalfeatures are hyperandrogenism and polycystic ovary morphology.1 Its clinical

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Best Practice & Research Clinical Obstetrics and GynaecologyVol. 18, No. 5, pp. 671–683, 2004doi:10.1016/j.bpobgyn.2004.05.001

available online at http://www.sciencedirect.com

* Corresponding author. Tel.: þ61-8-9340-1328; Fax: þ61-08-9381-3031.E-mail address: rhart@obsgyn.uwa.edu.au (R. Hart).

manifestations can include infertility, menstrual irregularity or absence, signs ofandrogen excess and obesity. Although PCOS is the most common endocrinedisturbance to affect women of reproductive age2, its definition has been controversialand aspects of its pathophysiology and natural history remain unclear. Therapy is aimedat amelioration of symptoms and a variety of interventions have been proposed,ranging from modifications in lifestyle2, to medical therapy3 or ovarian surgery.4

DEFINITIONS OF POLYCYSTIC OVARIES5

The characteristic appearance of polycystic ovaries was recognised in only 1.4% of12 160 laparotomies conducted in women of reproductive age by Vara and Niemineva.6

However, modern high-resolution ultrasonography provides a much more precise andnon-invasive technique to assess ovarian size and morphology. Using ultrasoundcriteria, polycystic ovaries are defined by the presence of 12 or more follicles in eachovary, each measuring 2–9 mm in diameter, and/or increased ovarian volume (.10 ml).The subjective appearance of an increased stromal volume or echogenicity is notincluded in the definition.5 The presence of a single polycystic ovary is sufficient toprovide the diagnosis.

It is intended that this definition will supersede the previous criteria describing aminimum of 10 follicles (between 2 and 8 mm in size) arranged peripherally around adense core of ovarian stroma in one plane or scattered throughout an increasedamount of stroma.7 Surprisingly, transvaginal scanning does not appear to increase thedetection rate of polycystic ovaries, although abdominal ultrasound findings in obesewomen might be limited.8

On histopathological assessment, polycystic ovaries contain increased numbers offollicles, hypertrophy and luteinization of the inner theca cell layer, and a thickenedovarian tunica.9 A good correlation appears to exist between these ultrasound andhistopathological diagnostic criteria.10

Although polycystic ovaries per se (without PCOS) appear to have no long-termimplications for the patient, they constitute a risk factor for the development of ovarianhyperstimulation syndrome (OHSS).11 However, women with polycystic ovaries mightbenefit from an improved outcome when undergoing in vitro fertilisation (IVF)treatment if they do not also suffer from OHSS. On average, women with polycysticovaries but no symptoms of PCOS produce more follicles, oocytes and embryos, andhave an 80% greater chance of having a live birth than matched women with normalovaries; however, the fertilization, cleavage and miscarriage rates are similar.12

The findings of a recent study demonstrated fundamental differences betweenpolycystic and normal ovaries with regard to early follicular development as assessed byhistological analysis.13 This would suggest that an intrinsic ovarian abnormality exists inwomen with polycystic ovaries. The authors suggest that an increased density of small,preantral follicles in polycystic ovaries could result from an increased initial totalpopulation of germ cells in the fetal ovary, or from a decreased rate of loss of oocytesduring late gestation, childhood and puberty.13

Definitions of polycystic ovary syndrome

The recent review of the definition of PCOS reflects increasing awareness that theclinical expression of PCOS might be broader than that defined by the 1990 NIH

672 R. Hart et al

criteria.5 The previous diagnostic criteria of PCOS were not universally accepted;indeed there were markedly disparate views, which made it difficult to interpret andcompare studies from different centres. Before 1990 it was recognised that womenwith regular cycles and either clinical or biochemical hyperandrogenism, or womenwith regular cycles and polycystic ovaries, might be part of the polycystic ovarysyndrome.7,14

The previously held diagnostic criteria were established by the 1990 NIH/NICHHDconsensus statement for the diagnosis of PCOS.15 This definition relied on acombination of oligomenorrhoea or amenorrhoea and clinical or biochemical evidenceof hyperandrogenaemia (in the absence of non-classical adrenal hyperplasia andhyperprolactinemia and thyroid dysfunction). Hence, in countries that used thisdefinition (e.g. North America and Australia), PCOS was diagnosed in the absence of anultrasound appearance of polycystic ovaries. By contrast, the European definition ofPCOS centred around the presence of polycystic ovaries on ultrasound in associationwith one or more of the following features: clinical and/or biochemical androgen excess(acne, hirsutism or alopecia), obesity, oligo-/amenorrhoea, or amenorrhoea and araised luteinising hormone (LH) level (see Table 1).16 According to this definition, themere presence of a polycystic ovary on ultrasound, plus obesity, was sufficient to makethe diagnosis, even though it was recognised that more than one symptom, sign orbiochemical disturbance usually coexisted with polycystic ovaries and that thecondition of PCOS is dynamic, such that the features in an individual can changeover time.9

In developing the consensus statement it was recognised that the reported incidenceof the clinical features of PCOS might be biased by the study population. For example,studies of fertility in PCOS will place greater emphasis on anovulation as the identifyingsymptom, rather than clinical hyperandrogenism or the presence of polycystic ovaries;studies of the treatment of hirsutism in PCOS would focus on terminal hair growth asopposed to ovulatory disorder for entry. It is known that women with chronicanovulation and hyperandrogenism and/or polycystic ovaries are at a greater riskof insulin resistance than those with hyperandrogenism and regular cycles.17,18

Table 1. Clinical symptoms and signs in women with polycystic ovary syndrome.

Percentage frequency of symptom or sign

Balen et al44 Franks14 Goldzieher et al53

n ¼ 1741 (%) n ¼ 300 (%) n ¼ 1079 (%) No. of casesa

Menstrual cycle disturbance

Oligomenorrhoea 47 52 29 547

Amenorrhoea 19 28 51 640

Hirsutism 66.2 64 69 819

Obesity 38 35 41 600

Acne 35 27 – –

Alopoecia 6 3 – –

Acanthosis nigricans 3 ,1 – –

Infertility (primary/secondary) 20 42 74 596

Reprinted from Ref. 9 with permission of Oxford University Press.a In the Goldzieher study clinical details were not available for the entire group of 1079 women, thus the

number of cases used to determine the frequency of each symptom is stated.

PCOS: definitions, prevalence and symptoms 673

Consequently, studies of the metabolic features of PCOS should stratify women withthe condition according to ovulatory function.

Elevated androgens cannot be ascribed to PCOS without excluding other causessuch as congenital adrenal hyperplasia, Cushing’s syndrome and androgen-secretingtumours. These are uncommon conditions, with characteristic features that can usuallybe detected on history and/or examination. Late-onset (non-classical) congenitaladrenal hyperplasia (in most cases due to 21-hydroxylase deficiency) can be difficult todistinguish clinically from PCOS and it is debatable whether routine screening isnecessary. Much depends on the frequency of non-classical 21-hydroxylase deficiencyas a cause of hirsutism in any given clinic (it is low in most reproductive endocrineclinics, including SF’s in London).5 If necessary, non-classical adrenal hyperplasia with21-hydroxylase deficiency can be excluded using a basal morning 17-hydroxypro-gesterone level, with upper limits ranging between 2 and 3 ng/ml.19 Similarly, othercauses of oligo- or amenorrhoea such as premature ovarian failure, hyperprolactinae-mia, hyper- and hypothroidism, and hypogonadotropic hypogonadism should beexcluded.

The revised definition of PCOS encompasses clinical and biochemical criteria as wellas ovarian morphology. It is recognised that women with regular cycles andhyperandrogenism may be part of the syndrome. PCOS is diagnosed in the presenceof two of the following three criteria: (i) polycystic ovaries; (ii) oligo-/anovulation;(iii) or clinical or biochemical evidence of hyperandrogenism.5

Ultrasound diagnostic criteria for polycystic ovaries

The ultrasound criteria for polycystic ovaries are now agreed to be the presence of12 or more follicles measuring 2–9 mm in diameter and/or an increased ovarianvolume greater than 10 cm3 on either vaginal or abdominal ultrasound. If on ultrasoundexamination there is a follicle in excess of 10 mm in diameter, the ultrasound scanshould be repeated at a time of ovarian inactivity to calculate its volume.5 Onepolycystic ovary is sufficient to provide the diagnosis. The distribution of the folliclesand the description of the stroma are not included in these criteria. Increased stromalechogenicity and/or stromal volume are specific to polycystic ovaries20 but themeasurement of the ovarian volume (or area) is a good surrogate for the quantificationof the stroma in clinical practice.21 This description of polycystic ovaries does not applyif the woman is taking the oral contraceptive pill. The optimal time to perform thisassessment in regularly menstruating women is between the third and the fifth day ofthe menstrual cycle.

Hyperandrogenaemia

Hirsutism has frequently been used as the primary clinical indicator of androgen excess.However, although hirsutism is an important clinical sign, and often distressing forpatients, the assessment of hirsutism is often very subjective as few clinicians usestandardised scoring methods22 and many women will have undergone treatment forhirsutism prior to assessment. More information is needed regarding the normal rangeof hirsutism patterns, particularly between racial groups.

Acne is a reasonable indicator of hyperandrogenism, although studies are somewhatconflicting regarding the exact prevalence of androgen excess in these patients.23,24 Thesole presence of androgenic alopecia as an indicator of hyperandrogenism has been lesswell studied, although a recent study suggests that polycystic ovaries are present in

674 R. Hart et al

most women with a primary complaint of alopecia.25 However, alopecia is a relativelypoor marker of androgen excess, unless present in the oligo-ovulatory patient.26

The diagnosis of androgen excess using measurements of circulating androgens isproblematic. Substantial variability has been seen between assays and there is a lack ofnormative data as well as wide variability in the normal population. Furthermore,androgens may remain suppressed after discontinuation of hormonal treatment. Giventhese caveats, the measurement of serum androgens remains intrinsic to the definitionof PCOS and serum-free testosterone, or the free androgen index, appear to be themost sensitive methods of assessing hyperandrogenaemia, although a few patients withPCOS might have isolated elevations in dehydroepiandrosterone sulphate.5

Although LH is often raised in anovulatory PCOS (Table 2), this is not a particularlyhelpful diagnostic feature.27 LH is raised due to both an increased amplitude andfrequency of LH pulses.28 Tonically raised LH can have detrimental effects on oocytematurity and fertilization29, pregnancy and miscarriage rates30, although suppression ofLH has not been shown to improve pregnancy outcome.31

Insulin resistance

PCOS constitutes a major risk factor for gestational diabetes32 and type 2 diabetes.33

Of 254 overweight women with PCOS, 31% had impaired glucose tolerance (IGT) and7.5% were diabetic by WHO criteria. These percentages were 10.3 and 1.5% in thosewith PCOS and normal weight.33 There is a steady increase in the development of IGTand type 2 diabetes over time in PCOS. Norman et al34 observed the glycaemic controlof 67 women with PCOS over 6 years. Of those who were normoglycaemic at the startof the study, 9% developed impaired glucose tolerance and 8% developed type 2diabetes. For those with impaired glucose tolerance at the start of the study, 54%developed type 2 diabetes over the 6 years. Consequently, in view of the highprevalence of insulin resistance35 and impaired glucose tolerance in obese women withPCOS33,34, it is now recommended that an oral glucose tolerance test and a metabolicscreen for obese women (BMI . 27 kg/m2) is carried out in women with PCOS.

PREVALENCE OF POLYCYSTIC OVARY SYNDROME

The use of different diagnostic criteria for PCOS have undermined attempts to derivean accurate, population-based prevalence for this condition. The incidental finding ofpolycystic ovaries at the time of ultrasound examination is relatively frequent, occurring

Table 2. Percentage frequency of biochemical features of women with polycystic ovary syndrome.

Percentage frequency

Balen et al44, n ¼ 1741 (%) Franks14, n ¼ 300 (%)

Elevated serum LH 40 51

Elevated serum testosterone 29 50

Elevated serum prolactin 12 7

Reprinted from Ref. 9 with permission of Oxford University Press.

PCOS: definitions, prevalence and symptoms 675

Table 3. The prevalence of polycystic ovaries in the general population.

Authors Polson et al37 Tayob et al78 Clayton et al38 Farquhar et al39 Botis et al40 Cresswell et al62

Study population Volunteers recruited

from clinical and

secretarial staff at

St Mary’s Hospital,

London

Volunteers using a

low-dose combined

oral contraceptive pill,

recruited from

routine clinics at the

Margaret Pyke centre

and the Royal Free

Hospital, London

Volunteers born

between 1952 and

1969 recruited from a

list of a GP group

practice in Harrow,

London, by random

postal invitation

Volunteers recruited

from two electoral

rolls in Auckland New

Zealand, by random

postal invitation

Volunteers recruited

from women present-

ing to an outpatient

clinic for routine Papa

nicolaou smear

Volunteers born

between and 1953

recruited from Jessop

Hospital, Sheffield, by

invitation and per-

sonal interview

n n ¼ 257 n ¼ 120 n ¼ 190 n ¼ 183 n ¼ 1078 n ¼ 235

Response rate Unknown Unknown 18% 16% Unknown 68%

Age range 18–36 years 18–30 years

mean 24 years

18–36 years 18–45 years

mean 33 years

17–40 years 40–42 years

Prevalence (%) 22 22 22 21 17 21

95% CI 17–27% 14–30% 16–28% 14–27% 14–19% 16–26%

Reprinted from Ref. 9 with permission of Oxford University Press.

676

R.H

artet

al

in up to 33% of women36, although most studies report an incidence around 22% in anunselected population (see Table 3).37–40

In a study of 173 symptomatic women, the ultrasonographic appearance ofpolycystic ovaries was found in 92% of women with hirsutism with regular menstrualcycles, 87% of women with oligomenorrhoea, 57% of anovulatory women and 26% ofwomen with amenorrhoea.7 Interestingly, of those women with the sonographicappearance consistent with polycystic ovaries, up to 25% will be asymptomatic. Afurther study of women who had regular menstrual cycles but were anovulatorydemonstrated polycystic ovaries in 91% of cases.41

Using the NIH/NICHHD criteria for the diagnosis of PCOS, Knochenhauer et al42

estimated that 6.2% of 129 white and 3.4% of 145 black women attending for amandatory pre-employment medical examination had PCOS.

SYMPTOMS OF POLYCYSTIC OVARY SYNDROME

Women with polycystic ovaries and no other features of PCOS are regarded asasymptomatic, and do not report an increased time to conceive.43 However, they dodemonstrate a predisposition towards the development of OHSS.

Menstrual disturbance

In the largest series of women with PCOS, Balen et al44 reported that of the 1871women with at least one symptom of PCOS (using the older diagnostic criteria),approximately 30% had a regular menstrual cycle, 50% had oligomenorrhoea and 20%were amenorrhoeic. Consequently, the majority of women with PCOS have anabnormal menstrual cycle and the most frequent pattern is infrequent menstruationassociated with anovulation.

Goldzieher and Green45 suggested that approximately 85–90% of women witholigoamenorrhoea, and up to 30–40% of those with amenorrhoea, will have PCOS.Obesity appears to augment anovulation in PCOS through increased peripheraloestrogen production and increased pancreatic insulin production interfering with thehypothalamic–pituitary–ovarian axis and resulting in elevated LH levels, whichinterfere with follicular maturation.46 Weight increase might induce oligo- oramenorrhoea and weight loss can restore ovulation and regular cycles.2

Obesity

The reported prevalence of obesity in women with PCOS depends, to a large extent,on the type of clinic to which the patient presents and on the diagnostic criteria used.However, in most large studies 35–50% of women with PCOS are overweight(BMI . 25) or obese (BMI . 27 kg/m2).47,48 Abdominal adiposity is common, with anincreased waist–hip ratio.49 Obesity increases the risk for type 2 diabetes and up to30% of obese PCOS women have IGTand a further 7.5% will develop frank diabetes bytheir forties.33 Central obesity is thought to be a significant factor leading to the seven-fold increased risk of myocardial infarction in women with PCOS.50 However, thebeneficial effects of weight loss are consistently shown, in improving menstrual cyclefrequency, restoring ovulation and normalising biochemical indices, particularly insulinresistance.2,51,52 Due to the high prevalence of IGT and type 2 diabetes among obese

PCOS: definitions, prevalence and symptoms 677

women with PCOS, the consensus group advocates the screening of obese women(BMI . 27 kg/m2) with PCOS with an oral glucose tolerance test.33

The association of obesity and PCOS is not completely understood, although it isknown that in addition to raised serum insulin, LH and androgens, hypothalamicendorphins and leptin are raised in anovulatory overweight women. However, on losingweight the LH pulse frequency and amplitude and the leptin levels do not appear toalter prior to resumption of menstruation.46

Hirsutism

Hirsutism in women describes the growth of terminal hair in an adult male distribution.Common presentations are excess facial hair, hair on the chest between the breasts andhair on the lower abdomen. Hirsutism is affected by familial and racial factors.Knochenhauer et al42 described a prevalence of ‘abnormal’ Ferriman–Gallwey scoresof at least 6, 8 and 10 in the unselected female population of 8.0, 2.8 and 1.6% in whitewomen and 7.1, 6.1 and 2.1% in black women. In those with PCOS the incidence was ashigh as 70%.53

The prevalence and extent of hirsutism is partially racially determined and it is morecommon with darker skin and rare in Japanese women with PCOS.54 Hirsutism inPCOS reflects androgen excess, predominantly local dihydrotestosterone. The dermalpapillae express androgen receptors that directly influence the size of the hair follicleand hence the hair produced. Weight loss has been shown to reduce hirsutism.51,55

Exogenous oestrogens (such as the combined oral contraceptive pill) will suppressovarian androgen production and stimulate sex-hormone binding globulin, hencereducing free circulating testosterone.

Androgenic alopecia

This describes the progressive pattern of loss of scalp terminal hair that is commonwith baldness in men and much less common in women, although probablyunderdiagnosed in those with PCOS.14 To present with alopecia requires a familialpredisposition to baldness and an associated increase in circulating androgens,consequently not all women with an excess of circulating androgens will suffer fromandrogenic alopecia. A recent study of 89 women, of mixed ethnic origin, withandrogenic alopecia demonstrated a 67% incidence of polycystic ovaries. The controlgroup of women had polycystic ovaries in 27% of cases, consistent with previousstudies.25 Of women with androgenic alopecia, 21% were also hirsute, compared with4% of the control group. Interestingly, the women with alopecia had highertestosterone, androstenedione and free androgen index than controls but few hadfrankly abnormal androgen levels.25

Acne

Acne is an inflammatory disorder of the hair follicle and its associated sebaceous andapocrine gland. It is present in up to one-third of women with PCOS.14,44 Unlikeandrogenic alopecia and hirsutism, the principal problem for women with acne is anincreased sebaceous secretion and serum androgen levels are often not raised.23,24

678 R. Hart et al

Acanthosis nigricans

Acanthosis nigricans is a mucocutaneous eruption that occurs most frequently in theaxillae, skin flexures and the nape of the neck. It is manifest by increased pigmentationand papillomatosis. It is a marker associated with insulin resistance and compensatoryincreased insulin secretion.56 It is thought to be present in women with PCOS inbetween 1 and 3% of cases14,44 and may present more commonly in adolescents withPCOS.57

THE NATURAL HISTORY OF POLYCYSTIC OVARY SYNDROME

Although PCOS cannot be diagnosed until 2–3 years after menarche, the condition islikely to originate in early childhood or even fetal life. Excessive androgen exposure inutero has been demonstrated in animal models to produce a PCOS-like syndrome.58

Similarly, the clinical and biochemical features of PCOS might also arise as aconsequence of genetically determined hypersecretion of androgens by the ovaryduring early childhood or puberty.59 Androgens might play a part in abnormal earlyovarian folliculogenesis, which could, in turn, lead to abnormal function of theca cells inmature follicles, thus setting up a self-propagating cycle of abnormal follicular growthand function.59 The resulting hyperandrogenism ‘programmes’ the hypothalamic–pituitary unit, causing excess LH secretion, and encourages the preferential abdominaladiposity that predisposes to insulin resistance. The severity of hyperinsulinaemia andinsulin resistance is further influenced by both genetic factors and environmentalfactors, notably obesity.59

The familial clustering of PCOS would suggest that there is a strong geneticcomponent to the origin of PCOS. To date, the candidate genes for PCOS that havebeen analysed and possibly associated with the condition have been those involved withsteroid hormone synthesis (CYP11A, CYP17 and the androgen receptor), carbo-hydrate metabolism (insulin receptor, insulin gene), gonadotrophin action (follistatingene) and genes in the histocompatibility region.60,61

Impaired fetal growth, as well as a normal and even higher weight at birth, have beenreported as a factor in the aetiology of PCOS.62–64 The effect of PCOS on the age ofmenarche is unclear but there is evidence for an increased risk of precocious puberty ingirls who will develop PCOS.65,66 However, there is also evidence to the contrary,suggesting that menarche occurs later in these girls.64

In later life, women with PCOS are potentially at a seven times increased risk ofdeveloping type 2 diabetes.17,33,67 There is evidence to suggest that women with PCOSare also at increased risk of cardiovascular disease50, although some epidemiologicalstudies have demonstrated no increased incidence of coronary disease events inwomen with a history of PCOS.67,68 Despite this report, hyperinsulinaemic womenwith PCOS have an adverse lipid profile of the type associated with an increased risk ofcoronary heart disease.69,70 Indeed, women with PCOS are at increased risk foratherosclerosis, as there is evidence that they have an increased coronary arterycalcification, compared to age- and weight-matched controls.71

Unopposed oestrogen arising from chronic anovulation may constitute a risk factorfor endometrial hyperplasia and cancer, although epidemiological evidence to linkPCOS and endometrial cancer is limited.72 The presentation and implications of PCOSin later life, particularly around the time of menopause, require further investigation.

PCOS: definitions, prevalence and symptoms 679

There is some evidence that menstrual cyclicity returns with age73 and that serumtestosterone levels decrease.74

The most common presentations of PCOS in adolescence include menstrualdysfunction and hyperandrogenism.75 Early maturation of pubic hair might be an earlyindication of PCOS.76 Oligomenorrhoea in adolescence is relatively common and hastraditionally been seen to represent normal physiological maturation of thehypothalamus–pituitary–ovarian axis. There is now increasing evidence thatoligomenorrhoea in adolescents is likely to represent PCOS.77 However, few publishedstudies have followed-up menstrual patterns in large populations of adolescents orsystematically assessed circulating androgens or ovarian morphology.

SUMMARY

PCOS is the most common endocrine disorder of women in their reproductive years. Italso has a huge implication for society as a whole, as these women are at an increasedrisk of obesity, have a markedly increased risk of diabetes and death after a myocardialevent and might also be at long-term risk for other cardiovascular disease. A recentconsensus meeting has led to the formulation of unifying diagnostic criteria for thedefinition of PCOS to enable an internationally agreed terminology to be used. Thesecriteria rely on the presence of two of the following: (i) oligo-/anovulation; (ii) clinical orbiochemical evidence of hyperandrogenism; and (iii) the presence of polycytic ovaries.

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Practice points

The new internationally agreed definition of PCOS – two out of three of:

† presence of polycystic ovaries on ultrasound examination† oligo-/anovulation† clinical or biochemical evidence of androgen excess† incidence of symptoms in women with PCOS: menstrual cycle disturbance

(70%), obesity (50%), hirsutism (70%), androgenic alopecia (10%) and acne(30%)

† the incidence of PCOS is approximately 1 in 12 women of reproductive age

Research agenda

† development of normative data for androgens, particularly in adolescents andolder women

† clarification of the relevance and implications of a high LH in PCOS† long-term follow-up of PCOS women to quantify their cardiovascular risk

680 R. Hart et al

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