Polycystic ovary syndrome: Difference between revisions

Polycystic ovary syndrome
Polycystic ovary syndrome
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Polycystic ovary syndrome (PCOS), also called hyperandrogenic anovulation (HA),^[1] or Stein-Leventhal syndrome,^[2] is one of the most common endocrine disorders among people with ovaries. PCOS has a diverse range of causes that are not entirely understood, but there is evidence that it is largely a genetic disease.^[3]^[4]^[5] Others say it is generally a metabolic dysfunction, since it is reversible. Even though considered as a gynecological problem, PCOS consists of 28 clinical symptoms.

Even though the name suggest that the ovaries are the cornerstone of disease pathology, cysts are the 'result' , not the cause of the disease. Symptoms of PCOS will persist even if both ovaries are removed; the disease can appear even if cysts are absent. Since its first description by Stein and Leventhal in 1935, the criteria of diagnosis, symptoms, and causative factors are subject to debate. Gynecologists often see it as a gynecological problem, with ovary as the primary organ affected. However, recent insights shows a multisystem disorder, with the primary problems lying in hormonal regulation in hypothalamus, with involvement of many organs. The name PCOD is used when there is ultrasonographic evidence. The term PCOS is used since there is a wide spectrum of symptoms possible, and cysts in the ovaries are seen only in 15% of people.^[6] Treatments like wedge resection or laparoscopic drilling of ovaries are still performed around the world, based on this false 'ovary-focused' belief.

PCOS produces symptoms in approximately 5% to 10% of people with ovaries of reproductive age (approximately 12 to 45 years old). It is thought to be one of the leading causes of subfertility in people with ovaries^[7]^[8]^[9] and the most frequent endocrine problem in people with ovaries of reproductive age.^[10] Finding that the ovaries appear polycystic on ultrasound is common, but it is not an absolute requirement in all definitions of the disorder.

The most common immediate symptoms are anovulation, excess androgenic hormones, and insulin resistance. Anovulation results in irregular menstruation, amenorrhea, and ovulation-related infertility. Hormone imbalance generally causes acne and hirsutism. Insulin resistance is associated with obesity, type 2 diabetes, and high cholesterol levels.^[11] The symptoms and severity of the syndrome vary greatly among affected people.

Signs and symptoms

Common symptoms of PCOS include the following:

Menstrual disorders: PCOS mostly produces oligomenorrhea (few menstrual periods) or amenorrhea (no menstrual periods), but other types of menstrual disorders may also occur.^[10]^[12]
Infertility:[12] This generally results directly from chronic anovulation (lack of ovulation).[10]
High levels of masculinizing hormones: The most common signs are acne and hirsutism (male pattern of hair growth), but it may produce hypermenorrhea (heavy and prolonged menstrual periods), androgenic alopecia (increase hair thinning or diffuse hair loss), or other symptoms.^[10]^[13] Approximately three-quarters of people with PCOS (by the diagnostic criteria of NIH/NICHD 1990) have evidence of hyperandrogenemia.^[14]
Metabolic syndrome:^[12] This appears as a tendency towards central obesity and other symptoms associated with insulin resistance.^[10] Serum insulin, insulin resistance, and homocysteine levels are higher in people with PCOS.^[15]

When Asian people with ovaries are affected with PCOS, they are less likely to develop hirsutism than people of other ethnic backgrounds.^[16]

Cause

PCOS is a heterogeneous disorder of uncertain cause.^[3]^[4]^[12] There is strong evidence that it is a genetic disease. Such evidence includes the familial clustering of cases, greater concordance in monozygotic compared with dizygotic twins and heritability of endocrine and metabolic features of PCOS.^[3]^[4]^[5]

The genetic component appears to be inherited in an autosomal dominant fashion with high genetic penetrance but variable expressivity in females; this means that each child has a 50% chance of inheriting the predisposing genetic variant(s) from a parent, and, if a daughter receives the variant(s), the daughter will have the disease to some extent.^[4]^[17]^[18]^[19] The genetic variant(s) can be inherited from either the father or the mother, and can be passed along to both sons (who may be asymptomatic carriers or may have symptoms such as early baldness and/or excessive hair) and daughters, who will show signs of PCOS.^[17]^[19] The allele appears to manifest itself at least partially via heightened androgen levels secreted by ovarian follicle theca cells from people with the allele.^[18] The exact gene affected has not yet been identified.^[4]^[5]^[20]

The clinical severity of PCOS symptoms appears to be largely determined by factors such as obesity.^[5]^[10]

Diagnosis

Not all people with PCOS have polycystic ovaries (PCO), nor do all people with ovarian cysts have PCOS; although a pelvic ultrasound is a major diagnostic tool, it is not the only one.^[21] The diagnosis is straightforward using the Rotterdam criteria, even when the syndrome is associated with a wide range of symptoms.

Polycystic Ovary as seen on Sonography
Transvaginal ultrasound scan of polycystic ovary
Polycystic Ovary as seen on Sonography

Definition

Two definitions are commonly used:

NIH

In 1990 a consensus workshop sponsored by the NIH/NICHD suggested that a person has PCOS if she has all of the following:^[22]

oligoovulation
signs of androgen excess (clinical or biochemical)
exclusion of other disorders that can result in menstrual irregularity and hyperandrogenism

Rotterdam

In 2003 a consensus workshop sponsored by ESHRE/ASRM in Rotterdam indicated PCOS to be present if any 2 out of 3 criteria are met^[23]

oligoovulation and/or anovulation
excess androgen activity
polycystic ovaries (by gynecologic ultrasound)
Other entities are excluded that would cause these.^[10]^[24]

The Rotterdam definition is wider, including many more people with ovaries, the most notable ones being designated people with ovaries without androgen excess. Critics say that findings obtained from the study of people with ovaries with androgen excess cannot necessarily be extrapolated to people with ovaries without androgen excess.^[25]^[26]

Androgen Excess PCOS Society: In 2006, the Androgen Excess PCOS Society suggested a tightening of the diagnostic criteria to all of:^[10]

excess androgen activity
oligoovulation/anovulation and/or polycystic ovaries
exclusion of other entities that would cause excess androgen activity

Standard diagnostic assessments

History-taking, specifically for menstrual pattern, obesity, hirsutism, and the absence of breast development. A clinical prediction rule found that these four questions can diagnose PCOS with a sensitivity of 77.1% (95% confidence interval [CI] 62.7%–88.0%) and a specificity of 93.8% (95% CI 82.8%–98.7%).^[27]
Gynecologic ultrasonography, specifically looking for small ovarian follicles. These are believed to be the result of disturbed ovarian function with failed ovulation, reflected by the infrequent or absent menstruation that is typical of the condition. In a normal menstrual cycle, one egg is released from a dominant follicle – in essence, a cyst that bursts to release the egg. After ovulation, the follicle remnant is transformed into a progesterone-producing corpus luteum, which shrinks and disappears after approximately 12–14 days. In PCOS, there is a so-called "follicular arrest"; i.e., several follicles develop to a size of 5–7 mm, but not further. No single follicle reaches the preovulatory size (16 mm or more). According to the Rotterdam criteria, 12 or more small follicles should be seen in an ovary on ultrasound examination.^[22] More recent research suggests that there should be at least 25 follicles in an ovary to designate it as having polycystic ovarian morphology (PCOM) in people with ovaries aged 18–35 years.^[28] The follicles may be oriented in the periphery, giving the appearance of a 'string of pearls'.^[29] If a high resolution transvaginal ultrasonography machine is not available, an ovarian volume of at least 10 ml is regarded as an acceptable definition of having polycystic ovarian morphology instead of follicle count.^[28]
Laparoscopic examination may reveal a thickened, smooth, pearl-white outer surface of the ovary. (This would usually be an incidental finding if laparoscopy were performed for some other reason, as it would not be routine to examine the ovaries in this way to confirm a diagnosis of PCOS.)^{[citation needed]}
Serum (blood) levels of androgens (male hormones), including androstenedione and testosterone may be elevated.^[10] Dehydroepiandrosterone sulfate levels above 700-800 µg/dL are highly suggestive of adrenal dysfunction because DHEA-S is made exclusively by the adrenal glands.^[30]^[31] The free testosterone level is thought to be the best measure,^[31]^[32] with ~60% of PCOS patients demonstrating supranormal levels.^[14] The Free androgen index (FAI) of the ratio of testosterone to sex hormone-binding globulin (SHBG) is high^[10]^[31] and is meant to be a predictor of free testosterone, but is a poor parameter for this and is no better than testosterone alone as a marker for PCOS,^[33] possibly because FAI is correlated with the degree of obesity.^[34]

Some other blood tests are suggestive but not diagnostic. The ratio of LH (Luteinizing hormone) to FSH (Follicle-stimulating hormone), when measured in international units, is elevated in people with ovaries with PCOS. Common cut-offs to designate abnormally high LH/FSH ratios are 2:1^[35] or 3:1^[31] as tested on Day 3 of the menstrual cycle. The pattern is not very specific and a ratio of 2:1 or higher was present in less than 50% of people with ovaries with PCOS in one study.^[35] There are often low levels of sex hormone-binding globulin,^[31] in particular among obese or overweight people with ovaries.^{[citation needed]}

Anti-Müllerian hormone (AMH) is increased in PCOS, and may become part of its diagnostic criteria.^[36]^[37]

Associated conditions

Fasting biochemical screen and lipid profile^[31]
2-Hour oral glucose tolerance test (GTT) in people with ovaries with risk factors (obesity, family history, history of gestational diabetes)^[10] may indicate impaired glucose tolerance (insulin resistance) in 15–33% of people with PCOS.^[31] Frank diabetes can be seen in 65–68% of people with this condition.^{[citation needed]} Insulin resistance can be observed in both normal weight and overweight people, although it is more common in the latter (and in those matching the stricter NIH criteria for diagnosis); 50–80% of people with PCOS may have insulin resistance at some level.^[10]
Fasting insulin level or GTT with insulin levels (also called IGTT). Elevated insulin levels have been helpful to predict response to medication and may indicate needing higher dosages of metformin or the use of a second medication to significantly lower insulin levels. Elevated blood sugar and insulin values do not predict who responds to an insulin-lowering medication, low-glycemic diet, and exercise. Many people with normal levels may benefit from combination therapy. A hypoglycemic response in which the two-hour insulin level is higher and the blood sugar lower than fasting is consistent with insulin resistance. A mathematical derivation known as the HOMAI, calculated from the fasting values in glucose and insulin concentrations, allows a direct and moderately accurate measure of insulin sensitivity (glucose-level x insulin-level/22.5).^{[citation needed]}
Glucose tolerance testing (GTT) instead of fasting glucose can increase diagnosis of increased glucose tolerance and frank diabetes among people with PCOS according to a prospective controlled trial.^[38] While fasting glucose levels may remain within normal limits, oral glucose tests revealed that up to 38% of asymptomatic people with PCOS (versus 8.5% in the general population) actually had impaired glucose tolerance, 7.5% of those with frank diabetes according to ADA guidelines.^[38]

Differential diagnosis

Other causes of irregular or absent menstruation and hirsutism, such as hypothyroidism, congenital adrenal hyperplasia (21-hydroxylase deficiency), Cushing's syndrome, hyperprolactinemia, androgen secreting neoplasms, and other pituitary or adrenal disorders, should be investigated.^[10]^[24]^[31] PCOS has been reported in other insulin-resistant situations such as acromegaly.^{[citation needed]}

Pathogenesis

Polycystic ovaries develop when the ovaries are stimulated to produce excessive amounts of male hormones (androgens), in particular testosterone, by either one or a combination of the following (almost certainly combined with genetic susceptibility^[18]):

the release of excessive luteinizing hormone (LH) by the anterior pituitary gland^{[citation needed]}
through high levels of insulin in the blood (hyperinsulinaemia) in people whose ovaries are sensitive to this stimulus^[12]

Also, reduced levels of sex-hormone-binding globulin can result in increased free androgens.^{[citation needed]}

The syndrome acquired its most widely used name due to the common sign on ultrasound examination of multiple (poly) ovarian cysts. These "cysts" are actually immature follicles not cysts. The follicles have developed from primordial follicles, but the development has stopped ("arrested") at an early antral stage due to the disturbed ovarian function. The follicles may be oriented along the ovarian periphery, appearing as a 'string of pearls' on ultrasound examination.^{[citation needed]}

People with PCOS experience an increased frequency of hypothalamic GnRH pulses, which in turn results in an increase in the LH/FSH ratio.^[39]

A majority of people with PCOS have insulin resistance and/or are obese. Their elevated insulin levels contribute to or cause the abnormalities seen in the hypothalamic-pituitary-ovarian axis that lead to PCOS. Hyperinsulinemia increases GnRH pulse frequency, LH over FSH dominance, increased ovarian androgen production,^[12] decreased follicular maturation, and decreased SHBG binding; all these steps contribute to the development of PCOS.^{[citation needed]} Insulin resistance is a common finding among people with a normal weight as well as overweight people.^[10]^[15]

In many cases, PCOS is characterised by a complex positive feedback loop of insulin resistance and hyperandrogenism. In most cases, it cannot be determined which (if any) of those two should be regarded causative. Experimental treatment with either antiandrogens or insulin-sensitizing agents improves both hyperandrogenism and insulin resistance.^{[citation needed]}

Adipose tissue possesses aromatase, an enzyme that converts androstenedione to estrone and testosterone to estradiol. The excess of adipose tissue in obese people creates the paradox of having both excess androgens (which are responsible for hirsutism and virilization) and estrogens (which inhibits FSH via negative feedback).^[40]

PCOS may be associated with chronic inflammation,^[12]^[41] with several investigators correlating inflammatory mediators with anovulation and other PCOS symptoms.^[42]^[43] Similarly, there seems to be a relation between PCOS and increased level of oxidative stress.^[44]

It has previously been suggested that the excessive androgen production in PCOS could be caused by a decreased serum level of IGFBP-1, in turn increasing the level of free IGF-I, which stimulates ovarian androgen production, but recent data concludes this mechanism to be unlikely.^[45]

PCOS has also been associated with a specific FMR1 sub-genotype. The research suggests that people with ovaries with heterozygous-normal/low FMR1 have polycystic-like symptoms of excessive follicle-activity and hyperactive ovarian function.^[46]

Management

Medical treatment of PCOS is tailored to the woman's goals. In broad terms, these may be considered under four categories:

Lowering of insulin resistance levels
Restoration of fertility
Treatment of hirsutism or acne
Restoration of regular menstruation, and prevention of endometrial hyperplasia and endometrial cancer

In each of these areas, there is considerable debate as to the optimal treatment. One of the major reasons for this is the lack of large-scale clinical trials comparing different treatments. Smaller trials tend to be less reliable and hence may produce conflicting results.

General interventions that help to reduce weight or insulin resistance can be beneficial for all these aims, because they address what is believed to be the underlying cause.

As PCOS appears to cause significant emotional distress, appropriate support may be useful.^[47]

Diet

Where PCOS is associated with overweight or obesity, successful weight loss is the most effective method of restoring normal ovulation/menstruation, but many people find it very difficult to achieve and sustain significant weight loss. A scientific review in 2013 found similar decreases in weight and body composition and improvements in pregnancy rate, menstrual regularity, ovulation, hyperandrogenism, insulin resistance, lipids, and quality of life to occur with weight loss independent of diet composition.^[48] Still, a low GI diet, in which a significant part of total carbohydrates are obtained from fruit, vegetables, and whole-grain sources, has resulted in greater menstrual regularity than a macronutrient-matched healthy diet.^[48] Vitamin D deficiency may play some role in the development of the metabolic syndrome, so treatment of any such deficiency is indicated.^[49]

Medications

Reducing insulin resistance by improving insulin sensitivity through medications such as metformin, and the newer thiazolidinedione (glitazones), have been an obvious approach and initial studies seemed to show effectiveness.^[12]^[49]^[50] Although metformin is not licensed for use in PCOS, the United Kingdom's National Institute for Health and Clinical Excellence recommended in 2004 that people with PCOS and a body mass index above 25 be given metformin when other therapy has failed to produce results.^[51] However subsequent reviews in 2008 and 2009 have noted that randomised control trials have in general not shown the promise suggested by the early observational studies.^[52]^[53] A review in 2014 concluded that there is no evidence that metformin could cause any increased risk of major birth defects in people affected by PCOS and treated during the first trimester.^[54]

Infertility

Not all people with PCOS have difficulty becoming pregnant. For those that do, anovulation or infrequent ovulation is a common cause. Other factors include changed levels of gonadotropins, hyperandrogenemia and hyperinsulinemia.^[55] Like people without PCOS, people with PCOS that are ovulating may be infertile due to other causes, such as tubal blockages due to a history of sexually transmitted diseases.

For overweight, anovulatory people with PCOS, weight loss and diet adjustments, especially to reduce the intake of simple carbohydrates, are associated with resumption of natural ovulation.

For those people that after weight loss still are anovulatory or for anovulatory lean people, then the ovulation-inducing medications clomiphene citrate^[49] and FSH are the principal treatments used to promote ovulation.^[12] Previously, the anti-diabetes medication metformin was recommended treatment for anovulation,^[12] but it appears less effective than clomiphene.^[56]

For people not responsive to clomiphene and diet and lifestyle modification, there are options available including assisted reproductive technology procedures such as controlled ovarian hyperstimulation with follicle-stimulating hormone (FSH) injections followed by in vitro fertilisation (IVF).

Though surgery is not commonly performed, the polycystic ovaries can be treated with a laparoscopic procedure called "ovarian drilling" (puncture of 4–10 small follicles with electrocautery, laser, or biopsy needles), which often results in either resumption of spontaneous ovulations^[49] or ovulations after adjuvant treatment with clomiphene or FSH.^{[citation needed]} (Ovarian wedge resection is no longer used as much due to complications such as adhesions and the presence of frequently effective medications.) There are, however, concerns about the long-term effects of ovarian drilling on ovarian function.^[49]

Hirsutism and acne

When appropriate (e.g., in people of child-bearing age who require contraception), a standard contraceptive pill is frequently effective in reducing hirsutism.^[12]^[49] A common choice of contraceptive pill is one that contains cyproterone acetate; in the UK, the available brands are Dianette/Diane. Cyproterone acetate is a progestogen with anti-androgen effects that block the action of male hormones that are believed to contribute to acne and the growth of unwanted facial and body hair.^{[citation needed]} On the other hand, progestogens such as norgestrel and levonorgestrel should be avoided due to their androgenic effects.^[49]

Other drugs with anti-androgen effects include flutamide,^[57] and spironolactone,^[12]^[49] which can give some improvement in hirsutism. Spironolactone is probably the most-commonly used drug in the US. Metformin can reduce hirsutism, perhaps by reducing insulin resistance, and is often used if there are other features such as insulin resistance, diabetes, or obesity that should also benefit from metformin. Eflornithine (Vaniqa) is a drug that is applied to the skin in cream form, and acts directly on the hair follicles to inhibit hair growth. It is usually applied to the face.^[49] Medications that reduce acne by indirect hormonal effects also include ergot dopamine agonists such as bromocriptine.^{[citation needed]} 5-alpha reductase inhibitors (such as finasteride and dutasteride) may also be used;^[58] they work by blocking the conversion of testosterone to dihydrotestosterone (the latter of which responsible for most hair growth alterations and androgenic acne).

Although these agents have shown significant efficacy in clinical trials (for oral contraceptives, in 60–100% of individuals^[49]), the reduction in hair growth may not be enough to eliminate the social embarrassment of hirsutism, or the inconvenience of plucking or shaving. Individuals vary in their response to different therapies. It is usually worth trying other drug treatments if one does not work, but drug treatments do not work well for all individuals. For removal of facial hairs, electrolysis, or laser treatments are – at least for some – faster and more efficient alternatives than the above-mentioned medical therapies.^{[citation needed]}

Menstrual irregularity and endometrial hyperplasia

If fertility is not the primary aim, then menstruation can usually be regulated with a contraceptive pill.^[12]^[49] The purpose of regulating menstruation, in essence, is for the woman's convenience, and perhaps her sense of well-being; there is no medical requirement for regular periods, as long as they occur sufficiently often.

If a regular menstrual cycle is not desired, then therapy for an irregular cycle is not necessarily required. Most experts say that, if a menstrual bleed occurs at least every three months, then the endometrium (womb lining) is being shed sufficiently often to prevent an increased risk of endometrial abnormalities or cancer.^[59] If menstruation occurs less often or not at all, some form of progestogen replacement is recommended.^[58] An alternative is oral progestogen taken at intervals (e.g., every three months) to induce a predictable menstrual bleeding.^[12]

Alternative medicine

There is insufficient evidence to conclude an effect from D-chiro-inositol.^[60] Myo-inositol however appears to be effective based on a systematic review.^[61]

Prognosis

People with PCOS are at risk for the following:

Endometrial hyperplasia and endometrial cancer (cancer of the uterine lining) are possible, due to overaccumulation of uterine lining, and also lack of progesterone resulting in prolonged stimulation of uterine cells by estrogen.^[12]^[22]^[62] It is not clear whether this risk is directly due to the syndrome or from the associated obesity, hyperinsulinemia, and hyperandrogenism.^[63]^[64]^[65]^[66]
Insulin resistance/Type II diabetes.^[12] A review published in 2010 concluded that people with PCOS have an elevated prevalence of insulin resistance and type II diabetes, even when controlling for body mass index (BMI).^[22]^[67] PCOS also makes a woman, particularly if obese, prone to gestational diabetes.^[12]
High blood pressure, in particular if obese and/or during pregnancy^[12]
Depression/Depression with Anxiety^[10]^[68]
Dyslipidemia^[12] – disorders of lipid metabolism — cholesterol and triglycerides. People with PCOS show a decreased removal of atherosclerosis-inducing remnants, seemingly independent of insulin resistance/Type II diabetes.^[69]
Cardiovascular disease,^[12]^[22] with a meta-analysis estimating a 2-fold risk of arterial disease for people with ovaries with PCOS relative to people with ovaries without PCOS, independent of BMI.^[70]
Strokes^[22]
Weight gain^[12]
Miscarriage^[7]^[8]
Sleep apnea, particularly if obesity is present^[12]
Non-alcoholic fatty liver disease, again particularly if obesity is present^[12]
Acanthosis nigricans (patches of darkened skin under the arms, in the groin area, on the back of the neck)^[22]
Autoimmune thyroiditis^[71]

Early diagnosis and treatment may reduce the risk of some of these, such as type 2 diabetes and heart disease.^[12]

The risk of ovarian cancer and breast cancer is not significantly increased overall.^[62]

Epidemiology

The prevalence of PCOS depends on the choice of diagnostic criteria. The World Health Organization estimates that it affects 116 million women worldwide as of 2010 (3.4% of women).^[72] One community-based prevalence study using the Rotterdam criteria found that about 18% of women had PCOS, and that 70% of them were previously undiagnosed.^[10]

One study in the United Kingdom concluded that the risk of PCOS development was higher in lesbian women than in heterosexuals.^[73] However, two subsequent studies of women with PCOS have not replicated this finding.^[74]^[75] Ultrasonographic findings of polycystic ovaries are found in 8-25% of normal women.^[76]^[77]^[78]^[79] 14% women on oral contraceptives are found to have polycystic ovaries.^[77]

History

The condition was first described in 1935 by American gynecologists Irving F. Stein, Sr. and Michael L. Leventhal, from whom its original name of Stein-Leventhal syndrome is taken.^[21]^[22]

The earliest published description of a person with what is now recognized as PCOS was in 1721 in Italy.^[80] Cyst-related changes to the ovaries were described in 1844.^[80]

Names

Other names for this syndrome include polycystic ovary disease, functional ovarian hyperandrogenism, ovarian hyperthecosis, sclerocystic ovary syndrome, and Stein-Leventhal syndrome. The eponymous last option is the original name; it is now used, if at all, only for the subset of people with ovaries with all the symptoms of amenorrhea with infertility, hirsutism, and enlarged polycystic ovaries.^[21]

Most common names for this disease derive from a typical finding on medical images, called a polycystic ovary.^[12] A polycystic ovary has an abnormally large number of developing eggs visible near its surface,^[21] looking like many small cysts^[81] or a string of pearls.

References

^ Kollmann M, Martins WP, Raine-Fenning N (2014). "Terms and thresholds for the ultrasound evaluation of the ovaries in people with hyperandrogenic anovulation". Hum. Reprod. Update. 20 (3): 463–4. doi:10.1093/humupd/dmu005. PMID 24516084.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ "USMLE-Rx". MedIQ Learning, LLC. 2014. Stein-Leventhal syndrome, also known as polycystic overy syndrome (PCOS), is a disorder characterized by hirsutism, obesity, and amenorrhea because of luteinizing hormone-resistant cystic ovaries. {{cite web}}: |access-date= requires |url= (help); Missing or empty |url= (help)
^ ^a ^b ^c Page 836 (Section:Polycystic ovary syndrome) in: Fauser BC, Diedrich K, Bouchard P, Domínguez F, Matzuk M, Franks S, Hamamah S, Simón C, Devroey P, Ezcurra D, Howles CM (2011). "Contemporary genetic technologies and female reproduction". Human Reproduction Update. 17 (6): 829–847. doi:10.1093/humupd/dmr033. PMC 3191938. PMID 21896560.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ ^a ^b ^c ^d ^e Legro RS, Strauss JF (September 2002). "Molecular progress in infertility: polycystic ovary syndrome". Fertility and Sterility. 78 (3): 569–576. doi:10.1016/S0015-0282(02)03275-2. PMID 12215335.
^ ^a ^b ^c ^d Diamanti-Kandarakis E, Kandarakis H, Legro RS (August 2006). "The role of genes and environment in the etiology of PCOS". Endocrine. 30 (1): 19–26. doi:10.1385/ENDO:30:1:19. PMID 17185788.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Dunaif, A; Fauser, BC (Nov 2013). "Renaming PCOS--a two-state solution". The Journal of clinical endocrinology and metabolism. 98 (11): 4325–8. PMID 24009134.
^ ^a ^b Goldenberg N, Glueck C (2008). "Medical therapy in women with polycystic ovary syndrome before and during pregnancy and lactation". Minerva Ginecol. 60 (1): 63–75. PMID 18277353.
^ ^a ^b Boomsma CM, Fauser BC, Macklon NS (2008). "Pregnancy complications in women with polycystic ovary syndrome". Semin. Reprod. Med. 26 (1): 72–84. doi:10.1055/s-2007-992927. PMID 18181085.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Azziz R, Woods KS, Reyna R, Key TJ, Knochenhauer ES, Yildiz BO (June 2004). "The Prevalence and Features of the Polycystic Ovary Syndrome in an Unselected Population". Journal of Clinical Endocrinology & Metabolism. 89 (6): 2745–9. doi:10.1210/jc.2003-032046. PMID 15181052.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p Teede H, Deeks A, Moran L (2010). "Polycystic ovary syndrome: a complex condition with psychological, reproductive and metabolic manifestations that impacts on health across the lifespan". BMC Med. 8: 41. doi:10.1186/1741-7015-8-41. PMC 2909929. PMID 20591140.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
^ "Polycystic ovary syndrome".
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p ^q ^r ^s ^t ^u ^v ^w ^x ^y Mayo Clinic Staff (4 April 2011). "Polycystic Ovary Syndrome – All". MayoClinic.com. Mayo Clinic. Retrieved 15 November 2011.
^ Christine Cortet-Rudelli, Didier Dewailly (Sep 21, 2006). "Diagnosis of Hyperandrogenism in Female Adolescents". Hyperandrogenism in Adolescent Girls. Armenian Health Network, Health.am. Retrieved 2006-11-21.
^ ^a ^b Huang A, Brennan K, Azziz R (April 2010). "Prevalence of hyperandrogenemia in the polycystic ovary syndrome diagnosed by the National Institutes of Health 1990 criteria". Fertil. Steril. 93 (6): 1938–41. doi:10.1016/j.fertnstert.2008.12.138. PMC 2859983. PMID 19249030.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ ^a ^b Nafiye Y, Sevtap K, Muammer D, Emre O, Senol K, Leyla M (April 2010). "The effect of serum and intrafollicular insulin resistance parameters and homocysteine levels of nonobese, nonhyperandrogenemic polycystic ovary syndrome patients on in vitro fertilization outcome". Fertil. Steril. 93 (6): 1864–9. doi:10.1016/j.fertnstert.2008.12.024. PMID 19171332.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Carmina E, Koyama T, Chang L, Stanczyk FZ, Lobo RA (December 1992). "Does ethnicity influence the prevalence of adrenal hyperandrogenism and insulin resistance in polycystic ovary syndrome?". American journal of obstetrics and gynecology. 167 (6): 1807–12. doi:10.1016/0002-9378(92)91779-a. PMID 1471702.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ ^a ^b Crosignani PG, Nicolosi AE (2001). "Polycystic ovarian disease: heritability and heterogeneity". Hum. Reprod. Update. 7 (1): 3–7. doi:10.1093/humupd/7.1.3. PMID 11212071.
^ ^a ^b ^c Strauss JF (November 2003). "Some new thoughts on the pathophysiology and genetics of polycystic ovary syndrome". Annals of the New York Academy of Sciences. 997: 42–48. doi:10.1196/annals.1290.005. PMID 14644808.
^ ^a ^b Ada Hamosh (12 September 2011). "POLYCYSTIC OVARY SYNDROME 1; PCOS1". OMIM. McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine. Retrieved 15 November 2011.
^ Amato P, Simpson JL (October 2004). "The genetics of polycystic ovary syndrome". Best Pract Res Clin Obstet Gynaecol. 18 (5): 707–18. doi:10.1016/j.bpobgyn.2004.05.002. PMID 15380142.
^ ^a ^b ^c ^d Marrinan, Greg (20 April 2011). Lin, Eugene C (ed.). "Imaging in Polycystic Ovary Disease". eMedicine. eMedicine. Retrieved 19 November 2011.
^ ^a ^b ^c ^d ^e ^f ^g ^h Richard Scott Lucidi (25 October 2011). "Polycystic Ovarian Syndrome". eMedicine. Retrieved 19 November 2011.
^ Azziz R (March 2006). "Diagnosis of Polycystic Ovarian Syndrome: The Rotterdam Criteria Are Premature". Journal of Clinical Endocrinology & Metabolism. 91 (3): 781–785. doi:10.1210/jc.2005-2153. PMID 16418211.
^ ^a ^b The Rotterdam ESHRE/ASRM‐sponsored PCOS consensus workshop group (2004). "Revised 2003 consensus on diagnostic criteria and long‐term health risks related to polycystic ovary syndrome (PCOS)". Human Reproduction. 19 (1): 41–47. doi:10.1093/humrep/deh098. PMID 14688154. Retrieved 14 November 2011.
^ Carmina E (February 2004). "Diagnosis of polycystic ovary syndrome: from NIH criteria to ESHRE-ASRM guidelines". Minerva ginecologica. 56 (1): 1–6. PMID 14973405.
^ Hart R, Hickey M, Franks S (October 2004). "Definitions, prevalence and symptoms of polycystic ovaries and polycystic ovary syndrome". Best Practice & Research Clinical Obstetrics & Gynaecology. 18 (5): 671–83. doi:10.1016/j.bpobgyn.2004.05.001. PMID 15380140.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Pedersen SD, Brar S, Faris P, Corenblum B (2007). "Polycystic ovary syndrome: validated questionnaire for use in diagnosis". Canadian Family Physician. 53 (6): 1042–7, 1041. PMC 1949220. PMID 17872783.{{cite journal}}: CS1 maint: multiple names: authors list (link) – see Table 5 Clinical tool for diagnosis of polycystic ovary syndrome
^ ^a ^b Dewailly D, Lujan ME, Carmina E, Cedars MI, Laven J, Norman RJ, Escobar-Morreale HF (2014). "Definition and significance of polycystic ovarian morphology: a task force report from the Androgen Excess and Polycystic Ovary Syndrome Society". Hum. Reprod. Update. 20 (3): 334–52. doi:10.1093/humupd/dmt061. PMID 24345633.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ O'Brien, William T. (1 January 2011). Top 3 Differentials in Radiology. Thieme. p. 369. ISBN 9781604062281. Retrieved 30 August 2014. Ultrasound findings in PCOS include enlarged ovaries with peripheral follicles in a "string of pearls" configuration.
^ Somani N, Harrison S, Bergfeld WF (2008). "The clinical evaluation of hirsutism". Dermatologic therapy. 21 (5): 376–91. doi:10.1111/j.1529-8019.2008.00219.x. PMID 18844715.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ ^a ^b ^c ^d ^e ^f ^g ^h "Polycystic Ovarian Syndrome Workup". eMedicine. 25 October 2011. Retrieved 19 November 2011.
^ Sharquie KE, Al-Bayatti AA, Al-Ajeel AI, Al-Bahar AJ, Al-Nuaimy AA (July 2007). "Free testosterone, luteinizing hormone/follicle stimulating hormone ratio and pelvic sonography in relation to skin manifestations in patients with polycystic ovary syndrome". Saudi Med J. 28 (7): 1039–43. PMID 17603706.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Robinson S, Rodin DA, Deacon A, Wheeler MJ, Clayton RN (March 1992). "Which hormone tests for the diagnosis of polycystic ovary syndrome?". Br J Obstet Gynaecol. 99 (3): 232–8. doi:10.1111/j.1471-0528.1992.tb14505.x. PMID 1296589.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Li X, Lin JF (December 2005). "[Clinical features, hormonal profile, and metabolic abnormalities of obese people with ovaries with obese polycystic ovary syndrome]". Zhonghua Yi Xue Za Zhi (in Chinese). 85 (46): 3266–71. PMID 16409817.
^ ^a ^b Banaszewska B, Spaczyński RZ, Pelesz M, Pawelczyk L (2003). "Incidence of elevated LH/FSH ratio in polycystic ovary syndrome women with normo- and hyperinsulinemia". Rocz. Akad. Med. Bialymst. 48: 131–4. PMID 14737959.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Dewailly D, Andersen CY, Balen A, Broekmans F, Dilaver N, Fanchin R, Griesinger G, Kelsey TW, La Marca A, Lambalk C, Mason H, Nelson SM, Visser JA, Wallace WH, Anderson RA (2014). "The physiology and clinical utility of anti-Mullerian hormone in women". Hum. Reprod. Update. 20 (3): 370–85. doi:10.1093/humupd/dmt062. PMID 24430863.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Broer, S. L.; Broekmans, F. J. M.; Laven, J. S. E.; Fauser, B. C. J. M. (2014). "Anti-Mullerian hormone: ovarian reserve testing and its potential clinical implications". Human Reproduction Update. 20 (5): 688–701. doi:10.1093/humupd/dmu020. ISSN 1355-4786.
^ ^a ^b Legro RS, Kunselman AR, Dodson WC, Dunaif A (1999). "Prevalence and predictors of risk for type 2 diabetes mellitus and impaired glucose tolerance in polycystic ovary syndrome: a prospective, controlled study in 254 affected women". J. Clin. Endocrinol. Metab. 84 (1): 165–9. doi:10.1210/jc.84.1.165. PMID 9920077.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ http://www.ncbi.nlm.nih.gov/pubmed/21528473
^ Kumar Cotran Robbins: Basic Pathology 6th ed. / Saunders 1996
^ Sathyapalan T, Atkin SL (2010). "Mediators of Inflammation in Polycystic Ovary Syndrome in Relation to Adiposity". Mediators of Inflammation. 2010. Hindawi: 758656. doi:10.1155/2010/758656. PMC 2852606. PMID 20396393.{{cite journal}}: CS1 maint: unflagged free DOI (link)
^ Fukuoka M, Yasuda K, Fujiwara H, Kanzaki H, Mori T (1992). "Interactions between interferon gamma, tumour necrosis factor alpha, and interleukin-1 in modulating progesterone and oestradiol production by human luteinized granulosa cells in culture". Hum Reprod. 7 (10): 1361–4. PMID 1291559.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ González F, Rote NS, Minium J, Kirwan JP (2006). "Reactive oxygen species-induced oxidative stress in the development of insulin resistance and hyperandrogenism in polycystic ovary syndrome". J Clin Endocrinol Metab. 91 (1): 336–40. doi:10.1210/jc.2005-1696. PMID 16249279.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Murri M, Luque-Ramírez M, Insenser M, Ojeda-Ojeda M, Escobar-Morreale HF (2013). "Circulating markers of oxidative stress and polycystic ovary syndrome (PCOS): a systematic review and meta-analysis". Hum. Reprod. Update. 19 (3): 268–288. doi:10.1093/humupd/dms059. PMID 23303572. {{cite journal}}: Invalid |display-authors=2 (help)CS1 maint: multiple names: authors list (link)
^ Kelly CJ, Stenton SR, Lashen H (2010). "Insulin-like growth factor binding protein-1 in PCOS: a systematic review and meta-analysis". Human Reproduction Update. 17 (1): 4–16. doi:10.1093/humupd/dmq027. PMID 20634211.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Gleicher N, Weghofer A, Lee IH, Barad DH (2010). Mailund, Thomas (ed.). "FMR1 Genotype with Autoimmunity-Associated Polycystic Ovary-Like Phenotype and Decreased Pregnancy Chance". PLoS ONE. 5 (12): e15303. doi:10.1371/journal.pone.0015303. PMC 3002956. PMID 21179569.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
^ Veltman-Verhulst SM, Boivin J, Eijkemans MJ, Fauser BJ (2012). "Emotional distress is a common risk in people with polycystic ovary syndrome: a systematic review and meta-analysis of 28 studies". Hum. Reprod. Update. 18 (6): 638–51. doi:10.1093/humupd/dms029. PMID 22824735.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ ^a ^b Moran LJ, Ko H, Misso M, Marsh K, Noakes M, Talbot M, Frearson M, Thondan M, Stepto N, Teede HJ (Sep–Oct 2013). "Dietary composition in the treatment of polycystic ovary syndrome: a systematic review to inform evidence-based guidelines". Human reproduction update. 19 (5): 432. doi:10.1093/humupd/dmt015. PMID 23727939.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k "Polycystic Ovarian Syndrome Treatment & Management". eMedicine. 25 October 2011. Retrieved 19 November 2011.
^ Lord JM, Flight IH, Norman RJ (2003). "Metformin in polycystic ovary syndrome: systematic review and meta-analysis". BMJ. 327 (7421): 951–3. doi:10.1136/bmj.327.7421.951. PMC 259161. PMID 14576245.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ National Institute for Health and Clinical Excellence. 11 Clinical guideline 11 : Fertility: assessment and treatment for people with fertility problems . London, 2004.
^ Balen A (December 2008). "Metformin therapy for the management of infertility in people with polycystic ovary syndrome" (PDF). Scientific Advisory Committee Opinion Paper 13. Royal College of Obstetricians and Gynaecologists. Retrieved 2009-12-13.
^ Leeman L, Acharya U (August 2009). "The use of metformin in the management of polycystic ovary syndrome and associated anovulatory infertility: the current evidence". J Obstet Gynaecol. 29 (6): 467–72. doi:10.1080/01443610902829414. PMID 19697191.
^ Cassina, M.; Dona, M.; Di Gianantonio, E.; Litta, P.; Clementi, M. (2014). "First-trimester exposure to metformin and risk of birth defects: a systematic review and meta-analysis". Human Reproduction Update. 20 (5): 656–669. doi:10.1093/humupd/dmu022. ISSN 1355-4786.
^ Qiao J, Feng HL (2010). "Extra- and intra-ovarian factors in polycystic ovary syndrome: impact on oocyte maturation and embryo developmental competence". Human Reproduction Update. 17 (1): 17–33. doi:10.1093/humupd/dmq032. PMC 3001338. PMID 20639519.
^ Legro RS, Barnhart HX, Schlaff WD, Carr BR, Diamond MP, Carson SA, Steinkampf MP, Coutifaris C, McGovern PG, Cataldo NA, Gosman GG, Nestler JE, Giudice LC, Leppert PC, Myers ER (2007). "Clomiphene, Metformin, or Both for Infertility in the Polycystic Ovary Syndrome". N Engl J Med. 356 (6): 551–66. doi:10.1056/NEJMoa063971. PMID 17287476.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ "Polycystic ovary syndrome – Treatment". United Kingdom: National Health Service. 17 October 2011. Retrieved 19 November 2011.
^ ^a ^b Richard Scott Lucidi (25 October 2011). "Polycystic Ovarian Syndrome Medication". eMedicine. Retrieved 19 November 2011.
^ "What are the health risks of PCOS?". Verity – PCOS Charity. Verity. 2011. Retrieved 21 November 2011.
^ Galazis N, Galazi M, Atiomo W (April 2011). "D-Chiro-inositol and its significance in polycystic ovary syndrome: a systematic review". Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology. 27 (4): 256–62. doi:10.3109/09513590.2010.538099. PMID 21142777.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Unfer V, Carlomagno G, Dante G, Facchinetti F (July 2012). "Effects of myo-inositol in women with PCOS: a systematic review of randomized controlled trials" (PDF). Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology. 28 (7): 509–15. doi:10.3109/09513590.2011.650660. PMID 22296306.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ ^a ^b Barry, J. A.; Azizia, M. M.; Hardiman, P. J. (2014). "Risk of endometrial, ovarian and breast cancer in women with polycystic ovary syndrome: a systematic review and meta-analysis". Human Reproduction Update. 20 (5): 748–758. doi:10.1093/humupd/dmu012. ISSN 1355-4786.
^ New MI (May 1993). "Nonclassical congenital adrenal hyperplasia and the polycystic ovarian syndrome". Annals of the New York Academy of Sciences. 687 (1 Intraovarian): 193–205. doi:10.1111/j.1749-6632.1993.tb43866.x. PMID 8323173.
^ Hardiman P, Pillay OC, Atiomo W (May 2003). "Polycystic ovary syndrome and endometrial carcinoma". Lancet. 361 (9371): 1810–2. doi:10.1016/S0140-6736(03)13409-5. PMID 12781553.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Mather KJ, Kwan F, Corenblum B (January 2000). "Hyperinsulinemia in polycystic ovary syndrome correlates with increased cardiovascular risk independent of obesity". Fertility and Sterility. 73 (1): 150–6. doi:10.1016/S0015-0282(99)00468-9. PMID 10632431.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Unfer V, Zacchè M, Serafini A, Redaelli A, Papaleo E (October 2008). "Treatment of hyperandrogenism and hyperinsulinemia in PCOS patients with essential amino acids. A pilot clinical study". Minerva ginecologica. 60 (5): 363–8. PMID 18854802.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Moran LJ, Misso ML, Wild RA, Norman RJ (May 2010). "Impaired glucose tolerance, type 2 diabetes and metabolic syndrome in polycystic ovary syndrome: a systematic review and meta-analysis". Hum Reprod Update. 16 (4): 347–63. doi:10.1093/humupd/dmq001. PMID 20159883.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Barry JA, Kuczmierczyk AR, Hardiman PJ (July 2011). "Anxiety and depression in polycystic ovary syndrome: a systematic review and meta-analysis". Hum. Reprod. 93 (6): 1948–56. doi:10.1093/humrep/der197. PMID 21725075.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Rocha MP, Maranhão RC, Seydell TM, Barcellos CR, Baracat EC, Hayashida SA, Bydlowski SP, Marcondes JA (April 2010). "Metabolism of triglyceride-rich lipoproteins and lipid transfer to high-density lipoprotein in young obese and normal-weight patients with polycystic ovary syndrome". Fertil. Steril. 93 (6): 1948–56. doi:10.1016/j.fertnstert.2008.12.044. PMID 19765700.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ de Groot PC, Dekkers OM, Romijn JA, Dieben SW, Helmerhorst FM (2011). "PCOS, coronary heart disease, stroke and the influence of obesity: A systematic review and meta-analysis". Human Reproduction Update. 17 (4): 495–500. doi:10.1093/humupd/dmr001. PMID 21335359.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Troischt MJ, Mehlman TR, and Nield LS (November 1, 2008). "Polycystic Ovary Syndrome: An Intriguing Diagnosis". Consultant for Pediatricians.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M, Shibuya K, Salomon JA, Abdalla S, Aboyans V; et al. (Dec 15, 2012). "Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet. 380 (9859): 2163–96. doi:10.1016/S0140-6736(12)61729-2. PMID 23245607. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
^ Agrawal R, Sharma S, Bekir J, Conway G, Bailey J, Balen AH, Prelevic G (2004). "Prevalence of polycystic ovaries and polycystic ovary syndrome in lesbian women compared with heterosexual women". J Fertil Steril. 82 (5): 1352–1357. doi:10.1016/j.fertnstert.2004.04.041. PMID 15533359.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ De Sutter P, Dutré T, Vanden Meerschaut F, Stuyver I, Van Maele G, Dhont M (September 2008). "PCOS in lesbian and heterosexual women treated with artificial donor insemination". Reprod. Biomed. Online. 17 (3): 398–402. doi:10.1016/S1472-6483(10)60224-6. PMID 18765011.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Smith HA, Markovic N, Matthews AK, Danielson ME, Kalro BN, Youk AO, Talbott EO (2011). "A comparison of polycystic ovary syndrome and related factors between lesbian and heterosexual women". Womens Health Issues. 21 (3): 191–8. doi:10.1016/j.whi.2010.11.001. PMID 21310628.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Polson DW, Adams J, Wadsworth J, Franks S (Apr 16, 1988). "Polycystic ovaries--a common finding in normal women". Lancet. 1 (8590): 870–2. PMID 2895373.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ ^a ^b Clayton RN, Ogden V, Hodgkinson J, Worswick L, Rodin DA, Dyer S, Meade TW (August 1992). "How common are polycystic ovaries in normal women and what is their significance for the fertility of the population?". Clinical endocrinology. 37 (2): 127–34. doi:10.1111/j.1365-2265.1992.tb02296.x. PMID 1395063.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Farquhar CM, Birdsall M, Manning P, Mitchell JM, France JT (February 1994). "The prevalence of polycystic ovaries on ultrasound scanning in a population of randomly selected women". The Australian & New Zealand journal of obstetrics & gynaecology. 34 (1): 67–72. doi:10.1111/j.1479-828X.1994.tb01041.x. PMID 8053879.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ van Santbrink EJ, Hop WC, Fauser BC (March 1997). "Classification of normogonadotropic infertility: polycystic ovaries diagnosed by ultrasound versus endocrine characteristics of polycystic ovary syndrome". Fertility and Sterility. 67 (3): 452–8. doi:10.1016/S0015-0282(97)80068-4. PMID 9091329.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ ^a ^b Kovacs, Gabor T.; Norman, Robert (2007-02-22). Polycystic Ovary Syndrome. Cambridge University Press. p. 4. ISBN 9781139462037. Retrieved 29 March 2013.
^ "What is Polycystic Ovary Syndrome (PCOS)?". Verity – PCOS Charity. Verity. 2011. Retrieved 21 November 2011.

External links

This template is no longer used; please see Template:Endocrine pathology for a suitable replacement

Template:Link GA

[KollmannMartins2014-1] Kollmann M, Martins WP, Raine-Fenning N (2014). "Terms and thresholds for the ultrasound evaluation of the ovaries in people with hyperandrogenic anovulation". Hum. Reprod. Update. 20 (3): 463–4. doi:10.1093/humupd/dmu005. PMID 24516084.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[2] "USMLE-Rx". MedIQ Learning, LLC. 2014. Stein-Leventhal syndrome, also known as polycystic overy syndrome (PCOS), is a disorder characterized by hirsutism, obesity, and amenorrhea because of luteinizing hormone-resistant cystic ovaries. {{cite web}}: |access-date= requires |url= (help); Missing or empty |url= (help)

[Fauser2011-3] Page 836 (Section:Polycystic ovary syndrome) in: Fauser BC, Diedrich K, Bouchard P, Domínguez F, Matzuk M, Franks S, Hamamah S, Simón C, Devroey P, Ezcurra D, Howles CM (2011). "Contemporary genetic technologies and female reproduction". Human Reproduction Update. 17 (6): 829–847. doi:10.1093/humupd/dmr033. PMC 3191938. PMID 21896560.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[FertSter_molecular-4] Legro RS, Strauss JF (September 2002). "Molecular progress in infertility: polycystic ovary syndrome". Fertility and Sterility. 78 (3): 569–576. doi:10.1016/S0015-0282(02)03275-2. PMID 12215335.

[Endocrine_role-5] Diamanti-Kandarakis E, Kandarakis H, Legro RS (August 2006). "The role of genes and environment in the etiology of PCOS". Endocrine. 30 (1): 19–26. doi:10.1385/ENDO:30:1:19. PMID 17185788.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[6] Dunaif, A; Fauser, BC (Nov 2013). "Renaming PCOS--a two-state solution". The Journal of clinical endocrinology and metabolism. 98 (11): 4325–8. PMID 24009134.

[pmid18277353-7] Goldenberg N, Glueck C (2008). "Medical therapy in women with polycystic ovary syndrome before and during pregnancy and lactation". Minerva Ginecol. 60 (1): 63–75. PMID 18277353.

[pmid18181085-8] Boomsma CM, Fauser BC, Macklon NS (2008). "Pregnancy complications in women with polycystic ovary syndrome". Semin. Reprod. Med. 26 (1): 72–84. doi:10.1055/s-2007-992927. PMID 18181085.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[9] Azziz R, Woods KS, Reyna R, Key TJ, Knochenhauer ES, Yildiz BO (June 2004). "The Prevalence and Features of the Polycystic Ovary Syndrome in an Unselected Population". Journal of Clinical Endocrinology & Metabolism. 89 (6): 2745–9. doi:10.1210/jc.2003-032046. PMID 15181052.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[BMC_Teede-10] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p Teede H, Deeks A, Moran L (2010). "Polycystic ovary syndrome: a complex condition with psychological, reproductive and metabolic manifestations that impacts on health across the lifespan". BMC Med. 8: 41. doi:10.1186/1741-7015-8-41. PMC 2909929. PMID 20591140.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)

[11] "Polycystic ovary syndrome".

[MayoClinic-12] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p ^q ^r ^s ^t ^u ^v ^w ^x ^y Mayo Clinic Staff (4 April 2011). "Polycystic Ovary Syndrome – All". MayoClinic.com. Mayo Clinic. Retrieved 15 November 2011.

[AMN-13] Christine Cortet-Rudelli, Didier Dewailly (Sep 21, 2006). "Diagnosis of Hyperandrogenism in Female Adolescents". Hyperandrogenism in Adolescent Girls. Armenian Health Network, Health.am. Retrieved 2006-11-21.

[huang-14] Huang A, Brennan K, Azziz R (April 2010). "Prevalence of hyperandrogenemia in the polycystic ovary syndrome diagnosed by the National Institutes of Health 1990 criteria". Fertil. Steril. 93 (6): 1938–41. doi:10.1016/j.fertnstert.2008.12.138. PMC 2859983. PMID 19249030.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[FertSter_insulin-15] Nafiye Y, Sevtap K, Muammer D, Emre O, Senol K, Leyla M (April 2010). "The effect of serum and intrafollicular insulin resistance parameters and homocysteine levels of nonobese, nonhyperandrogenemic polycystic ovary syndrome patients on in vitro fertilization outcome". Fertil. Steril. 93 (6): 1864–9. doi:10.1016/j.fertnstert.2008.12.024. PMID 19171332.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[16] Carmina E, Koyama T, Chang L, Stanczyk FZ, Lobo RA (December 1992). "Does ethnicity influence the prevalence of adrenal hyperandrogenism and insulin resistance in polycystic ovary syndrome?". American journal of obstetrics and gynecology. 167 (6): 1807–12. doi:10.1016/0002-9378(92)91779-a. PMID 1471702.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid11212071-17] Crosignani PG, Nicolosi AE (2001). "Polycystic ovarian disease: heritability and heterogeneity". Hum. Reprod. Update. 7 (1): 3–7. doi:10.1093/humupd/7.1.3. PMID 11212071.

[AnnNYAS_thoughts-18] Strauss JF (November 2003). "Some new thoughts on the pathophysiology and genetics of polycystic ovary syndrome". Annals of the New York Academy of Sciences. 997: 42–48. doi:10.1196/annals.1290.005. PMID 14644808.

[OMIM-19] Ada Hamosh (12 September 2011). "POLYCYSTIC OVARY SYNDROME 1; PCOS1". OMIM. McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine. Retrieved 15 November 2011.

[pmid15380142-20] Amato P, Simpson JL (October 2004). "The genetics of polycystic ovary syndrome". Best Pract Res Clin Obstet Gynaecol. 18 (5): 707–18. doi:10.1016/j.bpobgyn.2004.05.002. PMID 15380142.

[emedicine_imaging-21] Marrinan, Greg (20 April 2011). Lin, Eugene C (ed.). "Imaging in Polycystic Ovary Disease". eMedicine. eMedicine. Retrieved 19 November 2011.

[emedicine_main-22] ^ ^a ^b ^c ^d ^e ^f ^g ^h Richard Scott Lucidi (25 October 2011). "Polycystic Ovarian Syndrome". eMedicine. Retrieved 19 November 2011.

[23] Azziz R (March 2006). "Diagnosis of Polycystic Ovarian Syndrome: The Rotterdam Criteria Are Premature". Journal of Clinical Endocrinology & Metabolism. 91 (3): 781–785. doi:10.1210/jc.2005-2153. PMID 16418211.

[HumRep_Rotterdam-24] The Rotterdam ESHRE/ASRM‐sponsored PCOS consensus workshop group (2004). "Revised 2003 consensus on diagnostic criteria and long‐term health risks related to polycystic ovary syndrome (PCOS)". Human Reproduction. 19 (1): 41–47. doi:10.1093/humrep/deh098. PMID 14688154. Retrieved 14 November 2011.

[25] Carmina E (February 2004). "Diagnosis of polycystic ovary syndrome: from NIH criteria to ESHRE-ASRM guidelines". Minerva ginecologica. 56 (1): 1–6. PMID 14973405.

[26] Hart R, Hickey M, Franks S (October 2004). "Definitions, prevalence and symptoms of polycystic ovaries and polycystic ovary syndrome". Best Practice & Research Clinical Obstetrics & Gynaecology. 18 (5): 671–83. doi:10.1016/j.bpobgyn.2004.05.001. PMID 15380140.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid17872783-27] Pedersen SD, Brar S, Faris P, Corenblum B (2007). "Polycystic ovary syndrome: validated questionnaire for use in diagnosis". Canadian Family Physician. 53 (6): 1042–7, 1041. PMC 1949220. PMID 17872783.{{cite journal}}: CS1 maint: multiple names: authors list (link) – see Table 5 Clinical tool for diagnosis of polycystic ovary syndrome

[DewaillyLujan2013-28] Dewailly D, Lujan ME, Carmina E, Cedars MI, Laven J, Norman RJ, Escobar-Morreale HF (2014). "Definition and significance of polycystic ovarian morphology: a task force report from the Androgen Excess and Polycystic Ovary Syndrome Society". Hum. Reprod. Update. 20 (3): 334–52. doi:10.1093/humupd/dmt061. PMID 24345633.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[O'Brien2011-29] O'Brien, William T. (1 January 2011). Top 3 Differentials in Radiology. Thieme. p. 369. ISBN 9781604062281. Retrieved 30 August 2014. Ultrasound findings in PCOS include enlarged ovaries with peripheral follicles in a "string of pearls" configuration.

[pmid18844715-30] Somani N, Harrison S, Bergfeld WF (2008). "The clinical evaluation of hirsutism". Dermatologic therapy. 21 (5): 376–91. doi:10.1111/j.1529-8019.2008.00219.x. PMID 18844715.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[emedicine_workup-31] ^ ^a ^b ^c ^d ^e ^f ^g ^h "Polycystic Ovarian Syndrome Workup". eMedicine. 25 October 2011. Retrieved 19 November 2011.

[pmid17603706-32] Sharquie KE, Al-Bayatti AA, Al-Ajeel AI, Al-Bahar AJ, Al-Nuaimy AA (July 2007). "Free testosterone, luteinizing hormone/follicle stimulating hormone ratio and pelvic sonography in relation to skin manifestations in patients with polycystic ovary syndrome". Saudi Med J. 28 (7): 1039–43. PMID 17603706.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid1296589-33] Robinson S, Rodin DA, Deacon A, Wheeler MJ, Clayton RN (March 1992). "Which hormone tests for the diagnosis of polycystic ovary syndrome?". Br J Obstet Gynaecol. 99 (3): 232–8. doi:10.1111/j.1471-0528.1992.tb14505.x. PMID 1296589.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid16409817-34] Li X, Lin JF (December 2005). "[Clinical features, hormonal profile, and metabolic abnormalities of obese people with ovaries with obese polycystic ovary syndrome]". Zhonghua Yi Xue Za Zhi (in Chinese). 85 (46): 3266–71. PMID 16409817.

[Banaszewska2003-35] Banaszewska B, Spaczyński RZ, Pelesz M, Pawelczyk L (2003). "Incidence of elevated LH/FSH ratio in polycystic ovary syndrome women with normo- and hyperinsulinemia". Rocz. Akad. Med. Bialymst. 48: 131–4. PMID 14737959.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[DewaillyAndersen2014-36] Dewailly D, Andersen CY, Balen A, Broekmans F, Dilaver N, Fanchin R, Griesinger G, Kelsey TW, La Marca A, Lambalk C, Mason H, Nelson SM, Visser JA, Wallace WH, Anderson RA (2014). "The physiology and clinical utility of anti-Mullerian hormone in women". Hum. Reprod. Update. 20 (3): 370–85. doi:10.1093/humupd/dmt062. PMID 24430863.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[BroerBroekmans2014-37] Broer, S. L.; Broekmans, F. J. M.; Laven, J. S. E.; Fauser, B. C. J. M. (2014). "Anti-Mullerian hormone: ovarian reserve testing and its potential clinical implications". Human Reproduction Update. 20 (5): 688–701. doi:10.1093/humupd/dmu020. ISSN 1355-4786.

[pmid9920077-38] Legro RS, Kunselman AR, Dodson WC, Dunaif A (1999). "Prevalence and predictors of risk for type 2 diabetes mellitus and impaired glucose tolerance in polycystic ovary syndrome: a prospective, controlled study in 254 affected women". J. Clin. Endocrinol. Metab. 84 (1): 165–9. doi:10.1210/jc.84.1.165. PMID 9920077.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[39] ttp://www.ncbi.nlm.nih.gov/pubmed/21528473

[40] Kumar Cotran Robbins: Basic Pathology 6th ed. / Saunders 1996

[Mediators_Inflammation-41] Sathyapalan T, Atkin SL (2010). "Mediators of Inflammation in Polycystic Ovary Syndrome in Relation to Adiposity". Mediators of Inflammation. 2010. Hindawi: 758656. doi:10.1155/2010/758656. PMC 2852606. PMID 20396393.{{cite journal}}: CS1 maint: unflagged free DOI (link)

[42] Fukuoka M, Yasuda K, Fujiwara H, Kanzaki H, Mori T (1992). "Interactions between interferon gamma, tumour necrosis factor alpha, and interleukin-1 in modulating progesterone and oestradiol production by human luteinized granulosa cells in culture". Hum Reprod. 7 (10): 1361–4. PMID 1291559.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[43] González F, Rote NS, Minium J, Kirwan JP (2006). "Reactive oxygen species-induced oxidative stress in the development of insulin resistance and hyperandrogenism in polycystic ovary syndrome". J Clin Endocrinol Metab. 91 (1): 336–40. doi:10.1210/jc.2005-1696. PMID 16249279.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid23303572-44] Murri M, Luque-Ramírez M, Insenser M, Ojeda-Ojeda M, Escobar-Morreale HF (2013). "Circulating markers of oxidative stress and polycystic ovary syndrome (PCOS): a systematic review and meta-analysis". Hum. Reprod. Update. 19 (3): 268–288. doi:10.1093/humupd/dms059. PMID 23303572. {{cite journal}}: Invalid |display-authors=2 (help)CS1 maint: multiple names: authors list (link)

[45] Kelly CJ, Stenton SR, Lashen H (2010). "Insulin-like growth factor binding protein-1 in PCOS: a systematic review and meta-analysis". Human Reproduction Update. 17 (1): 4–16. doi:10.1093/humupd/dmq027. PMID 20634211.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[46] Gleicher N, Weghofer A, Lee IH, Barad DH (2010). Mailund, Thomas (ed.). "FMR1 Genotype with Autoimmunity-Associated Polycystic Ovary-Like Phenotype and Decreased Pregnancy Chance". PLoS ONE. 5 (12): e15303. doi:10.1371/journal.pone.0015303. PMC 3002956. PMID 21179569.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)

[pmid22824735-47] Veltman-Verhulst SM, Boivin J, Eijkemans MJ, Fauser BJ (2012). "Emotional distress is a common risk in people with polycystic ovary syndrome: a systematic review and meta-analysis of 28 studies". Hum. Reprod. Update. 18 (6): 638–51. doi:10.1093/humupd/dms029. PMID 22824735.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[Moran2013-48] Moran LJ, Ko H, Misso M, Marsh K, Noakes M, Talbot M, Frearson M, Thondan M, Stepto N, Teede HJ (Sep–Oct 2013). "Dietary composition in the treatment of polycystic ovary syndrome: a systematic review to inform evidence-based guidelines". Human reproduction update. 19 (5): 432. doi:10.1093/humupd/dmt015. PMID 23727939.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[emedicine_treatment-49] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k "Polycystic Ovarian Syndrome Treatment & Management". eMedicine. 25 October 2011. Retrieved 19 November 2011.

[Lord-50] Lord JM, Flight IH, Norman RJ (2003). "Metformin in polycystic ovary syndrome: systematic review and meta-analysis". BMJ. 327 (7421): 951–3. doi:10.1136/bmj.327.7421.951. PMC 259161. PMID 14576245.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[NICE2004-51] National Institute for Health and Clinical Excellence. 11 Clinical guideline 11 : Fertility: assessment and treatment for people with fertility problems . London, 2004.

[52] Balen A (December 2008). "Metformin therapy for the management of infertility in people with polycystic ovary syndrome" (PDF). Scientific Advisory Committee Opinion Paper 13. Royal College of Obstetricians and Gynaecologists. Retrieved 2009-12-13.

[pmid19697191-53] Leeman L, Acharya U (August 2009). "The use of metformin in the management of polycystic ovary syndrome and associated anovulatory infertility: the current evidence". J Obstet Gynaecol. 29 (6): 467–72. doi:10.1080/01443610902829414. PMID 19697191.

[CassinaDona2014-54] Cassina, M.; Dona, M.; Di Gianantonio, E.; Litta, P.; Clementi, M. (2014). "First-trimester exposure to metformin and risk of birth defects: a systematic review and meta-analysis". Human Reproduction Update. 20 (5): 656–669. doi:10.1093/humupd/dmu022. ISSN 1355-4786.

[Qiao2011-55] Qiao J, Feng HL (2010). "Extra- and intra-ovarian factors in polycystic ovary syndrome: impact on oocyte maturation and embryo developmental competence". Human Reproduction Update. 17 (1): 17–33. doi:10.1093/humupd/dmq032. PMC 3001338. PMID 20639519.

[56] Legro RS, Barnhart HX, Schlaff WD, Carr BR, Diamond MP, Carson SA, Steinkampf MP, Coutifaris C, McGovern PG, Cataldo NA, Gosman GG, Nestler JE, Giudice LC, Leppert PC, Myers ER (2007). "Clomiphene, Metformin, or Both for Infertility in the Polycystic Ovary Syndrome". N Engl J Med. 356 (6): 551–66. doi:10.1056/NEJMoa063971. PMID 17287476.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[flutamide-57] "Polycystic ovary syndrome – Treatment". United Kingdom: National Health Service. 17 October 2011. Retrieved 19 November 2011.

[emedicine_medications-58] Richard Scott Lucidi (25 October 2011). "Polycystic Ovarian Syndrome Medication". eMedicine. Retrieved 19 November 2011.

[verity_risks-59] "What are the health risks of PCOS?". Verity – PCOS Charity. Verity. 2011. Retrieved 21 November 2011.

[pmid21142777-60] Galazis N, Galazi M, Atiomo W (April 2011). "D-Chiro-inositol and its significance in polycystic ovary syndrome: a systematic review". Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology. 27 (4): 256–62. doi:10.3109/09513590.2010.538099. PMID 21142777.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid22296306-61] Unfer V, Carlomagno G, Dante G, Facchinetti F (July 2012). "Effects of myo-inositol in women with PCOS: a systematic review of randomized controlled trials" (PDF). Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology. 28 (7): 509–15. doi:10.3109/09513590.2011.650660. PMID 22296306.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[BarryAzizia2014-62] Barry, J. A.; Azizia, M. M.; Hardiman, P. J. (2014). "Risk of endometrial, ovarian and breast cancer in women with polycystic ovary syndrome: a systematic review and meta-analysis". Human Reproduction Update. 20 (5): 748–758. doi:10.1093/humupd/dmu012. ISSN 1355-4786.

[63] New MI (May 1993). "Nonclassical congenital adrenal hyperplasia and the polycystic ovarian syndrome". Annals of the New York Academy of Sciences. 687 (1 Intraovarian): 193–205. doi:10.1111/j.1749-6632.1993.tb43866.x. PMID 8323173.

[64] Hardiman P, Pillay OC, Atiomo W (May 2003). "Polycystic ovary syndrome and endometrial carcinoma". Lancet. 361 (9371): 1810–2. doi:10.1016/S0140-6736(03)13409-5. PMID 12781553.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[65] Mather KJ, Kwan F, Corenblum B (January 2000). "Hyperinsulinemia in polycystic ovary syndrome correlates with increased cardiovascular risk independent of obesity". Fertility and Sterility. 73 (1): 150–6. doi:10.1016/S0015-0282(99)00468-9. PMID 10632431.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[66] Unfer V, Zacchè M, Serafini A, Redaelli A, Papaleo E (October 2008). "Treatment of hyperandrogenism and hyperinsulinemia in PCOS patients with essential amino acids. A pilot clinical study". Minerva ginecologica. 60 (5): 363–8. PMID 18854802.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[67] Moran LJ, Misso ML, Wild RA, Norman RJ (May 2010). "Impaired glucose tolerance, type 2 diabetes and metabolic syndrome in polycystic ovary syndrome: a systematic review and meta-analysis". Hum Reprod Update. 16 (4): 347–63. doi:10.1093/humupd/dmq001. PMID 20159883.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[68] Barry JA, Kuczmierczyk AR, Hardiman PJ (July 2011). "Anxiety and depression in polycystic ovary syndrome: a systematic review and meta-analysis". Hum. Reprod. 93 (6): 1948–56. doi:10.1093/humrep/der197. PMID 21725075.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[69] Rocha MP, Maranhão RC, Seydell TM, Barcellos CR, Baracat EC, Hayashida SA, Bydlowski SP, Marcondes JA (April 2010). "Metabolism of triglyceride-rich lipoproteins and lipid transfer to high-density lipoprotein in young obese and normal-weight patients with polycystic ovary syndrome". Fertil. Steril. 93 (6): 1948–56. doi:10.1016/j.fertnstert.2008.12.044. PMID 19765700.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[70] Groot PC, Dekkers OM, Romijn JA, Dieben SW, Helmerhorst FM (2011). "PCOS, coronary heart disease, stroke and the influence of obesity: A systematic review and meta-analysis". Human Reproduction Update. 17 (4): 495–500. doi:10.1093/humupd/dmr001. PMID 21335359.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[71] Troischt MJ, Mehlman TR, and Nield LS (November 1, 2008). "Polycystic Ovary Syndrome: An Intriguing Diagnosis". Consultant for Pediatricians.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[LancetEpi2012-72] Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M, Shibuya K, Salomon JA, Abdalla S, Aboyans V; et al. (Dec 15, 2012). "Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet. 380 (9859): 2163–96. doi:10.1016/S0140-6736(12)61729-2. PMID 23245607. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)

[73] Agrawal R, Sharma S, Bekir J, Conway G, Bailey J, Balen AH, Prelevic G (2004). "Prevalence of polycystic ovaries and polycystic ovary syndrome in lesbian women compared with heterosexual women". J Fertil Steril. 82 (5): 1352–1357. doi:10.1016/j.fertnstert.2004.04.041. PMID 15533359.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[74] De Sutter P, Dutré T, Vanden Meerschaut F, Stuyver I, Van Maele G, Dhont M (September 2008). "PCOS in lesbian and heterosexual women treated with artificial donor insemination". Reprod. Biomed. Online. 17 (3): 398–402. doi:10.1016/S1472-6483(10)60224-6. PMID 18765011.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[75] Smith HA, Markovic N, Matthews AK, Danielson ME, Kalro BN, Youk AO, Talbott EO (2011). "A comparison of polycystic ovary syndrome and related factors between lesbian and heterosexual women". Womens Health Issues. 21 (3): 191–8. doi:10.1016/j.whi.2010.11.001. PMID 21310628.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[76] Polson DW, Adams J, Wadsworth J, Franks S (Apr 16, 1988). "Polycystic ovaries--a common finding in normal women". Lancet. 1 (8590): 870–2. PMID 2895373.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[clayton-77] Clayton RN, Ogden V, Hodgkinson J, Worswick L, Rodin DA, Dyer S, Meade TW (August 1992). "How common are polycystic ovaries in normal women and what is their significance for the fertility of the population?". Clinical endocrinology. 37 (2): 127–34. doi:10.1111/j.1365-2265.1992.tb02296.x. PMID 1395063.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid8053879-78] Farquhar CM, Birdsall M, Manning P, Mitchell JM, France JT (February 1994). "The prevalence of polycystic ovaries on ultrasound scanning in a population of randomly selected women". The Australian & New Zealand journal of obstetrics & gynaecology. 34 (1): 67–72. doi:10.1111/j.1479-828X.1994.tb01041.x. PMID 8053879.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[pmid9091329-79] van Santbrink EJ, Hop WC, Fauser BC (March 1997). "Classification of normogonadotropic infertility: polycystic ovaries diagnosed by ultrasound versus endocrine characteristics of polycystic ovary syndrome". Fertility and Sterility. 67 (3): 452–8. doi:10.1016/S0015-0282(97)80068-4. PMID 9091329.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[Kovacs2007-80] Kovacs, Gabor T.; Norman, Robert (2007-02-22). Polycystic Ovary Syndrome. Cambridge University Press. p. 4. ISBN 9781139462037. Retrieved 29 March 2013.

[verity_what_is_PCOS-81] "What is Polycystic Ovary Syndrome (PCOS)?". Verity – PCOS Charity. Verity. 2011. Retrieved 21 November 2011.

[1]

[2]

[3]

[4]

[5]

[6]

[7]

[8]

[9]

[10]

[11]

[12]

[13]

[14]

[15]

[16]

[17]

[18]

[19]

[20]

[21]

[22]

[23]

[24]

[25]

[26]

[27]

[28]

[29]

[30]

[31]

[32]

[33]

[34]

[35]

[36]

[37]

[38]

[39]

[40]

[41]

[42]

[43]

[44]

[45]

[46]

[47]

[48]

[49]

[50]

[51]

[52]

[53]

[54]

[55]

[56]

[57]

[58]

[59]

[60]

[61]

[62]

[63]

[64]

[65]

[66]

[67]

[68]

[69]

[70]

[71]

[72]

[73]

[74]

[75]

[76]

[77]

[78]

[79]

[80]

[81]

@@ Line 3: / Line 3: @@
  | Name           = Polycystic Ovary Syndrome.
  | Image          = PCOS.jpg
- | Caption        = A polycystic ovary (aka PCO) shown on an [[Medical ultrasonography|ultrasound image]]. PCO is not necessary for diagnosing PCOS, but it is a common sign. As many as 30% or more of women with PCOS do not have PCO as a sign.
+ | Caption        = A polycystic ovary (aka PCO) shown on an [[Medical ultrasonography|ultrasound image]]. PCO is not necessary for diagnosing PCOS, but it is a common sign. As many as 30% or more of people with PCOS do not have PCO as a sign.
  | ICD10          = {{ICD10|E|28|2|e|20}}
  | ICD9           = {{ICD9|256.4}}
@@ Line 14: / Line 14: @@
  | MeshID         = D011085
 }}
-'''Polycystic ovary syndrome''' ('''PCOS'''), also called '''hyperandrogenic anovulation''' ('''HA'''),<ref name="KollmannMartins2014">{{cite journal | author = Kollmann M, Martins WP, Raine-Fenning N | title = Terms and thresholds for the ultrasound evaluation of the ovaries in women with hyperandrogenic anovulation | journal = Hum. Reprod. Update | volume = 20 | issue = 3 | pages = 463–4 | year = 2014 | pmid = 24516084 | doi = 10.1093/humupd/dmu005 }}</ref> or '''Stein-Leventhal syndrome''',<ref>{{cite web|title=USMLE-Rx|year=2014|publisher=MedIQ Learning, LLC|accessdate=15 May 2014|quote=Stein-Leventhal syndrome, also known as polycystic overy syndrome (PCOS), is a disorder characterized by hirsutism, obesity, and amenorrhea because of luteinizing hormone-resistant cystic ovaries.}}</ref> is one of the most common [[endocrine]] disorders among females. PCOS has a diverse range of causes that are not entirely understood, but there is evidence that it is largely a [[genetic disease]].<ref name=Fauser2011>Page 836 (Section:''Polycystic ovary syndrome'') in: {{cite journal | author = Fauser BC, Diedrich K, Bouchard P, Domínguez F, Matzuk M, Franks S, Hamamah S, Simón C, Devroey P, Ezcurra D, Howles CM | title = Contemporary genetic technologies and female reproduction | journal = Human Reproduction Update | volume = 17 | issue = 6 | pages = 829–847 | year = 2011 | pmid = 21896560 | pmc = 3191938 | doi = 10.1093/humupd/dmr033 }}</ref><ref name=FertSter_molecular>{{cite journal | author = Legro RS, Strauss JF | title = Molecular progress in infertility: polycystic ovary syndrome | journal = Fertility and Sterility | volume = 78 | issue = 3 | pages = 569–576 | date = September 2002 | pmid = 12215335 | doi = 10.1016/S0015-0282(02)03275-2 }}</ref><ref name=Endocrine_role>{{cite journal | author = Diamanti-Kandarakis E, Kandarakis H, Legro RS | title = The role of genes and environment in the etiology of PCOS | journal = Endocrine | volume = 30 | issue = 1 | pages = 19–26 | date = August 2006 | pmid = 17185788 | doi = 10.1385/ENDO:30:1:19 }}</ref> Others say it is generally a metabolic dysfunction, since it is reversible. Even though considered as a gynecological problem, PCOS consists of 28 clinical symptoms.
+'''Polycystic ovary syndrome''' ('''PCOS'''), also called '''hyperandrogenic anovulation''' ('''HA'''),<ref name="KollmannMartins2014">{{cite journal | author = Kollmann M, Martins WP, Raine-Fenning N | title = Terms and thresholds for the ultrasound evaluation of the ovaries in people with hyperandrogenic anovulation | journal = Hum. Reprod. Update | volume = 20 | issue = 3 | pages = 463–4 | year = 2014 | pmid = 24516084 | doi = 10.1093/humupd/dmu005 }}</ref> or '''Stein-Leventhal syndrome''',<ref>{{cite web|title=USMLE-Rx|year=2014|publisher=MedIQ Learning, LLC|accessdate=15 May 2014|quote=Stein-Leventhal syndrome, also known as polycystic overy syndrome (PCOS), is a disorder characterized by hirsutism, obesity, and amenorrhea because of luteinizing hormone-resistant cystic ovaries.}}</ref> is one of the most common [[endocrine]] disorders among people with ovaries. PCOS has a diverse range of causes that are not entirely understood, but there is evidence that it is largely a [[genetic disease]].<ref name=Fauser2011>Page 836 (Section:''Polycystic ovary syndrome'') in: {{cite journal | author = Fauser BC, Diedrich K, Bouchard P, Domínguez F, Matzuk M, Franks S, Hamamah S, Simón C, Devroey P, Ezcurra D, Howles CM | title = Contemporary genetic technologies and female reproduction | journal = Human Reproduction Update | volume = 17 | issue = 6 | pages = 829–847 | year = 2011 | pmid = 21896560 | pmc = 3191938 | doi = 10.1093/humupd/dmr033 }}</ref><ref name=FertSter_molecular>{{cite journal | author = Legro RS, Strauss JF | title = Molecular progress in infertility: polycystic ovary syndrome | journal = Fertility and Sterility | volume = 78 | issue = 3 | pages = 569–576 | date = September 2002 | pmid = 12215335 | doi = 10.1016/S0015-0282(02)03275-2 }}</ref><ref name=Endocrine_role>{{cite journal | author = Diamanti-Kandarakis E, Kandarakis H, Legro RS | title = The role of genes and environment in the etiology of PCOS | journal = Endocrine | volume = 30 | issue = 1 | pages = 19–26 | date = August 2006 | pmid = 17185788 | doi = 10.1385/ENDO:30:1:19 }}</ref> Others say it is generally a metabolic dysfunction, since it is reversible. Even though considered as a gynecological problem, PCOS consists of 28 clinical symptoms.
 Even though the name suggest that the ovaries are the cornerstone of disease pathology, cysts are the 'result' , not the cause of the disease. Symptoms of PCOS will persist even if both ovaries are removed; the disease can appear even if cysts are absent. Since its first description by Stein and Leventhal  in 1935, the criteria of diagnosis, symptoms, and causative factors are subject to debate. Gynecologists often see it as a gynecological problem, with ovary as the primary organ affected. However, recent insights shows a multisystem disorder, with the primary problems lying in hormonal regulation in hypothalamus, with involvement of many organs. The name PCOD is used when there is ultrasonographic evidence. The term PCOS is used since there is a wide spectrum of symptoms possible, and cysts in the ovaries are seen only in 15% of people.<ref>{{cite journal|last1=Dunaif|first1=A|last2=Fauser|first2=BC|title=Renaming PCOS--a two-state solution.|journal=The Journal of clinical endocrinology and metabolism|date=Nov 2013|volume=98|issue=11|pages=4325–8|pmid=24009134}}</ref> Treatments like wedge resection or laparoscopic drilling of ovaries are still performed around the world, based on this false 'ovary-focused' belief.
-PCOS produces symptoms in approximately 5% to 10% of women of reproductive age (approximately 12 to 45 years old). It is thought to be one of the leading causes of [[female subfertility]]<ref name="pmid18277353">{{cite journal | author = Goldenberg N, Glueck C | title = Medical therapy in women with polycystic [[ovary]] syndrome before and during pregnancy and lactation | journal = Minerva Ginecol | volume = 60 | issue = 1 | pages = 63–75 | year = 2008 | pmid = 18277353 | doi =  }}</ref><ref name="pmid18181085">{{cite journal | author = Boomsma CM, Fauser BC, Macklon NS | title = Pregnancy complications in women with polycystic ovary syndrome | journal = Semin. Reprod. Med. | volume = 26 | issue = 1 | pages = 72–84 | year = 2008 | pmid = 18181085 | doi = 10.1055/s-2007-992927 }}</ref><ref>{{cite journal | author = Azziz R, Woods KS, Reyna R, Key TJ, Knochenhauer ES, Yildiz BO | title = The Prevalence and Features of the Polycystic Ovary Syndrome in an Unselected Population | journal = Journal of Clinical Endocrinology & Metabolism | volume = 89 | issue = 6 | pages = 2745–9 | date = June 2004 | pmid = 15181052 | doi = 10.1210/jc.2003-032046 }}</ref> and the most frequent endocrine problem in women of reproductive age.<ref name=BMC_Teede>{{cite journal | author = Teede H, Deeks A, Moran L | title = Polycystic ovary syndrome: a complex condition with psychological, reproductive and metabolic manifestations that impacts on health across the lifespan | journal = BMC Med | volume = 8 | issue = | pages = 41 | year = 2010 | pmid = 20591140 | pmc = 2909929 | doi = 10.1186/1741-7015-8-41 }}</ref> Finding that the ovaries appear polycystic on ultrasound is common, but it is not an absolute requirement in all definitions of the disorder.
+PCOS produces symptoms in approximately 5% to 10% of people with ovaries of reproductive age (approximately 12 to 45 years old). It is thought to be one of the leading causes of [[subfertility]] in people with ovaries<ref name="pmid18277353">{{cite journal | author = Goldenberg N, Glueck C | title = Medical therapy in women with polycystic [[ovary]] syndrome before and during pregnancy and lactation | journal = Minerva Ginecol | volume = 60 | issue = 1 | pages = 63–75 | year = 2008 | pmid = 18277353 | doi =  }}</ref><ref name="pmid18181085">{{cite journal | author = Boomsma CM, Fauser BC, Macklon NS | title = Pregnancy complications in women with polycystic ovary syndrome | journal = Semin. Reprod. Med. | volume = 26 | issue = 1 | pages = 72–84 | year = 2008 | pmid = 18181085 | doi = 10.1055/s-2007-992927 }}</ref><ref>{{cite journal | author = Azziz R, Woods KS, Reyna R, Key TJ, Knochenhauer ES, Yildiz BO | title = The Prevalence and Features of the Polycystic Ovary Syndrome in an Unselected Population | journal = Journal of Clinical Endocrinology & Metabolism | volume = 89 | issue = 6 | pages = 2745–9 | date = June 2004 | pmid = 15181052 | doi = 10.1210/jc.2003-032046 }}</ref> and the most frequent endocrine problem in people with ovaries of reproductive age.<ref name=BMC_Teede>{{cite journal | author = Teede H, Deeks A, Moran L | title = Polycystic ovary syndrome: a complex condition with psychological, reproductive and metabolic manifestations that impacts on health across the lifespan | journal = BMC Med | volume = 8 | issue = | pages = 41 | year = 2010 | pmid = 20591140 | pmc = 2909929 | doi = 10.1186/1741-7015-8-41 }}</ref> Finding that the ovaries appear polycystic on ultrasound is common, but it is not an absolute requirement in all definitions of the disorder.
-The most common immediate symptoms are [[anovulation]], excess [[androgen]]ic hormones, and [[insulin resistance]]. Anovulation results in irregular [[menstruation]], [[amenorrhea]], and ovulation-related infertility. [[Hormone imbalance]] generally causes [[acne]] and [[hirsutism]]. Insulin resistance is associated with [[obesity]], [[type 2 diabetes]], and [[hypercholesterolemia|high cholesterol levels]].<ref>{{cite web|title=Polycystic ovary syndrome|url=http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001408/}}</ref>  The symptoms and severity of the syndrome vary greatly among affected women.
+The most common immediate symptoms are [[anovulation]], excess [[androgen]]ic hormones, and [[insulin resistance]]. Anovulation results in irregular [[menstruation]], [[amenorrhea]], and ovulation-related infertility. [[Hormone imbalance]] generally causes [[acne]] and [[hirsutism]]. Insulin resistance is associated with [[obesity]], [[type 2 diabetes]], and [[hypercholesterolemia|high cholesterol levels]].<ref>{{cite web|title=Polycystic ovary syndrome|url=http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001408/}}</ref>  The symptoms and severity of the syndrome vary greatly among affected people.
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@@ Line 30: / Line 30: @@
 * [[Infertility]]:<ref name=MayoClinic />  This generally results directly from chronic [[anovulation]] (lack of ovulation).<ref name=BMC_Teede /> {{Further|Infertility in polycystic ovary syndrome}}
 * [[hyperandrogenism|High levels of masculinizing hormones]]:  The most common signs are [[acne]] and [[hirsutism]] (male pattern of hair growth), but it may produce [[hypermenorrhea]] (heavy and prolonged menstrual periods), [[androgenic alopecia]] (increase hair thinning or diffuse hair loss), or other symptoms.<ref name=BMC_Teede /><ref name=AMN>{{cite web |author=Christine Cortet-Rudelli, Didier Dewailly|title=Diagnosis of Hyperandrogenism in Female Adolescents| work=Hyperandrogenism in Adolescent Girls |url=http://www.health.am/gyneco/more/diagnosis-of-hyperandrogenism-in-female/|date=Sep 21, 2006|publisher=Armenian Health Network, Health.am|accessdate=2006-11-21}}</ref> Approximately three-quarters of people with PCOS (by the diagnostic criteria of NIH/NICHD 1990) have evidence of [[hyperandrogenemia]].<ref name=huang>{{cite journal | author = Huang A, Brennan K, Azziz R | title = Prevalence of hyperandrogenemia in the polycystic ovary syndrome diagnosed by the National Institutes of Health 1990 criteria | journal = Fertil. Steril. | volume = 93 | issue = 6 | pages = 1938–41 | date = April 2010 | pmid = 19249030 | pmc = 2859983 | doi = 10.1016/j.fertnstert.2008.12.138 | url =  }}</ref>
-* [[Metabolic syndrome]]:<ref name=MayoClinic />  This appears as a tendency towards [[central obesity]] and other symptoms associated with [[insulin resistance]].<ref name=BMC_Teede /> Serum [[insulin]], insulin resistance, and [[homocysteine]] levels are higher in women with PCOS.<ref name=FertSter_insulin>{{cite journal | author = Nafiye Y, Sevtap K, Muammer D, Emre O, Senol K, Leyla M | title = The effect of serum and intrafollicular insulin resistance parameters and homocysteine levels of nonobese, nonhyperandrogenemic polycystic ovary syndrome patients on in vitro fertilization outcome | journal = Fertil. Steril. | volume = 93 | issue = 6 | pages = 1864–9 | date = April 2010 | pmid = 19171332 | doi = 10.1016/j.fertnstert.2008.12.024 }}</ref>
+* [[Metabolic syndrome]]:<ref name=MayoClinic />  This appears as a tendency towards [[central obesity]] and other symptoms associated with [[insulin resistance]].<ref name=BMC_Teede /> Serum [[insulin]], insulin resistance, and [[homocysteine]] levels are higher in people with PCOS.<ref name=FertSter_insulin>{{cite journal | author = Nafiye Y, Sevtap K, Muammer D, Emre O, Senol K, Leyla M | title = The effect of serum and intrafollicular insulin resistance parameters and homocysteine levels of nonobese, nonhyperandrogenemic polycystic ovary syndrome patients on in vitro fertilization outcome | journal = Fertil. Steril. | volume = 93 | issue = 6 | pages = 1864–9 | date = April 2010 | pmid = 19171332 | doi = 10.1016/j.fertnstert.2008.12.024 }}</ref>
-When Asian women are affected with PCOS, they are less likely to develop hirsutism than women of other ethnic backgrounds.<ref>{{cite journal | author = Carmina E, Koyama T, Chang L, Stanczyk FZ, Lobo RA | title = Does ethnicity influence the prevalence of adrenal hyperandrogenism and insulin resistance in polycystic ovary syndrome? | journal = American journal of obstetrics and gynecology | volume = 167 | issue = 6 | pages = 1807–12 | date = December 1992 | pmid = 1471702 | doi = 10.1016/0002-9378(92)91779-a }}</ref>
+When Asian people with ovaries are affected with PCOS, they are less likely to develop hirsutism than people of other ethnic backgrounds.<ref>{{cite journal | author = Carmina E, Koyama T, Chang L, Stanczyk FZ, Lobo RA | title = Does ethnicity influence the prevalence of adrenal hyperandrogenism and insulin resistance in polycystic ovary syndrome? | journal = American journal of obstetrics and gynecology | volume = 167 | issue = 6 | pages = 1807–12 | date = December 1992 | pmid = 1471702 | doi = 10.1016/0002-9378(92)91779-a }}</ref>
 == Cause ==
 PCOS is a heterogeneous disorder of uncertain [[etiology|cause]].<ref name="Fauser2011"/><ref name=FertSter_molecular /><ref name=MayoClinic /> There is strong evidence that it is a [[genetic disease]]. Such evidence includes the familial clustering of cases, greater [[Concordance (genetics)|concordance]] in [[monozygotic twin|monozygotic]] compared with [[dizygotic]] twins and heritability of endocrine and metabolic features of PCOS.<ref name=Fauser2011/><ref name="FertSter_molecular"/><ref name="Endocrine_role"/>
-The genetic component appears to be inherited in an [[autosomal dominant]] fashion with high [[genetic penetrance]] but variable [[expressivity]] in females; this means that each child has a 50% chance of inheriting the predisposing genetic variant(s) from a parent, and, if a daughter receives the variant(s), the daughter will have the disease to some extent.<ref name=FertSter_molecular /><ref name="pmid11212071" /><ref name=AnnNYAS_thoughts /><ref name=OMIM />  The genetic variant(s) can be inherited from either the father or the mother, and can be passed along to both sons (who may be asymptomatic carriers or may have symptoms such as early [[baldness]] and/or excessive hair) and daughters, who will show signs of PCOS.<ref name="pmid11212071">{{cite journal | author = Crosignani PG, Nicolosi AE | title = Polycystic ovarian disease: heritability and heterogeneity | journal = Hum. Reprod. Update | volume = 7 | issue = 1 | pages = 3–7 | year = 2001 | pmid = 11212071 | doi = 10.1093/humupd/7.1.3 }}</ref><ref name=OMIM>{{cite web|url=http://omim.org/entry/184700|work=[[OMIM]]|title=POLYCYSTIC OVARY SYNDROME 1; PCOS1|accessdate=15 November 2011|publisher=McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine|author=Ada Hamosh|date=12 September 2011}}</ref> The [[allele]] appears to manifest itself at least partially via heightened androgen levels secreted by [[ovarian follicle]] [[theca]] cells from women with the allele.<ref name=AnnNYAS_thoughts>{{cite journal | author = Strauss JF | title = Some new thoughts on the pathophysiology and genetics of polycystic ovary syndrome | journal = Annals of the New York Academy of Sciences | volume = 997 | pages = 42–48 | date = November 2003 | pmid = 14644808 | doi = 10.1196/annals.1290.005 }}</ref> The exact gene affected has not yet been identified.<ref name=FertSter_molecular /><ref name=Endocrine_role /><ref name="pmid15380142">{{cite journal | author = Amato P, Simpson JL | title = The genetics of polycystic ovary syndrome | journal = Best Pract Res Clin Obstet Gynaecol | volume = 18 | issue = 5 | pages = 707–18 | date = October 2004 | pmid = 15380142 | doi = 10.1016/j.bpobgyn.2004.05.002 }}</ref>
+The genetic component appears to be inherited in an [[autosomal dominant]] fashion with high [[genetic penetrance]] but variable [[expressivity]] in females; this means that each child has a 50% chance of inheriting the predisposing genetic variant(s) from a parent, and, if a daughter receives the variant(s), the daughter will have the disease to some extent.<ref name=FertSter_molecular /><ref name="pmid11212071" /><ref name=AnnNYAS_thoughts /><ref name=OMIM />  The genetic variant(s) can be inherited from either the father or the mother, and can be passed along to both sons (who may be asymptomatic carriers or may have symptoms such as early [[baldness]] and/or excessive hair) and daughters, who will show signs of PCOS.<ref name="pmid11212071">{{cite journal | author = Crosignani PG, Nicolosi AE | title = Polycystic ovarian disease: heritability and heterogeneity | journal = Hum. Reprod. Update | volume = 7 | issue = 1 | pages = 3–7 | year = 2001 | pmid = 11212071 | doi = 10.1093/humupd/7.1.3 }}</ref><ref name=OMIM>{{cite web|url=http://omim.org/entry/184700|work=[[OMIM]]|title=POLYCYSTIC OVARY SYNDROME 1; PCOS1|accessdate=15 November 2011|publisher=McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine|author=Ada Hamosh|date=12 September 2011}}</ref> The [[allele]] appears to manifest itself at least partially via heightened androgen levels secreted by [[ovarian follicle]] [[theca]] cells from people with the allele.<ref name=AnnNYAS_thoughts>{{cite journal | author = Strauss JF | title = Some new thoughts on the pathophysiology and genetics of polycystic ovary syndrome | journal = Annals of the New York Academy of Sciences | volume = 997 | pages = 42–48 | date = November 2003 | pmid = 14644808 | doi = 10.1196/annals.1290.005 }}</ref> The exact gene affected has not yet been identified.<ref name=FertSter_molecular /><ref name=Endocrine_role /><ref name="pmid15380142">{{cite journal | author = Amato P, Simpson JL | title = The genetics of polycystic ovary syndrome | journal = Best Pract Res Clin Obstet Gynaecol | volume = 18 | issue = 5 | pages = 707–18 | date = October 2004 | pmid = 15380142 | doi = 10.1016/j.bpobgyn.2004.05.002 }}</ref>
 The clinical severity of PCOS symptoms appears to be largely determined by factors such as obesity.<ref name=Endocrine_role /><ref name=BMC_Teede />
 == Diagnosis ==
-Not all women with PCOS have polycystic ovaries (PCO), nor do all women with ovarian cysts have PCOS; although a [[pelvic ultrasound]] is a major diagnostic tool, it is not the only one.<ref name=emedicine_imaging /> The diagnosis is straightforward using the Rotterdam criteria, even when the syndrome is associated with a wide range of symptoms.
+Not all people with PCOS have polycystic ovaries (PCO), nor do all people with ovarian cysts have PCOS; although a [[pelvic ultrasound]] is a major diagnostic tool, it is not the only one.<ref name=emedicine_imaging /> The diagnosis is straightforward using the Rotterdam criteria, even when the syndrome is associated with a wide range of symptoms.
 <gallery>
 File:PCOS.jpg|Polycystic Ovary as seen on Sonography
@@ Line 65: / Line 65: @@
 #Other entities are excluded that would cause these.<ref name=BMC_Teede /><ref name=HumRep_Rotterdam>{{cite journal | author = The Rotterdam ESHRE/ASRM‐sponsored PCOS consensus workshop group | title = Revised 2003 consensus on diagnostic criteria and long‐term health risks related to polycystic ovary syndrome (PCOS) | journal = Human Reproduction | volume = 19 | issue = 1 | pages = 41–47 | year = 2004 | pmid = 14688154 | doi = 10.1093/humrep/deh098 | url = http://humrep.oxfordjournals.org/content/19/1/41.long | accessdate = 14 November 2011 }}</ref>
-The Rotterdam definition is wider, including many more women, the most notable ones being women without androgen excess. Critics say that findings obtained from the study of women with androgen excess cannot necessarily be extrapolated to women without androgen excess.<ref>{{cite journal | author = Carmina E | title = Diagnosis of polycystic ovary syndrome: from NIH criteria to ESHRE-ASRM guidelines. | journal = Minerva ginecologica | volume = 56 | issue = 1 | pages = 1–6 | date = February 2004 | pmid = 14973405 }}</ref><ref>{{cite journal | author = Hart R, Hickey M, Franks S | title = Definitions, prevalence and symptoms of polycystic ovaries and polycystic ovary syndrome | journal = Best Practice & Research Clinical Obstetrics & Gynaecology | volume = 18 | issue = 5 | pages = 671–83 | date = October 2004 | pmid = 15380140 | doi = 10.1016/j.bpobgyn.2004.05.001 }}</ref>
+The Rotterdam definition is wider, including many more people with ovaries, the most notable ones being designated people with ovaries without androgen excess. Critics say that findings obtained from the study of people with ovaries with androgen excess cannot necessarily be extrapolated to people with ovaries without androgen excess.<ref>{{cite journal | author = Carmina E | title = Diagnosis of polycystic ovary syndrome: from NIH criteria to ESHRE-ASRM guidelines. | journal = Minerva ginecologica | volume = 56 | issue = 1 | pages = 1–6 | date = February 2004 | pmid = 14973405 }}</ref><ref>{{cite journal | author = Hart R, Hickey M, Franks S | title = Definitions, prevalence and symptoms of polycystic ovaries and polycystic ovary syndrome | journal = Best Practice & Research Clinical Obstetrics & Gynaecology | volume = 18 | issue = 5 | pages = 671–83 | date = October 2004 | pmid = 15380140 | doi = 10.1016/j.bpobgyn.2004.05.001 }}</ref>
 ;Androgen Excess PCOS Society
@@ Line 75: / Line 75: @@
 === Standard diagnostic assessments ===
 * History-taking, specifically for menstrual pattern, obesity, hirsutism, and the absence of breast development. A [[clinical prediction rule]] found that these four questions can diagnose PCOS with a [[sensitivity (tests)|sensitivity]] of 77.1% (95% [[confidence interval]] [CI] 62.7%–88.0%) and a [[specificity (tests)|specificity]] of 93.8% (95% CI 82.8%–98.7%).<ref name="pmid17872783">{{cite journal | author = Pedersen SD, Brar S, Faris P, Corenblum B | title = Polycystic ovary syndrome: validated questionnaire for use in diagnosis | journal = Canadian Family Physician | volume = 53 | issue = 6 | pages = 1042–7, 1041 | year = 2007 | pmid = 17872783 | pmc = 1949220 | doi =  | url = http://www.cfp.ca/cgi/content/full/53/6/1041#T50531041 }}&nbsp;– see [http://www.cfp.ca/cgi/content/full/53/6/1041/T50531041 Table 5 Clinical tool for diagnosis of polycystic ovary syndrome]</ref>
-* [[Gynecologic ultrasonography]], specifically looking for small [[ovarian follicles]]. These are believed to be the result of disturbed ovarian function with failed ovulation, reflected by the infrequent or absent menstruation that is typical of the condition. In a normal [[menstrual cycle]], one egg is released from a dominant follicle&nbsp;– in essence, a cyst that bursts to release the egg. After ovulation, the follicle remnant is transformed into a [[progesterone]]-producing [[corpus luteum]], which shrinks and disappears after approximately 12–14 days. In PCOS, there is a so-called "follicular arrest"; i.e., several follicles develop to a size of 5–7&nbsp;mm, but not further. No single follicle reaches the preovulatory size (16&nbsp;mm or more). According to the Rotterdam criteria, 12 or more small follicles should be seen in an ovary on ultrasound examination.<ref name=emedicine_main /> More recent research suggests that there should be at least 25 follicles in an ovary to designate it as having polycystic ovarian morphology (PCOM) in women aged 18–35 years.<ref name="DewaillyLujan2013">{{cite journal | author = Dewailly D, Lujan ME, Carmina E, Cedars MI, Laven J, Norman RJ, Escobar-Morreale HF | title = Definition and significance of polycystic ovarian morphology: a task force report from the Androgen Excess and Polycystic Ovary Syndrome Society | journal = Hum. Reprod. Update | volume = 20 | issue = 3 | pages = 334–52 | year = 2014 | pmid = 24345633 | doi = 10.1093/humupd/dmt061 }}</ref> The follicles may be oriented in the periphery, giving the appearance of a 'string of pearls'.<ref name="O'Brien2011">{{cite book|last=O'Brien|first=William T.|title=Top 3 Differentials in Radiology|url=http://books.google.com/books?id=l9BmkWhvcXYC&pg=PA369|accessdate=30 August 2014|date=1 January 2011|publisher=Thieme|isbn=9781604062281|page=369|quote=Ultrasound findings in PCOS include enlarged ovaries with peripheral follicles in a "string of pearls" configuration.}}</ref> If a high resolution transvaginal ultrasonography machine is not available, an ovarian volume of at least 10 ml is regarded as an acceptable definition of having polycystic ovarian morphology instead of follicle count.<ref name="DewaillyLujan2013"/>
+* [[Gynecologic ultrasonography]], specifically looking for small [[ovarian follicles]]. These are believed to be the result of disturbed ovarian function with failed ovulation, reflected by the infrequent or absent menstruation that is typical of the condition. In a normal [[menstrual cycle]], one egg is released from a dominant follicle&nbsp;– in essence, a cyst that bursts to release the egg. After ovulation, the follicle remnant is transformed into a [[progesterone]]-producing [[corpus luteum]], which shrinks and disappears after approximately 12–14 days. In PCOS, there is a so-called "follicular arrest"; i.e., several follicles develop to a size of 5–7&nbsp;mm, but not further. No single follicle reaches the preovulatory size (16&nbsp;mm or more). According to the Rotterdam criteria, 12 or more small follicles should be seen in an ovary on ultrasound examination.<ref name=emedicine_main /> More recent research suggests that there should be at least 25 follicles in an ovary to designate it as having polycystic ovarian morphology (PCOM) in people with ovaries aged 18–35 years.<ref name="DewaillyLujan2013">{{cite journal | author = Dewailly D, Lujan ME, Carmina E, Cedars MI, Laven J, Norman RJ, Escobar-Morreale HF | title = Definition and significance of polycystic ovarian morphology: a task force report from the Androgen Excess and Polycystic Ovary Syndrome Society | journal = Hum. Reprod. Update | volume = 20 | issue = 3 | pages = 334–52 | year = 2014 | pmid = 24345633 | doi = 10.1093/humupd/dmt061 }}</ref> The follicles may be oriented in the periphery, giving the appearance of a 'string of pearls'.<ref name="O'Brien2011">{{cite book|last=O'Brien|first=William T.|title=Top 3 Differentials in Radiology|url=http://books.google.com/books?id=l9BmkWhvcXYC&pg=PA369|accessdate=30 August 2014|date=1 January 2011|publisher=Thieme|isbn=9781604062281|page=369|quote=Ultrasound findings in PCOS include enlarged ovaries with peripheral follicles in a "string of pearls" configuration.}}</ref> If a high resolution transvaginal ultrasonography machine is not available, an ovarian volume of at least 10 ml is regarded as an acceptable definition of having polycystic ovarian morphology instead of follicle count.<ref name="DewaillyLujan2013"/>
 * [[laparoscopic surgery|Laparoscopic]] examination may reveal a thickened, smooth, pearl-white outer surface of the ovary. (This would usually be an incidental finding if laparoscopy were performed for some other reason, as it would not be routine to examine the ovaries in this way to confirm a diagnosis of PCOS.){{Citation needed|date=November 2011}}
-* Serum (blood) levels of [[androgen]]s (male hormones), including [[androstenedione]] and [[testosterone]] may be elevated.<ref name=BMC_Teede /> [[Dehydroepiandrosterone sulfate]] levels above 700-800&nbsp;µg/dL are highly suggestive of adrenal dysfunction because DHEA-S is made exclusively by the adrenal glands.<ref name="pmid18844715">{{cite journal | author = Somani N, Harrison S, Bergfeld WF | title = The clinical evaluation of hirsutism | journal = Dermatologic therapy | volume = 21 | issue = 5 | pages = 376–91 | year = 2008 | pmid = 18844715 | doi = 10.1111/j.1529-8019.2008.00219.x }}</ref><ref name=emedicine_workup>{{cite web|url=http://emedicine.medscape.com/article/256806-workup#showall|title=Polycystic Ovarian Syndrome Workup|publisher=[[eMedicine]]|date=25 October 2011|accessdate=19 November 2011}}</ref> The free testosterone level is thought to be the best measure,<ref name=emedicine_workup /><ref name="pmid17603706">{{cite journal | author = Sharquie KE, Al-Bayatti AA, Al-Ajeel AI, Al-Bahar AJ, Al-Nuaimy AA | title = Free testosterone, luteinizing hormone/follicle stimulating hormone ratio and pelvic sonography in relation to skin manifestations in patients with polycystic ovary syndrome | journal = Saudi Med J | volume = 28 | issue = 7 | pages = 1039–43 | date = July 2007 | pmid = 17603706 | doi =  | url =  }}</ref> with ~60% of PCOS patients demonstrating supranormal levels.<ref name="huang"/> The [[Free androgen index]] (FAI) of the ratio of testosterone to [[sex hormone-binding globulin]] (SHBG) is high<ref name=BMC_Teede /><ref name=emedicine_workup /> and is meant to be a predictor of free testosterone, but is a poor parameter for this and is no better than testosterone alone as a marker for PCOS,<ref name="pmid1296589">{{cite journal | author = Robinson S, Rodin DA, Deacon A, Wheeler MJ, Clayton RN | title = Which hormone tests for the diagnosis of polycystic ovary syndrome? | journal = Br J Obstet Gynaecol | volume = 99 | issue = 3 | pages = 232–8 | date = March 1992 | pmid = 1296589 | doi = 10.1111/j.1471-0528.1992.tb14505.x }}</ref> possibly because FAI is correlated with the degree of obesity.<ref name="pmid16409817">{{cite journal | author = Li X, Lin JF | title = [Clinical features, hormonal profile, and metabolic abnormalities of obese women with obese polycystic ovary syndrome] | language = Chinese | journal = Zhonghua Yi Xue Za Zhi | volume = 85 | issue = 46 | pages = 3266–71 | date = December 2005 | pmid = 16409817 }}</ref>
+* Serum (blood) levels of [[androgen]]s (male hormones), including [[androstenedione]] and [[testosterone]] may be elevated.<ref name=BMC_Teede /> [[Dehydroepiandrosterone sulfate]] levels above 700-800&nbsp;µg/dL are highly suggestive of adrenal dysfunction because DHEA-S is made exclusively by the adrenal glands.<ref name="pmid18844715">{{cite journal | author = Somani N, Harrison S, Bergfeld WF | title = The clinical evaluation of hirsutism | journal = Dermatologic therapy | volume = 21 | issue = 5 | pages = 376–91 | year = 2008 | pmid = 18844715 | doi = 10.1111/j.1529-8019.2008.00219.x }}</ref><ref name=emedicine_workup>{{cite web|url=http://emedicine.medscape.com/article/256806-workup#showall|title=Polycystic Ovarian Syndrome Workup|publisher=[[eMedicine]]|date=25 October 2011|accessdate=19 November 2011}}</ref> The free testosterone level is thought to be the best measure,<ref name=emedicine_workup /><ref name="pmid17603706">{{cite journal | author = Sharquie KE, Al-Bayatti AA, Al-Ajeel AI, Al-Bahar AJ, Al-Nuaimy AA | title = Free testosterone, luteinizing hormone/follicle stimulating hormone ratio and pelvic sonography in relation to skin manifestations in patients with polycystic ovary syndrome | journal = Saudi Med J | volume = 28 | issue = 7 | pages = 1039–43 | date = July 2007 | pmid = 17603706 | doi =  | url =  }}</ref> with ~60% of PCOS patients demonstrating supranormal levels.<ref name="huang"/> The [[Free androgen index]] (FAI) of the ratio of testosterone to [[sex hormone-binding globulin]] (SHBG) is high<ref name=BMC_Teede /><ref name=emedicine_workup /> and is meant to be a predictor of free testosterone, but is a poor parameter for this and is no better than testosterone alone as a marker for PCOS,<ref name="pmid1296589">{{cite journal | author = Robinson S, Rodin DA, Deacon A, Wheeler MJ, Clayton RN | title = Which hormone tests for the diagnosis of polycystic ovary syndrome? | journal = Br J Obstet Gynaecol | volume = 99 | issue = 3 | pages = 232–8 | date = March 1992 | pmid = 1296589 | doi = 10.1111/j.1471-0528.1992.tb14505.x }}</ref> possibly because FAI is correlated with the degree of obesity.<ref name="pmid16409817">{{cite journal | author = Li X, Lin JF | title = [Clinical features, hormonal profile, and metabolic abnormalities of obese people with ovaries with obese polycystic ovary syndrome] | language = Chinese | journal = Zhonghua Yi Xue Za Zhi | volume = 85 | issue = 46 | pages = 3266–71 | date = December 2005 | pmid = 16409817 }}</ref>
-Some other blood tests are suggestive but not diagnostic. The ratio of LH ([[Luteinizing hormone]]) to FSH ([[Follicle-stimulating hormone]]), when measured in [[international unit]]s, is elevated in women with PCOS. Common [[cut-off (reference value)|cut-off]]s to designate abnormally high LH/FSH ratios are 2:1<ref name=Banaszewska2003/> or 3:1<ref name=emedicine_workup /> as tested on Day 3 of the menstrual cycle. The pattern is not very specific and a ratio of 2:1 or higher was present in less than 50% of women with PCOS in one study.<ref name=Banaszewska2003>{{cite journal | author = Banaszewska B, Spaczyński RZ, Pelesz M, Pawelczyk L | title = Incidence of elevated LH/FSH ratio in polycystic ovary syndrome women with normo- and hyperinsulinemia | journal = Rocz. Akad. Med. Bialymst. | volume = 48 | issue =  | pages = 131–4 | year = 2003 | pmid = 14737959 | doi =  }}</ref> There are often low levels of [[sex hormone-binding globulin]],<ref name=emedicine_workup /> in particular among obese or overweight women.{{Citation needed|date=November 2011}}
+Some other blood tests are suggestive but not diagnostic. The ratio of LH ([[Luteinizing hormone]]) to FSH ([[Follicle-stimulating hormone]]), when measured in [[international unit]]s, is elevated in people with ovaries with PCOS. Common [[cut-off (reference value)|cut-off]]s to designate abnormally high LH/FSH ratios are 2:1<ref name=Banaszewska2003/> or 3:1<ref name=emedicine_workup /> as tested on Day 3 of the menstrual cycle. The pattern is not very specific and a ratio of 2:1 or higher was present in less than 50% of people with ovaries with PCOS in one study.<ref name=Banaszewska2003>{{cite journal | author = Banaszewska B, Spaczyński RZ, Pelesz M, Pawelczyk L | title = Incidence of elevated LH/FSH ratio in polycystic ovary syndrome women with normo- and hyperinsulinemia | journal = Rocz. Akad. Med. Bialymst. | volume = 48 | issue =  | pages = 131–4 | year = 2003 | pmid = 14737959 | doi =  }}</ref> There are often low levels of [[sex hormone-binding globulin]],<ref name=emedicine_workup /> in particular among obese or overweight people with ovaries.{{Citation needed|date=November 2011}}
 [[Anti-Müllerian hormone]] (AMH) is increased in PCOS, and may become part of its diagnostic criteria.<ref name="DewaillyAndersen2014">{{cite journal | author = Dewailly D, Andersen CY, Balen A, Broekmans F, Dilaver N, Fanchin R, Griesinger G, Kelsey TW, La Marca A, Lambalk C, Mason H, Nelson SM, Visser JA, Wallace WH, Anderson RA | title = The physiology and clinical utility of anti-Mullerian hormone in women | journal = Hum. Reprod. Update | volume = 20 | issue = 3 | pages = 370–85 | year = 2014 | pmid = 24430863 | doi = 10.1093/humupd/dmt062 }}</ref><ref name="BroerBroekmans2014">{{cite journal|last1=Broer|first1=S. L.|last2=Broekmans|first2=F. J. M.|last3=Laven|first3=J. S. E.|last4=Fauser|first4=B. C. J. M.|title=Anti-Mullerian hormone: ovarian reserve testing and its potential clinical implications|journal=Human Reproduction Update|volume=20|issue=5|year=2014|pages=688–701|issn=1355-4786|doi=10.1093/humupd/dmu020}}</ref>
@@ Line 85: / Line 85: @@
 === Associated conditions===
 * Fasting biochemical screen and lipid profile<ref name="emedicine_workup"/>
-* 2-Hour oral [[glucose tolerance test]] (GTT) in women with risk factors (obesity, family history, history of gestational diabetes)<ref name=BMC_Teede /> may indicate impaired glucose tolerance (insulin resistance) in 15–33% of women with PCOS.<ref name=emedicine_workup /> Frank diabetes can be seen in 65–68% of women with this condition.{{Citation needed|date=November 2011|reason=Also, which criteria is this using? NIH or Rotterdam?}} Insulin resistance can be observed in both normal weight and overweight people, although it is more common in the latter (and in those matching the stricter NIH criteria for diagnosis); 50–80% of people with PCOS may have insulin resistance at some level.<ref name=BMC_Teede />
+* 2-Hour oral [[glucose tolerance test]] (GTT) in people with ovaries with risk factors (obesity, family history, history of gestational diabetes)<ref name=BMC_Teede /> may indicate impaired glucose tolerance (insulin resistance) in 15–33% of people with PCOS.<ref name=emedicine_workup /> Frank diabetes can be seen in 65–68% of people with this condition.{{Citation needed|date=November 2011|reason=Also, which criteria is this using? NIH or Rotterdam?}} Insulin resistance can be observed in both normal weight and overweight people, although it is more common in the latter (and in those matching the stricter NIH criteria for diagnosis); 50–80% of people with PCOS may have insulin resistance at some level.<ref name=BMC_Teede />
-* Fasting insulin level or GTT with insulin levels (also called IGTT). Elevated insulin levels have been helpful to predict response to medication and may indicate women needing higher dosages of metformin or the use of a second medication to significantly lower insulin levels. Elevated [[blood sugar]] and insulin values do not predict who responds to an insulin-lowering medication, low-glycemic diet, and exercise. Many women with normal levels may benefit from combination therapy. A hypoglycemic response in which the two-hour insulin level is higher and the blood sugar lower than fasting is consistent with insulin resistance. A mathematical derivation known as the HOMAI, calculated from the fasting values in glucose and insulin concentrations, allows a direct and moderately accurate measure of insulin sensitivity (glucose-level x insulin-level/22.5).{{Citation needed|date=November 2011}}
+* Fasting insulin level or GTT with insulin levels (also called IGTT). Elevated insulin levels have been helpful to predict response to medication and may indicate needing higher dosages of metformin or the use of a second medication to significantly lower insulin levels. Elevated [[blood sugar]] and insulin values do not predict who responds to an insulin-lowering medication, low-glycemic diet, and exercise. Many people with normal levels may benefit from combination therapy. A hypoglycemic response in which the two-hour insulin level is higher and the blood sugar lower than fasting is consistent with insulin resistance. A mathematical derivation known as the HOMAI, calculated from the fasting values in glucose and insulin concentrations, allows a direct and moderately accurate measure of insulin sensitivity (glucose-level x insulin-level/22.5).{{Citation needed|date=November 2011}}
-*[[Glucose tolerance test]]ing (GTT) instead of fasting glucose can increase diagnosis of increased glucose tolerance and frank diabetes among people with PCOS according to a prospective controlled trial.<ref name="pmid9920077">{{cite journal | author = Legro RS, Kunselman AR, Dodson WC, Dunaif A | title = Prevalence and predictors of risk for type 2 diabetes mellitus and impaired glucose tolerance in polycystic ovary syndrome: a prospective, controlled study in 254 affected women | journal = J. Clin. Endocrinol. Metab. | volume = 84 | issue = 1 | pages = 165–9 | year = 1999 | pmid = 9920077 | doi = 10.1210/jc.84.1.165 | url = http://jcem.endojournals.org/cgi/pmidlookup?view=long&pmid=9920077 }}</ref> While fasting glucose levels may remain within normal limits, oral glucose tests revealed that up to 38% of asymptomatic women with PCOS (versus 8.5% in the general population) actually had impaired glucose tolerance, 7.5% of those with frank diabetes according to ADA guidelines.<ref name="pmid9920077"/>
+*[[Glucose tolerance test]]ing (GTT) instead of fasting glucose can increase diagnosis of increased glucose tolerance and frank diabetes among people with PCOS according to a prospective controlled trial.<ref name="pmid9920077">{{cite journal | author = Legro RS, Kunselman AR, Dodson WC, Dunaif A | title = Prevalence and predictors of risk for type 2 diabetes mellitus and impaired glucose tolerance in polycystic ovary syndrome: a prospective, controlled study in 254 affected women | journal = J. Clin. Endocrinol. Metab. | volume = 84 | issue = 1 | pages = 165–9 | year = 1999 | pmid = 9920077 | doi = 10.1210/jc.84.1.165 | url = http://jcem.endojournals.org/cgi/pmidlookup?view=long&pmid=9920077 }}</ref> While fasting glucose levels may remain within normal limits, oral glucose tests revealed that up to 38% of asymptomatic people with PCOS (versus 8.5% in the general population) actually had impaired glucose tolerance, 7.5% of those with frank diabetes according to ADA guidelines.<ref name="pmid9920077"/>
 === Differential diagnosis ===
@@ Line 95: / Line 95: @@
 Polycystic ovaries develop when the ovaries are stimulated to produce excessive amounts of male hormones (androgens), in particular testosterone, by either one or a combination of the following (almost certainly combined with genetic susceptibility<ref name="AnnNYAS_thoughts"/>):
 *the release of excessive [[luteinizing hormone]] (LH) by the anterior pituitary gland{{Citation needed|date=November 2011}}
-*through high levels of insulin in the blood (hyperinsulinaemia) in women whose ovaries are sensitive to this stimulus<ref name=MayoClinic>{{cite web|url=http://www.mayoclinic.com/health/polycystic-ovary-syndrome/DS00423/METHOD=print&DSECTION=all|author=Mayo Clinic Staff|publisher=Mayo Clinic|work=MayoClinic.com|title=Polycystic Ovary Syndrome&nbsp;– All|date=4 April 2011|accessdate=15 November 2011}}</ref>
+*through high levels of insulin in the blood (hyperinsulinaemia) in people whose ovaries are sensitive to this stimulus<ref name=MayoClinic>{{cite web|url=http://www.mayoclinic.com/health/polycystic-ovary-syndrome/DS00423/METHOD=print&DSECTION=all|author=Mayo Clinic Staff|publisher=Mayo Clinic|work=MayoClinic.com|title=Polycystic Ovary Syndrome&nbsp;– All|date=4 April 2011|accessdate=15 November 2011}}</ref>
 Also, reduced levels of sex-hormone-binding globulin can result in increased free androgens.{{Citation needed|date=November 2011}}
 The syndrome acquired its most widely used name due to the common sign on ultrasound examination of multiple (poly) ovarian [[cyst]]s. These "cysts" are actually immature [[ovarian follicle|follicles]] not cysts. The follicles have developed from primordial follicles, but the development has stopped ("arrested") at an early antral stage due to the disturbed ovarian function. The follicles may be oriented along the ovarian periphery, appearing as a 'string of pearls' on ultrasound examination.{{Citation needed|date=November 2011}}
-Women with PCOS experience an increased frequency of hypothalamic GnRH pulses, which in turn results in an increase in the LH/FSH ratio.<ref>http://www.ncbi.nlm.nih.gov/pubmed/21528473</ref>
+People with PCOS experience an increased frequency of hypothalamic GnRH pulses, which in turn results in an increase in the LH/FSH ratio.<ref>http://www.ncbi.nlm.nih.gov/pubmed/21528473</ref>
-A majority of people with PCOS have insulin resistance and/or are obese. Their elevated insulin levels contribute to or cause the abnormalities seen in the [[hypothalamic-pituitary-ovarian axis]] that lead to PCOS. Hyperinsulinemia increases [[GnRH]] pulse frequency, LH over FSH dominance, increased ovarian androgen production,<ref name=MayoClinic /> decreased follicular maturation, and decreased [[SHBG]] binding; all these steps contribute to the development of PCOS.{{Citation needed|date=November 2011}} Insulin resistance is a common finding among women with a normal weight as well as overweight women.<ref name=BMC_Teede /><ref name="FertSter_insulin"/>
+A majority of people with PCOS have insulin resistance and/or are obese. Their elevated insulin levels contribute to or cause the abnormalities seen in the [[hypothalamic-pituitary-ovarian axis]] that lead to PCOS. Hyperinsulinemia increases [[GnRH]] pulse frequency, LH over FSH dominance, increased ovarian androgen production,<ref name=MayoClinic /> decreased follicular maturation, and decreased [[SHBG]] binding; all these steps contribute to the development of PCOS.{{Citation needed|date=November 2011}} Insulin resistance is a common finding among people with a normal weight as well as overweight people.<ref name=BMC_Teede /><ref name="FertSter_insulin"/>
 In many cases, PCOS is characterised by a complex positive feedback loop of insulin resistance and hyperandrogenism. In most cases, it cannot be determined which (if any) of those two should be regarded causative. Experimental treatment with either antiandrogens or insulin-sensitizing agents improves both hyperandrogenism and insulin resistance.{{Citation needed|date=November 2011}}
-Adipose tissue possesses [[aromatase]], an enzyme that converts androstenedione to estrone and testosterone to estradiol. The excess of adipose tissue in obese women creates the paradox of having both excess androgens (which are responsible for hirsutism and [[virilization]]) and estrogens (which inhibits FSH via negative feedback).<ref>Kumar Cotran Robbins: Basic Pathology 6th ed. / Saunders 1996</ref>
+Adipose tissue possesses [[aromatase]], an enzyme that converts androstenedione to estrone and testosterone to estradiol. The excess of adipose tissue in obese people creates the paradox of having both excess androgens (which are responsible for hirsutism and [[virilization]]) and estrogens (which inhibits FSH via negative feedback).<ref>Kumar Cotran Robbins: Basic Pathology 6th ed. / Saunders 1996</ref>
 PCOS may be associated with chronic inflammation,<ref name=MayoClinic /><ref name=Mediators_Inflammation>{{cite journal | author = Sathyapalan T, Atkin SL | title = Mediators of Inflammation in Polycystic Ovary Syndrome in Relation to Adiposity | journal = Mediators of Inflammation | volume = 2010 | page = 758656 | year = 2010 | pmid = 20396393 | pmc = 2852606 | doi = 10.1155/2010/758656 | url = http://www.hindawi.com/journals/mi/2010/758656/ | publisher = Hindawi }}</ref> with several investigators correlating inflammatory mediators with anovulation and other PCOS symptoms.<!--
@@ Line 114: / Line 114: @@
 It has previously been suggested that the excessive androgen production in PCOS could be caused by a decreased serum level of [[IGFBP-1]], in turn increasing the level of free [[IGF-I]], which stimulates ovarian androgen production, but recent data concludes this mechanism to be unlikely.<ref>{{cite journal | author = Kelly CJ, Stenton SR, Lashen H | title = Insulin-like growth factor binding protein-1 in PCOS: a systematic review and meta-analysis | journal = Human Reproduction Update | volume = 17 | issue = 1 | pages = 4–16 | year = 2010 | pmid = 20634211 | doi = 10.1093/humupd/dmq027 }}</ref>
-PCOS has also been associated with a specific [[FMR1]] sub-genotype. The research suggests that women with ''heterozygous-normal/low'' FMR1 have polycystic-like symptoms of excessive follicle-activity and hyperactive ovarian function.<ref>{{cite journal | author = Gleicher N, Weghofer A, Lee IH, Barad DH | title = FMR1 Genotype with Autoimmunity-Associated Polycystic Ovary-Like Phenotype and Decreased Pregnancy Chance | journal = PLoS ONE | volume = 5 | issue = 12 | page = e15303 | year = 2010 | pmid = 21179569 | pmc = 3002956 | doi = 10.1371/journal.pone.0015303 | editor1-last = Mailund | editor1-first = Thomas }}</ref>
+PCOS has also been associated with a specific [[FMR1]] sub-genotype. The research suggests that people with ovaries with ''heterozygous-normal/low'' FMR1 have polycystic-like symptoms of excessive follicle-activity and hyperactive ovarian function.<ref>{{cite journal | author = Gleicher N, Weghofer A, Lee IH, Barad DH | title = FMR1 Genotype with Autoimmunity-Associated Polycystic Ovary-Like Phenotype and Decreased Pregnancy Chance | journal = PLoS ONE | volume = 5 | issue = 12 | page = e15303 | year = 2010 | pmid = 21179569 | pmc = 3002956 | doi = 10.1371/journal.pone.0015303 | editor1-last = Mailund | editor1-first = Thomas }}</ref>
 == Management ==
@@ Line 127: / Line 127: @@
 General interventions that help to reduce weight or insulin resistance can be beneficial for all these aims, because they address what is believed to be the underlying cause.
-As PCOS appears to cause significant emotional distress, appropriate support may be useful.<ref name="pmid22824735">{{cite journal | author = Veltman-Verhulst SM, Boivin J, Eijkemans MJ, Fauser BJ | title = Emotional distress is a common risk in women with polycystic ovary syndrome: a systematic review and meta-analysis of 28 studies | journal = Hum. Reprod. Update | volume = 18 | issue = 6 | pages = 638–51 | year = 2012 | pmid = 22824735 | doi = 10.1093/humupd/dms029 | url =  }}</ref>
+As PCOS appears to cause significant emotional distress, appropriate support may be useful.<ref name="pmid22824735">{{cite journal | author = Veltman-Verhulst SM, Boivin J, Eijkemans MJ, Fauser BJ | title = Emotional distress is a common risk in people with polycystic ovary syndrome: a systematic review and meta-analysis of 28 studies | journal = Hum. Reprod. Update | volume = 18 | issue = 6 | pages = 638–51 | year = 2012 | pmid = 22824735 | doi = 10.1093/humupd/dms029 | url =  }}</ref>
 === Diet ===
-Where PCOS is associated with overweight or obesity, successful weight loss is the most effective method of restoring normal ovulation/menstruation, but many women find it very difficult to achieve and sustain significant weight loss. A [[scientific review]] in 2013 found similar decreases in weight and body composition and improvements in [[pregnancy rate]], menstrual regularity, ovulation, hyperandrogenism, insulin resistance, lipids, and quality of life to occur with weight loss independent of diet composition.<ref name=Moran2013>{{cite journal | author = Moran LJ, Ko H, Misso M, Marsh K, Noakes M, Talbot M, Frearson M, Thondan M, Stepto N, Teede HJ | title = Dietary composition in the treatment of polycystic ovary syndrome: a systematic review to inform evidence-based guidelines. | journal = Human reproduction update | volume = 19 | issue = 5 | pages = 432 | date = Sep–Oct 2013 | pmid = 23727939 | doi = 10.1093/humupd/dmt015 }}</ref> Still, a [[low GI diet]], in which a significant part of total carbohydrates are obtained from fruit, vegetables, and whole-grain sources, has resulted in greater menstrual regularity than a [[macronutrient]]-matched healthy diet.<ref name=Moran2013/> [[Vitamin D deficiency]] may play some role in the development of the [[metabolic syndrome]], so treatment of any such deficiency is indicated.<ref name=emedicine_treatment />
+Where PCOS is associated with overweight or obesity, successful weight loss is the most effective method of restoring normal ovulation/menstruation, but many people find it very difficult to achieve and sustain significant weight loss. A [[scientific review]] in 2013 found similar decreases in weight and body composition and improvements in [[pregnancy rate]], menstrual regularity, ovulation, hyperandrogenism, insulin resistance, lipids, and quality of life to occur with weight loss independent of diet composition.<ref name=Moran2013>{{cite journal | author = Moran LJ, Ko H, Misso M, Marsh K, Noakes M, Talbot M, Frearson M, Thondan M, Stepto N, Teede HJ | title = Dietary composition in the treatment of polycystic ovary syndrome: a systematic review to inform evidence-based guidelines. | journal = Human reproduction update | volume = 19 | issue = 5 | pages = 432 | date = Sep–Oct 2013 | pmid = 23727939 | doi = 10.1093/humupd/dmt015 }}</ref> Still, a [[low GI diet]], in which a significant part of total carbohydrates are obtained from fruit, vegetables, and whole-grain sources, has resulted in greater menstrual regularity than a [[macronutrient]]-matched healthy diet.<ref name=Moran2013/> [[Vitamin D deficiency]] may play some role in the development of the [[metabolic syndrome]], so treatment of any such deficiency is indicated.<ref name=emedicine_treatment />
 === Medications ===
-Reducing insulin resistance by improving insulin sensitivity through medications such as [[metformin]], and the newer [[thiazolidinedione]] (glitazones), have been an obvious approach and initial studies seemed to show effectiveness.<ref name=MayoClinic /><ref name=emedicine_treatment /><ref name=Lord>{{cite journal | author = Lord JM, Flight IH, Norman RJ | title = Metformin in polycystic ovary syndrome: systematic review and meta-analysis | journal = BMJ | volume = 327 | issue = 7421 | pages = 951–3 | year = 2003 | pmid = 14576245 | pmc = 259161 | doi = 10.1136/bmj.327.7421.951 | url = http://www.bmj.com/cgi/content/full/327/7421/951 }}</ref> Although metformin is [[Off-label use|not licensed]] for use in PCOS, the United Kingdom's [[National Institute for Health and Clinical Excellence]] recommended in 2004 that women with PCOS and a [[body mass index]] above 25 be given metformin when other therapy has failed to produce results.<ref name="NICE2004">{{NICE | 11 | Fertility: assessment and treatment for people with fertility problems | 2004}}</ref> However subsequent reviews in 2008 and 2009 have noted that [[randomised control trial]]s have in general not shown the promise suggested by the early [[observational studies]].<ref>{{cite web |author=Balen A |title=Metformin therapy for the management of infertility in women with polycystic ovary syndrome |work=Scientific Advisory Committee Opinion Paper 13 |publisher=Royal College of Obstetricians and Gynaecologists |date=December 2008 |url=http://www.rcog.org.uk/files/rcog-corp/uploaded-files/SAC13metformin-minorrevision.pdf |format=PDF |accessdate=2009-12-13}}</ref><ref name="pmid19697191">{{cite journal | author = Leeman L, Acharya U | title = The use of metformin in the management of polycystic ovary syndrome and associated anovulatory infertility: the current evidence | journal = J Obstet Gynaecol | volume = 29 | issue = 6 | pages = 467–72 | date = August 2009 | pmid = 19697191 | doi = 10.1080/01443610902829414 | url =  }}</ref> A review in 2014 concluded that there is no evidence that metformin could cause any increased risk of major [[birth defect]]s in women affected by PCOS and treated during the first trimester.<ref name="CassinaDona2014">{{cite journal|last1=Cassina|first1=M.|last2=Dona|first2=M.|last3=Di Gianantonio|first3=E.|last4=Litta|first4=P.|last5=Clementi|first5=M.|title=First-trimester exposure to metformin and risk of birth defects: a systematic review and meta-analysis|journal=Human Reproduction Update|volume=20|issue=5|year=2014|pages=656–669|issn=1355-4786|doi=10.1093/humupd/dmu022}}</ref>
+Reducing insulin resistance by improving insulin sensitivity through medications such as [[metformin]], and the newer [[thiazolidinedione]] (glitazones), have been an obvious approach and initial studies seemed to show effectiveness.<ref name=MayoClinic /><ref name=emedicine_treatment /><ref name=Lord>{{cite journal | author = Lord JM, Flight IH, Norman RJ | title = Metformin in polycystic ovary syndrome: systematic review and meta-analysis | journal = BMJ | volume = 327 | issue = 7421 | pages = 951–3 | year = 2003 | pmid = 14576245 | pmc = 259161 | doi = 10.1136/bmj.327.7421.951 | url = http://www.bmj.com/cgi/content/full/327/7421/951 }}</ref> Although metformin is [[Off-label use|not licensed]] for use in PCOS, the United Kingdom's [[National Institute for Health and Clinical Excellence]] recommended in 2004 that people with PCOS and a [[body mass index]] above 25 be given metformin when other therapy has failed to produce results.<ref name="NICE2004">{{NICE | 11 | Fertility: assessment and treatment for people with fertility problems | 2004}}</ref> However subsequent reviews in 2008 and 2009 have noted that [[randomised control trial]]s have in general not shown the promise suggested by the early [[observational studies]].<ref>{{cite web |author=Balen A |title=Metformin therapy for the management of infertility in people with polycystic ovary syndrome |work=Scientific Advisory Committee Opinion Paper 13 |publisher=Royal College of Obstetricians and Gynaecologists |date=December 2008 |url=http://www.rcog.org.uk/files/rcog-corp/uploaded-files/SAC13metformin-minorrevision.pdf |format=PDF |accessdate=2009-12-13}}</ref><ref name="pmid19697191">{{cite journal | author = Leeman L, Acharya U | title = The use of metformin in the management of polycystic ovary syndrome and associated anovulatory infertility: the current evidence | journal = J Obstet Gynaecol | volume = 29 | issue = 6 | pages = 467–72 | date = August 2009 | pmid = 19697191 | doi = 10.1080/01443610902829414 | url =  }}</ref> A review in 2014 concluded that there is no evidence that metformin could cause any increased risk of major [[birth defect]]s in people affected by PCOS and treated during the first trimester.<ref name="CassinaDona2014">{{cite journal|last1=Cassina|first1=M.|last2=Dona|first2=M.|last3=Di Gianantonio|first3=E.|last4=Litta|first4=P.|last5=Clementi|first5=M.|title=First-trimester exposure to metformin and risk of birth defects: a systematic review and meta-analysis|journal=Human Reproduction Update|volume=20|issue=5|year=2014|pages=656–669|issn=1355-4786|doi=10.1093/humupd/dmu022}}</ref>
 === Infertility ===
 {{Main|Infertility in polycystic ovary syndrome}}
-Not all women with PCOS have difficulty becoming pregnant. For those that do, [[anovulation]] or infrequent ovulation is a common cause. Other factors include changed levels of [[gonadotropin]]s, [[hyperandrogenemia]] and [[hyperinsulinemia]].<ref name=Qiao2011>{{cite journal | author = Qiao J, Feng HL | title = Extra- and intra-ovarian factors in polycystic ovary syndrome: impact on oocyte maturation and embryo developmental competence | journal = Human Reproduction Update | volume = 17 | issue = 1 | pages = 17–33 | year = 2010 | pmid = 20639519 | pmc = 3001338 | doi = 10.1093/humupd/dmq032 }}</ref> Like women without PCOS, women with PCOS that are ovulating may be infertile due to other causes, such as tubal blockages due to a history of sexually transmitted diseases.
+Not all people with PCOS have difficulty becoming pregnant. For those that do, [[anovulation]] or infrequent ovulation is a common cause. Other factors include changed levels of [[gonadotropin]]s, [[hyperandrogenemia]] and [[hyperinsulinemia]].<ref name=Qiao2011>{{cite journal | author = Qiao J, Feng HL | title = Extra- and intra-ovarian factors in polycystic ovary syndrome: impact on oocyte maturation and embryo developmental competence | journal = Human Reproduction Update | volume = 17 | issue = 1 | pages = 17–33 | year = 2010 | pmid = 20639519 | pmc = 3001338 | doi = 10.1093/humupd/dmq032 }}</ref> Like people without PCOS, people with PCOS that are ovulating may be infertile due to other causes, such as tubal blockages due to a history of sexually transmitted diseases.
-For overweight, anovulatory women with PCOS, [[weight loss]] and diet adjustments, especially to reduce the intake of simple carbohydrates, are associated with resumption of natural ovulation.
+For overweight, anovulatory people with PCOS, [[weight loss]] and diet adjustments, especially to reduce the intake of simple carbohydrates, are associated with resumption of natural ovulation.
-For those women that after weight loss still are anovulatory or for anovulatory lean women, then the ovulation-inducing medications [[clomiphene citrate]]<ref name=emedicine_treatment /> and [[Follicle-stimulating hormone|FSH]] are the principal treatments used to promote ovulation.<ref name=MayoClinic />  Previously, the anti-diabetes medication metformin was recommended treatment for anovulation,<ref name=MayoClinic /> but it appears less effective than clomiphene.<ref>{{cite journal | author = Legro RS, Barnhart HX, Schlaff WD, Carr BR, Diamond MP, Carson SA, Steinkampf MP, Coutifaris C, McGovern PG, Cataldo NA, Gosman GG, Nestler JE, Giudice LC, Leppert PC, Myers ER | title = Clomiphene, Metformin, or Both for Infertility in the Polycystic Ovary Syndrome | journal = N Engl J Med | volume = 356 | issue = 6 | pages = 551–66 | year = 2007 | pmid = 17287476 | doi = 10.1056/NEJMoa063971 }}</ref>
+For those people that after weight loss still are anovulatory or for anovulatory lean people, then the ovulation-inducing medications [[clomiphene citrate]]<ref name=emedicine_treatment /> and [[Follicle-stimulating hormone|FSH]] are the principal treatments used to promote ovulation.<ref name=MayoClinic />  Previously, the anti-diabetes medication metformin was recommended treatment for anovulation,<ref name=MayoClinic /> but it appears less effective than clomiphene.<ref>{{cite journal | author = Legro RS, Barnhart HX, Schlaff WD, Carr BR, Diamond MP, Carson SA, Steinkampf MP, Coutifaris C, McGovern PG, Cataldo NA, Gosman GG, Nestler JE, Giudice LC, Leppert PC, Myers ER | title = Clomiphene, Metformin, or Both for Infertility in the Polycystic Ovary Syndrome | journal = N Engl J Med | volume = 356 | issue = 6 | pages = 551–66 | year = 2007 | pmid = 17287476 | doi = 10.1056/NEJMoa063971 }}</ref>
-For women not responsive to clomiphene and diet and lifestyle modification, there are options available including [[assisted reproductive technology]] procedures such as [[controlled ovarian hyperstimulation]] with [[follicle-stimulating hormone]] (FSH) injections followed by [[in vitro fertilisation]] (IVF).
+For people not responsive to clomiphene and diet and lifestyle modification, there are options available including [[assisted reproductive technology]] procedures such as [[controlled ovarian hyperstimulation]] with [[follicle-stimulating hormone]] (FSH) injections followed by [[in vitro fertilisation]] (IVF).
 Though surgery is not commonly performed, the polycystic ovaries can be treated with a laparoscopic procedure called "ovarian drilling" (puncture of 4–10 small follicles with electrocautery, laser, or biopsy needles), which often results in either resumption of spontaneous ovulations<ref name=emedicine_treatment /> or ovulations after adjuvant treatment with clomiphene or FSH.{{citation needed|date=November 2011}} (Ovarian wedge resection is no longer used as much due to complications such as [[adhesions]] and the presence of frequently effective medications.) There are, however, concerns about the long-term effects of ovarian drilling on ovarian function.<ref name=emedicine_treatment />
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 === Hirsutism and acne ===
 {{Details|Hirsutism}}
-When appropriate (e.g., in women of child-bearing age who require contraception), a standard contraceptive pill is frequently effective in reducing hirsutism.<ref name=MayoClinic /><ref name=emedicine_treatment /> A common choice of contraceptive pill is one that contains [[cyproterone acetate]]; in the UK, the available brands are Dianette/Diane. Cyproterone acetate is a [[progestogen]] with anti-[[androgen]] effects that block the action of male hormones that are believed to contribute to acne and the growth of unwanted facial and body hair.{{citation needed|date=November 2011}} On the other hand, progestogens such as norgestrel and levonorgestrel should be avoided due to their androgenic effects.<ref name=emedicine_treatment />
+When appropriate (e.g., in people of child-bearing age who require contraception), a standard contraceptive pill is frequently effective in reducing hirsutism.<ref name=MayoClinic /><ref name=emedicine_treatment /> A common choice of contraceptive pill is one that contains [[cyproterone acetate]]; in the UK, the available brands are Dianette/Diane. Cyproterone acetate is a [[progestogen]] with anti-[[androgen]] effects that block the action of male hormones that are believed to contribute to acne and the growth of unwanted facial and body hair.{{citation needed|date=November 2011}} On the other hand, progestogens such as norgestrel and levonorgestrel should be avoided due to their androgenic effects.<ref name=emedicine_treatment />
 Other drugs with anti-androgen effects include [[flutamide]],<ref name=flutamide>{{cite web|url=http://www.nhs.uk/Conditions/Polycystic-ovarian-syndrome/Pages/Treatment.aspx|title=Polycystic ovary syndrome&nbsp;– Treatment|publisher=National Health Service|location=United Kingdom|date=17 October 2011|accessdate=19 November 2011}}</ref> and [[spironolactone]],<ref name=MayoClinic /><ref name=emedicine_treatment /> which can give some improvement in hirsutism. Spironolactone is probably the most-commonly used drug in the US. Metformin can reduce hirsutism, perhaps by reducing insulin resistance, and is often used if there are other features such as insulin resistance, diabetes, or obesity that should also benefit from metformin. [[Eflornithine]] (Vaniqa) is a drug that is applied to the skin in cream form, and acts directly on the hair follicles to inhibit hair growth. It is usually applied to the face.<ref name=emedicine_treatment /> Medications that reduce acne by indirect hormonal effects also include ergot dopamine agonists such as [[bromocriptine]].{{citation needed|date=November 2011}} [[5-alpha reductase inhibitor]]s (such as [[finasteride]] and [[dutasteride]]) may also be used;<ref name=emedicine_medications>{{cite web|url=http://emedicine.medscape.com/article/256806-medication#showall|title=Polycystic Ovarian Syndrome Medication|publisher=eMedicine|author=Richard Scott Lucidi|date=25 October 2011|accessdate=19 November 2011}}</ref> they work by blocking the conversion of [[testosterone]] to [[dihydrotestosterone]] (the latter of which responsible for most hair growth alterations and androgenic acne).
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 == Prognosis ==
-Women with PCOS are at risk for the following:
+People with PCOS are at risk for the following:
 * [[Endometrial hyperplasia]] and [[endometrial cancer]] (cancer of the uterine lining) are possible, due to overaccumulation of uterine lining, and also lack of [[progesterone]] resulting in prolonged stimulation of uterine cells by estrogen.<ref name=MayoClinic /><ref name=emedicine_main /><ref name="BarryAzizia2014"/> It is not clear whether this risk is directly due to the syndrome or from the associated obesity, [[hyperinsulinemia]], and [[hyperandrogenism]].<ref>{{cite journal | author = New MI | title = Nonclassical congenital adrenal hyperplasia and the polycystic ovarian syndrome | journal = Annals of the New York Academy of Sciences | volume = 687 | issue = 1 Intraovarian | pages = 193–205 | date = May 1993 | pmid = 8323173 | doi = 10.1111/j.1749-6632.1993.tb43866.x }}</ref><ref>{{cite journal | author = Hardiman P, Pillay OC, Atiomo W | title = Polycystic ovary syndrome and endometrial carcinoma | journal = Lancet | volume = 361 | issue = 9371 | pages = 1810–2 | date = May 2003 | pmid = 12781553 | doi = 10.1016/S0140-6736(03)13409-5 }}</ref><ref>{{cite journal | author = Mather KJ, Kwan F, Corenblum B | title = Hyperinsulinemia in polycystic ovary syndrome correlates with increased cardiovascular risk independent of obesity | journal = Fertility and Sterility | volume = 73 | issue = 1 | pages = 150–6 | date = January 2000 | pmid = 10632431 | doi = 10.1016/S0015-0282(99)00468-9 }}</ref><ref>{{cite journal | author = Unfer V, Zacchè M, Serafini A, Redaelli A, Papaleo E | title = Treatment of hyperandrogenism and hyperinsulinemia in PCOS patients with essential amino acids. A pilot clinical study | journal = Minerva ginecologica | volume = 60 | issue = 5 | pages = 363–8 | date = October 2008 | pmid = 18854802 }}</ref>
-* [[Insulin resistance]]/[[Diabetes mellitus type 2|Type II diabetes]].<ref name=MayoClinic /> A review published in 2010 concluded that women with PCOS have an elevated prevalence of insulin resistance and type II diabetes, even when controlling for [[body mass index]] (BMI).<ref name=emedicine_main /><ref>{{cite journal | author = Moran LJ, Misso ML, Wild RA, Norman RJ | title = Impaired glucose tolerance, type 2 diabetes and metabolic syndrome in polycystic ovary syndrome: a systematic review and meta-analysis | journal = Hum Reprod Update | volume = 16 | issue = 4 | pages = 347–63 | date = May 2010 | pmid = 20159883 | doi = 10.1093/humupd/dmq001 | url =  }}</ref> PCOS also makes a woman, particularly if obese, prone to [[gestational diabetes]].<ref name=MayoClinic />
+* [[Insulin resistance]]/[[Diabetes mellitus type 2|Type II diabetes]].<ref name=MayoClinic /> A review published in 2010 concluded that people with PCOS have an elevated prevalence of insulin resistance and type II diabetes, even when controlling for [[body mass index]] (BMI).<ref name=emedicine_main /><ref>{{cite journal | author = Moran LJ, Misso ML, Wild RA, Norman RJ | title = Impaired glucose tolerance, type 2 diabetes and metabolic syndrome in polycystic ovary syndrome: a systematic review and meta-analysis | journal = Hum Reprod Update | volume = 16 | issue = 4 | pages = 347–63 | date = May 2010 | pmid = 20159883 | doi = 10.1093/humupd/dmq001 | url =  }}</ref> PCOS also makes a woman, particularly if obese, prone to [[gestational diabetes]].<ref name=MayoClinic />
 * [[High blood pressure]], in particular if obese and/or during pregnancy<ref name=MayoClinic />
 * [[Depression (mood)|Depression]]/Depression with [[Anxiety]]<ref name=BMC_Teede /><ref>{{cite journal | author = Barry JA, Kuczmierczyk AR, Hardiman PJ | title = Anxiety and depression in polycystic ovary syndrome: a systematic review and meta-analysis | journal = Hum. Reprod. | volume = 93 | issue = 6 | pages = 1948–56 | date = July 2011 | pmid = 21725075 | doi = 10.1093/humrep/der197 | url =  }}</ref>
-* [[Dyslipidemia]]<ref name=MayoClinic />&nbsp;– disorders of lipid metabolism&nbsp;— cholesterol and triglycerides. Women with PCOS show a decreased removal of [[atherosclerosis]]-inducing remnants, seemingly independent of insulin resistance/Type II diabetes.<ref>{{cite journal | author = Rocha MP, Maranhão RC, Seydell TM, Barcellos CR, Baracat EC, Hayashida SA, Bydlowski SP, Marcondes JA | title = Metabolism of triglyceride-rich lipoproteins and lipid transfer to high-density lipoprotein in young obese and normal-weight patients with polycystic ovary syndrome | journal = Fertil. Steril. | volume = 93 | issue = 6 | pages = 1948–56 | date = April 2010 | pmid = 19765700 | doi = 10.1016/j.fertnstert.2008.12.044 }}</ref>
+* [[Dyslipidemia]]<ref name=MayoClinic />&nbsp;– disorders of lipid metabolism&nbsp;— cholesterol and triglycerides. People with PCOS show a decreased removal of [[atherosclerosis]]-inducing remnants, seemingly independent of insulin resistance/Type II diabetes.<ref>{{cite journal | author = Rocha MP, Maranhão RC, Seydell TM, Barcellos CR, Baracat EC, Hayashida SA, Bydlowski SP, Marcondes JA | title = Metabolism of triglyceride-rich lipoproteins and lipid transfer to high-density lipoprotein in young obese and normal-weight patients with polycystic ovary syndrome | journal = Fertil. Steril. | volume = 93 | issue = 6 | pages = 1948–56 | date = April 2010 | pmid = 19765700 | doi = 10.1016/j.fertnstert.2008.12.044 }}</ref>
-* [[Cardiovascular disease]],<ref name=MayoClinic /><ref name=emedicine_main /> with a meta-analysis estimating a 2-fold risk of arterial disease for women with PCOS relative to women without PCOS, independent of BMI.<ref>{{cite journal | author = de Groot PC, Dekkers OM, Romijn JA, Dieben SW, Helmerhorst FM | title = PCOS, coronary heart disease, stroke and the influence of obesity: A systematic review and meta-analysis | journal = Human Reproduction Update | volume = 17 | issue = 4 | pages = 495–500 | year = 2011 | pmid = 21335359 | doi = 10.1093/humupd/dmr001 }}</ref>
+* [[Cardiovascular disease]],<ref name=MayoClinic /><ref name=emedicine_main /> with a meta-analysis estimating a 2-fold risk of arterial disease for people with ovaries with PCOS relative to people with ovaries without PCOS, independent of BMI.<ref>{{cite journal | author = de Groot PC, Dekkers OM, Romijn JA, Dieben SW, Helmerhorst FM | title = PCOS, coronary heart disease, stroke and the influence of obesity: A systematic review and meta-analysis | journal = Human Reproduction Update | volume = 17 | issue = 4 | pages = 495–500 | year = 2011 | pmid = 21335359 | doi = 10.1093/humupd/dmr001 }}</ref>
 * [[Stroke]]s<ref name=emedicine_main />
 * [[Weight gain]]<ref name=MayoClinic />
@@ Line 193: / Line 193: @@
 === Names ===
-Other names for this syndrome include '''polycystic ovary disease''', '''functional ovarian hyperandrogenism''', '''ovarian hyperthecosis''', '''sclerocystic ovary syndrome''', and '''Stein-Leventhal syndrome'''. The [[Medical eponyms|eponymous]] last option is the original name; it is now used, if at all, only for the subset of women with all the symptoms of amenorrhea with infertility, [[hirsutism]], and enlarged polycystic ovaries.<ref name=emedicine_imaging />
+Other names for this syndrome include '''polycystic ovary disease''', '''functional ovarian hyperandrogenism''', '''ovarian hyperthecosis''', '''sclerocystic ovary syndrome''', and '''Stein-Leventhal syndrome'''. The [[Medical eponyms|eponymous]] last option is the original name; it is now used, if at all, only for the subset of people with ovaries with all the symptoms of amenorrhea with infertility, [[hirsutism]], and enlarged polycystic ovaries.<ref name=emedicine_imaging />
 Most common names for this disease derive from a typical finding on medical images, called a polycystic ovary.<ref name=MayoClinic /> A polycystic ovary has an abnormally large number of developing eggs visible near its surface,<ref name=emedicine_imaging /> looking like many small [[cyst]]s<ref name=verity_what_is_PCOS>{{cite web|title=What is Polycystic Ovary Syndrome (PCOS)?|url=http://www.verity-pcos.org.uk/guide_to_pcos/what_is_pcos|year=2011|accessdate=21 November 2011|work=Verity&nbsp;– PCOS Charity|publisher=Verity}}</ref> or a [[Pearl#Pearls in jewelry|string of pearl]]s.