Wikipedia

Polyendocrine metabolic ovarian syndrome

(Redirected from PCOS)

Polyendocrine metabolic ovarian syndrome (PMOS), previously called polycystic ovary syndrome (PCOS),[11] is the most common hormonal disorder in women of reproductive age.

Polyendocrine metabolic ovarian syndrome
Other namesPolycystic ovary syndrome, Hyperandrogenic anovulation (HA),[1] Stein–Leventhal syndrome[2]
A polycystic ovary
SpecialtyGynecology, endocrinology
SymptomsIrregular menstrual periods, heavy periods, excess hair, acne, difficulty getting pregnant, patches of thick, darker, velvety skin[3]
ComplicationsType 2 diabetes, obesity, obstructive sleep apnea, heart disease, mood disorders, endometrial cancer[3]
DurationLong term[4]
CausesGenetic and environmental factors[5]
Risk factorsFamily history, obesity[6]
Diagnostic methodBased on irregular periods, high androgen levels, ovarian cysts[7]
Differential diagnosisAdrenal hyperplasia, hypothyroidism, high blood levels of prolactin[8]
ManagementHealthy lifestyle, medication[5]
MedicationBirth control pills, metformin, anti-androgens, fertility treatments such as letrozole[9][10]
Frequency5–18% of women of childbearing age[5]

PMOS is diagnosed when a woman has at least two of the following three features: irregular menstrual periods, high testosterone or related symptoms (like excess facial hair), or an excess of antral ovarian follicles on ultrasound; women with PMOS are not more likely than those without to have true ovarian cysts.[12] A blood test for high levels of anti-Müllerian hormone can replace the ultrasound in the diagnosis.[13] Other symptoms associated with PMOS are heavy periods, acne, difficulty getting pregnant, and patches of darker skin.[3][14]

The exact cause of PMOS remains uncertain.[15] There is a clear genetic component, but environmental factors are also thought to contribute. PMOS occurs in between 5% and 18% of women.[5] The disorder is linked to insulin resistance, which is made worse by obesity. Insulin resistance and related excess insulin levels increase the risk of complications such as type 2 diabetes and liver disease.[16] Women with PMOS also have higher risk of endometrial cancer.[17]

Management focuses on relieving symptoms and reducing long-term risks. A healthy lifestyle and weight control are recommended for general management. In addition, hormonal contraception can help regulate menstrual cycles and reduce acne and excess hair growth. Metformin, a common anti-diabetes drug, increases insulin sensitivity. For fertility, ovulation can be induced with letrozole, among other methods. In addition, women can be monitored for cardiometabolic risks, and during pregnancy.[5]

Signs and symptoms

edit

PMOS has a wide variety of signs and symptoms. They include issues with ovulation (such as irregular periods), excess levels of androgens (hormones that trigger male characteristics, such as facial hair growth), and metabolism (such as weight gain).[3] Symptoms usually start in puberty, but may be masked if oral contraceptives are started early.[18]

Common signs and symptoms of PMOS are:

The ovaries might be larger than normal, with many small fluid-filled sacs that surround eggs ("follicles").[21] Testosterone levels are usually elevated: one meta-analysis showed testosterone levels to be 1.5 times higher in women with PMOS compared to women without PMOS.[22]

Associated conditions

edit

Women with PMOS have an increased risk of a range of metabolic, cardiovascular, reproductive and mental health conditions. The likelihood of developing metabolic disorders is about three to seven times higher than in women without PMOS. Insulin resistance is common, even in lean women with PMOS.[23] Overweight or obese women with PMOS are at higher risk of type 2 diabetes than women without PMOS at the same BMI. Lean women with PMOS do not appear to be at higher risk of developing diabetes.[16] Other metabolic and cardiovascular complications commonly associated with PMOS include:

PMOS increases the risk of pregnancy complications, such as gestational diabetes, high blood pressure, low blood sugar levels, and pre-eclampsia. Miscarriages are more likely, and when a baby is delivered, they are more likely to require admission to the neonatal intensive care unit.[28]

PMOS is associated with mental health-related conditions including depression, anxiety, bipolar disorder, and obsessive–compulsive disorder.[29] Those with PMOS often report reduced quality of life due to excess body weight, and to a lesser extent due to hirsutism, infertility and menstrual cycles. In regions where infertility or hirsutism are stigmatised, the impact on mental health is more severe.[13] Body image can be negatively affected[30] and PMOS increases the risk of eating disorders,[31] such as binge eating.[5] In addition, sexual wellbeing is often lower in women with PMOS.[32]

Women with PMOS are about three times more likely to develop endometrial cancer. This is linked to lack of periods and lower levels of sex hormone-binding globulin (SHBG) and progesterone.[17] Women with PMOS more often have sleep apnea, particularly if obesity is present.[33]

Cause

edit

PMOS's root cause is unknown.[34] Risk factors include a family history of PMOS, early development of pubic hair and sweat gland development (adrenarche), and obesity. Low birth weight, exposure to androgens in the womb, and exposure to hormone disruptors may also predispose people to PMOS.[6]

Genetics

edit

PMOS has a clear genetic component and high heritability.[5] Evidence of the genetic basis comes from family and twin studies, as well as from large genome-wide association studies. The correlation in PMOS occurrence between identical twin sisters was found to be twice as high as that between non-identical twins, suggesting a significant genetic influence. Twenty-five different genetic loci have been found to correlate with PMOS in genome-wide association studies, of which thirteen were replicated in at least one other study. Variants in genes involved in insulin signaling and androgen synthesis, including those affecting ovarian steroidogenesis, have also been associated with increased susceptibility to PMOS. Genes near some of these loci imply neuroendocrine and metabolic dysfunction, but the role of other genes is not yet clear.[13]

Men with a family history of PMOS also display some of the symptoms associated with it. For instance, brothers of women with PMOS show a higher likelihood of high AMH levels, insulin resistance, and abnormal lipid levels in the blood. Men with the genetic risk factors associated with PMOS also have higher levels of obesity, type-2 diabetes, male pattern hair loss, and cardiovascular disease. Not all similarities between family members are likely due to genetics, as PMOS and obesity in mothers can have an impact on fetal development, making it more likely for men to get metabolic disorders with age.[13]

In Mendelian randomization, the question is whether exposure (e.g. obesity) causes outcome (e.g. PMOS). The technique assumes that there are genetic variants that increase the risk of the exposure, but do not directly impact the outcome, and are not impacted by a confounder .

Mendelian randomization is a method in genetic epidemiology that seeks to identify causal relationships between risk factors and diseases. It uses the randomness of inheriting different genes to do so. Using Mendelian randomization, it was found that PMOS has causal links to sex hormone-binding globulin level, anti-Müllerian hormone (AMH) level, menopause age, body fat percentage, insulin resistance, depression, breast cancer, ovarian cancer, obsessive-compulsive disorder, and lung capacity. Other factors do not seem causally linked: anxiety disorder, schizophrenia, type 2 diabetes, coronary heart disease, stroke, or birth weight.[35]

Environment

edit

PMOS may also be impacted by epigenetics, which regulates how active genes are. High levels of androgens and AMH during pregnancy and early weight gain can hinder the fetal environment.[13] In studies of PMOS in mice, exposure to AMH or the androgen dihydrotestosterone still has an effect three generations later. If that is so in humans, it implies that PMOS can be inherited via epigenetic changes.[5] Blood in the umbilical cord of babies whose mothers have PMOS shows specific epigenetic changes suggestive of PMOS.[13]

There is little evidence on the effect of environmental pollutants on PMOS risk.[13] Hormone disruptors are chemicals that disturb the hormonal system by blocking or mimicking natural hormones. Of these, bisphenol A and phthalates (both used in plastics), and possibly octocrylene exposure may raise the risks of PMOS.[36]

Obesity is implicated in PMOS development. As fat tissue can produce androgens, obesity leads to increased androgen levels. It also leads to suppression of the SHBG hormone, increased insulin resistance, and abnormally increased insulin levels. Some of the effects go both ways: PMOS might impact appetite, so that weight gain becomes more likely. Weight loss using diet is equally effective in people with and without PMOS.[5]

Mechanism

edit
see caption
Hormonal disruption: Increased gonadotropin-releasing hormone (GnRH) pulse frequency raises levels of luteinizing hormone (LH), which stimulates ovarian follicles to produce more androgens. Excess androgens slow follicle development, leading to the accumulation of small follicles that produce anti-Müllerian hormone (AMH), increasing testosterone levels. Insulin resistance raises blood sugar and insulin levels, lowering sex hormone-binding globulin (SHBG), which further raises testosterone levels. Insulin also enhances the effect of LH on androgen production.

PMOS involves both hormonal and metabolic changes. Women with PMOS often have higher levels of androgens, mainly produced by the ovaries, as part of a disrupted hypothalamus–pituitary–ovarian axis. In the brain, the hypothalamus sends out gonadotropin-releasing hormone (GnRH) pulses with higher frequency. This raises luteinising hormone (LH), while follicle-stimulating hormone (FSH) stays the same or is slightly lower. The higher LH stimulates theca cells in the ovary to produce more androgens.[13]

The disrupted hormonal environment, including high levels of androgens, suppresses the growth and development of ovarian follicles ("cysts"). This leads to an accumulation of many small follicles,[13] a feature referred to as polycystic ovarian morphology. The lack of ovarian follicle development also leads to a reduction in ovulation.[5] Granulosa cells in these small follicles produce high levels of anti-Müllerian hormone, which reduces the conversion of testosterone to oestradiol (oestrogen).[13]

Metabolic changes are common in PMOS. Many women develop insulin resistance, which causes the pancreas to produce extra insulin. High insulin levels reduce liver production of sex hormone-binding globulin (SHBG), increasing free circulating androgens. Low-grade inflammation can worsen insulin resistance, creating a reinforcing loop between metabolic and reproductive disturbances. Insulin resistance is not present only in overweight women with PMOS,[37] but obesity makes it worse.[16]

PMOS is associated with cardiovascular and liver dysfunction. For instance, women with PMOS can have coronary and aortic calcification. Obesity, impaired glucose metabolism, and excess androgens are all risk factors for liver dysfunction (MASLD).[13]

Diagnosis

edit

Diagnostic criteria

edit

Different criteria are used for diagnosing PMOS, but the (revised) Rotterdam criteria are recommended by clinical guidelines.[38][13] According to these criteria, an adult woman is diagnosed with PMOS if she meets two out of the following three:[38][13]

  1. Signs of androgen excess, either clinical (visible signs such as facial hair or acne) or biochemical (detected through a blood test). Androgens are "male" hormones like testosterone.[21]
  2. Irregular or absent menstrual cycles
  3. Polycystic ovaries on ultrasound or high levels of anti-Müllerian hormone (AMH)

Other causes of these issues need to be excluded for diagnosis. In adolescents, both androgen excess and irregular or absent periods are required, as it is normal for adolescents to have many follicles ("cysts") visible in their ovaries, so it does not help with diagnosis.[39] Adolescents who only meet one criterion are considered 'at risk', and are to be reassessed when they are adults.[13]

Older criteria are the 1990 NIH criteria and the 2006 Androgen Excess Society criteria.[5] The Androgen Excess Society criteria were never widely adopted. The old NIH criteria are stricter than the Rotterdam criteria, as both infrequent or irregular cycles and signs of androgen excess need to be present:[40]

  1. Infrequent or irregular cycles
  2. Signs of androgen excess (clinical or biochemical)
  3. Exclusion of other disorders that can result in the above

Assessment and testing

edit
Steps to diagnose PCOS
Steps to diagnose polycystic ovary syndrome in adults. In adolescents, only the first two steps are followed.

There is a three-step algorithm to diagnose PMOS. Step one assesses signs of androgen excess and irregular menstrual cycles. If someone has both, and other causes are excluded, PMOS is diagnosed. In step two, those with only irregular cycles undergo a blood test for testosterone. If elevated, again excluding other causes of the symptoms, PMOS is diagnosed. For adolescents, step two is the final step. Step three applies to adults with either irregular cycles or androgen excess. An ultrasound or AMH test (but not both, to avoid overdiagnosis) is performed. If polycystic ovaries or elevated AMH levels are detected, PMOS is diagnosed.[41]

Clinical androgen excess in adults can result in acne, hirsutism (male pattern of hair growth, such as on the chin or chest), and female pattern hair loss. Hirsutism can be assessed using the standardised Ferriman–Gallwey visual scoring system, with a score above four to six indicating clinical significance.[42] The recommended cut-off score depends on ethnicity, with a lower cut-off for Asian women, and a higher cut-off for Hispanic and Middle Eastern women.[43] Assessment may be complicated by self-treatment.[44] Hair loss can be assessed with the Ludwig visual score. In adolescents, androgen excess shows as severe acne and hirsutism.[42]

For individuals who had their first menstrual cycle more than three years ago, menstrual cycles are considered irregular if they occur less than 21 days apart or more than 35 days apart. For those whose first menstrual cycle was between one and three years ago, the cycle is considered irregular if it is less than 21 days apart or more than 45 days apart. Finally, for anyone whose first cycle was over a year ago, a single cycle lasting over 90 days is considered irregular.[41]

Biochemical androgen excess in PMOS is assessed using total and free testosterone. Accurate measurement requires tandem mass spectrometry assays, as direct free testosterone tests are not reliable. Interpretation is based on laboratory reference ranges. Hormonal contraception can interfere with hormone levels, so a withdrawal period of at least three months with alternative contraception may be needed. Severely elevated androgen levels may indicate other conditions.[41]

Three ultrasound images at different locations in the ovary (different planes), and a reconstructed 3D image of ovarian follicles.
Ultrasound image showing polycystic ovary morphology

In adults, an ultrasound can be used to look for small ovarian follicles. In adolescents, this is not assessed because larger numbers of follicles are normal at that age.[42] In PMOS, these follicles are often on the ovary's periphery, forming a "string of pearls".[45] To count as polycystic ovaries, at least 20 follicles must be present, smaller than 9 mm. (Older diagnostic criteria required only 12.[13]) A less clear marker of PMOS is enlarged ovaries.[42] Ovaries must be at least 10 cm3 to count as enlarged.[13] For sexually active people and those who consent, a transvaginal ultrasound approach is preferred.[42] If transvaginal ultrasound is unacceptable (for personal or cultural reasons), a transabdominal ultrasound can be performed.[46] Alternatively, AMH levels can be tested in the blood.[42]

Differential diagnosis

edit

To diagnose PMOS, other conditions must first be ruled out. These include thyroid disease (assessed via thyroid stimulating hormone), hyperprolactinemia (assessed via prolactin), and non-classic congenital adrenal hyperplasia (tested via 17-hydroxy progesterone). For those without any periods whatsoever or more severe signs or symptoms, further tests are recommended to exclude hypogonadotropic hypogonadism, any androgen-producing tumors or Cushing's disease. Overt virilisation (development of male sex characteristics) is not characteristic of PMOS and indicates that another underlying condition may be responsible.[39]

Management

edit

PMOS has no cure,[4] and management focuses on relief of symptoms.[5] Treatment usually involves lifestyle changes such as diet and exercise of moderate intensity.[47] Metabolic issues can further be treated with metformin or GLP-1 receptor agonists. For women with a BMI over 35, bariatric surgery may be an option.[13] Combined oral contraceptives are especially effective and used as the first line of treatment to reduce acne and hirsutism and regulate the menstrual cycle.[48] Other typical acne treatments and hair removal techniques may be used.[9] First-line treatment for fertility issues uses ovulation induction with clomiphene or letrozole.[5] As PMOS is associated with psychological disorders and cardiovascular risk, screening for both is recommended.[5]

Lifestyle

edit

Weight management and a healthy lifestyle are first-line treatments for PMOS. Weight management includes the prevention of weight gain, losing some weight, or maintaining weight loss.[5] Limited weight loss of 5% shows metabolic benefits, and possibly benefits for reproductive health.[13] There is little evidence that one type of healthy diet is better than another in PMOS.[5] In terms of exercise, the general population guidance of 150 minutes of moderate-intensity exercise per week is recommended to prevent weight gain. For weight loss, 250 minutes of moderate exercise is recommended.[5]

Lifestyle changes for people with PMOS have been proven to be difficult due to various factors. Some studies indicate that women with PMOS might have problems with feeling sated after eating, making weight loss more challenging. Sleep disorders, more prevalent in women with PMOS, cause fatigue, which further makes a healthy lifestyle more difficult. Finally, issues with body image, eating disorders, depression, or lack of intrinsic motivation (not enjoying exercise) may make lifestyle interventions more difficult.[49]

Lifestyle interventions for women with PMOS may include strategies such as setting goals, tracking progress, learning assertiveness, and relapse prevention. These approaches aim to support weight control, a healthy lifestyle, and emotional well-being. Support may also involve using SMART goals (specific, measurable, achievable, realistic, and timely). Broader behavioural or cognitive behavioural programmes may help increase motivation, continued participation, and long-term healthy habits.[50]

Medications

edit

Medications for PMOS include metformin and oral contraceptives. Metformin is a medication commonly used in type 2 diabetes mellitus, and is used frequently off-label in the management of PMOS.[13][51] It is recommended for those with a BMI over 25 to treat insulin resistance and normalise lipid profiles, and can also be considered for the treatment of irregular periods in adolescents and for those with a BMI under 25.[52] Metformin is associated with several side effects, including abdominal pain, metallic taste in the mouth, diarrhoea and vomiting.[53] It can also be used to help women get pregnant, but it is not the most effective drug for it.[54]

Combined oral contraceptives (COCs) can be used to reduce the symptoms of hirsutism and regulate menstrual periods.[55] They increase sex hormone binding globulin production, and reduce levels of androgens. A regular cycle reduces the risk of endometrial cancer. Contraceptive pills with only progestogens can be used to improve menstrual regularity, but not for symptoms of androgen excess.[5] Anti-androgens such as finasteride and flutamide do not show advantages over COCs for treating hirsutism, but can be an option for people for whom COCs are contraindicated or who do not tolerate them.[56] It may take six to twelve months for COCs to be effective for hirsutism.[5] For the treatment of androgenic alopecia, a combination of anti-androgens and combined oral contraceptives can be tried,[57] but it is difficult to treat.[5]

GLP-1 receptor agonists, such as liraglutide and semaglutide, may be more effective than metformin alone at metabolic improvements. Their combination has stronger effects than either therapy alone. Small trials have found positive effects on menstrual regularity and androgen levels. These drugs are not recommended when trying to conceive.[13] There is some evidence inositol may have positive effects on metabolic issues in PMOS. However, metformin is recommended over inositol supplements for hirsutism and abdominal fat reduction.[58]

Infertility

edit

It can be difficult to become pregnant with PMOS due to irregular ovulation. The first management step is to improve the general health of the mother, such as through lifestyle interventions.[13] GLP-1 agonist for weight loss can be used, but should be stopped at least 2 months before conception. As of 2025, there is not enough data to know if they are safe in pregnancy.[59] Pregnancy in PMOS is more risky than normal, and treatment is focused on getting a single pregnancy, rather than, for instance, twins (multiple pregnancy).[13] With treatment, the eventual family size of women with PMOS does not seem different to those without.[5]

The first-line medical treatment for infertility in women with PMOS is letrozole (Femara) to induce ovulation.[13] This is, in general, more effective than clomiphene citrate to improve both pregnancy rates and live births.[60] Other medications that can be used to treat infertility, listed from most to least effective, are metformin + clomiphene citrate, clomiphene citrate alone, and metformin alone.[13] Women may be more likely to experience gastrointestinal side effects with metformin.[61] Gonadotrophin therapy may be effective too, but requires monitoring and increases the risks of multiple pregnancies.[62]

When medication and lifestyle interventions are ineffective, infertility can be treated with a laparoscopic procedure called "ovarian drilling", which involves puncture of 4–10 small follicles with electrocautery, laser, or biopsy needles.[63] This procedure can induce ovulation, typically leads to a single pregnancy, but other risks may be higher compared to medication.[5][64] The procedure might lead to lower chance of live births compared to medication alone.[63] Ovarian wedge resection is no longer used as much due to complications such as adhesions and the presence of frequently effective medications.[65]

As a final treatment option, in vitro fertilisation (IVF) can be considered. IVF does increase the risk of ovarian hyperstimulation syndrome.[66] Using a 'freeze all' strategy makes it easier to transfer a single embryo and provides time for the ovaries to recover from hyperstimulation.[13] A less effective alternative, but with much lower risks of ovarian hyperstimulation syndrome, is in vitro maturation instead of full IVF.[66] This option avoids high-dose gonadotropin therapy.[5]

Hirsutism and acne

edit
Laser hair removal

Management of hirsutism involves lowering androgen levels and removing existing hair, for example, by laser treatment or shaving.[5] A standard contraceptive pill is frequently effective in reducing hirsutism and acne.[65] Progestogens such as norgestrel and levonorgestrel should be avoided due to their androgenic effects.[65] Metformin combined with an oral contraceptive may be more effective than the oral contraceptive on its own.[67] Although oral contraceptives have shown significant efficacy in clinical trials (60–100% of individuals for treatment of hirsutism), severe acne or hirsutism might require additional treatment.[65]

Other medications with anti-androgen effects include flutamide and spironolactone, which can improve hirsutism.[68] Antiandrogens are sometimes used, such as finasteride, but they are contraindicated in pregnancy. Finasteride inhibits the conversion of testosterone to its stronger form dihydrotestosterone.[69]

Mental health

edit

Women with PMOS are far more likely to have depression than women without PMOS. Symptoms of depression might be heightened by certain symptoms of the condition, such as hirsutism or obesity, that can lead to low self-esteem or poor body image.[29] Screening for depression and anxiety disorders is recommended using validated questionnaires, for instance, at diagnosis as well as afterwards, based on clinical judgement.[70] For eating disorders and body image distress, screening is only recommended when clinically indicated.[13] For sexually active women who give permission to discuss it, psychosexual dysfunction can be assessed too.[71]

Treatment of PMOS shows no to moderate effect on depression or anxiety, and standard therapies (such a psychotherapy and anti-depressants) are recommended instead.[13] Cognitive behaviour therapy can be used for girls and women with low self-esteem, poor body image, disordered eating or psychosexual dysfunction.[72]

Screening for cardiometabolic issues

edit

Given the higher risk of cardiometabolic conditions, monitoring is recommended.[5] This includes testing of glucose tolerance, using a two-hour oral glucose tolerance test (GTT) in all women with PMOS. After initial testing at diagnosis, follow-up assessments are advised every one to three years, depending on the presence of diabetes risk factors.[73] Screening for cardiovascular risk factors includes lipid profile tests and yearly blood pressure measurements.[74]

Epidemiology

edit

PMOS is the most common hormonal disorder (endocrine disorder) among women of reproductive age.[75] When someone is infertile due to a lack of ovulation, PMOS is the most common cause.[7]

According to the World Health Organization (WHO), PMOS affects over 6 to 13% of reproductive-aged women.[76] A 2022 review noted a prevalence between 5% and 18%.[5] The prevalence of PMOS depends on the choice of diagnostic criteria.[77] Using the Rotterdam criteria, around 10–13% of women have PMOS.[78] Based on the NIH criteria, the global prevalence was 5.5%, increasing to approximately 7.1% when using the Androgen Excess Society criteria. Irrespective of the criteria, the prevalence of PMOS is increasing, likely due to an aging population, more awareness, and increasing obesity rates.[77]

Prevalence seems fairly even among people with different ethnicities, but may be higher in people from Southeast Asia and the Eastern Mediterranean.[78] But PMOS can express differently. For instance, in African and Hispanic American people with PMOS, there is more insulin resistance compared to other ethnic groups.[13] The same is true for South Asian people with PMOS, who also have more metabolic symptoms and higher BMIs. East Asian women typically have less hirsutism and lower BMI compared to other groups.[5] While early small-scale studies found that transmasculine people were more likely to have PMOS than cis women, this was not found in a larger, more rigorous study.[79]

History

edit

Historical descriptions of possible PMOS symptoms date to ancient Greece, where Hippocrates described women with "thick, oily skin and absence of menstruation."[80] The earliest known description of what is now recognized as PMOS dates from 1721 in Italy, which described "Young married peasant women, moderately obese and infertile, with two larger than normal ovaries, bumpy, shiny and whitish, just like pigeon eggs".[81] Polycystic ovaries were likely first formally described in 1844 by the French doctor Achille Chereau.[82]

In 1935, American gynecologists Irving F. Stein and Michael L. Leventhal published a report linking polycystic ovaries to hirsutism, infertility, and lack of periods. The report also hypothesised that PMOS results from endocrine dysfunction, initiating research into its hormonal causes and giving rise to the term Stein–Leventhal syndrome.[83][82] By the 1980s, the metabolic side of PMOS started to be studied, before the start of genetics research in the 1990s.[82]

Terminology

edit

The name used until 2026, polycystic ovary syndrome, derived from a typical finding on medical images called polycystic ovary morphology. A polycystic ovary has an abnormally large number of developing follicles, looking like many small cysts. There were various objections to the name polycystic ovary syndrome: the "cysts" are not truly cysts, but arrested follicles. Having many follicles in the ovaries is also not unique to PMOS, and is often seen in women without PMOS, particularly adolescents.[84] Furthermore, the name implied that PMOS is a gynecological condition only, rather than a metabolic and endocrine condition.[85]

Other previous names for PMOS were Stein–Leventhal syndrome and polycystic ovary disease. Suggested names included hyperandrogenic (chronic) anovulation, estrogenic ovulatory dysfunction or functional female hyperandrogenism.[86][87] For specific subgroups, suggested names included multi-follicular ovarian disorder for those with polycystic ovary morphology,[84] and metabolic hyperandrogenic syndrome for those meeting the NIH PMOS criteria.[87] Following discussions among clinicians and people with PMOS, a majority of whom were in favour of renaming the condition, a survey was launched to find a new name.[85]

In 2026, an article by Helena Teede and others in The Lancet described the "multistep global consensus process" through which clinicians agreed to rename the condition "polyendocrine metabolic ovarian syndrome" (PMOS).[11] The previous term PCOS was considered "inaccurate, implying pathological ovarian cysts, obscuring diverse endocrine and metabolic features, and contributing to delayed diagnosis, fragmented care, and stigma, while curtailing research and policy framing." The new term reflects "the condition's multisystem pathophysiology", and is more accurate by omitting cysts.[11]

Research directions

edit

Key research questions in PMOS focus on the best way to manage the condition, including with new anti-obesity drugs. In terms of criteria for diagnosis, age-specific levels of AMH need to be specified. Biomarkers are needed for early diagnosis and to guide drug development. Another open question is how to define the male phenotype to assess male relatives of women with PMOS.[13]

Research is exploring better ways to assess and predict metabolic complications. Current clinical tests for insulin resistance lack accuracy and standardisation, and the gold-standard method is impractical in clinical settings. Emerging approaches include multi-omics, which may uncover biomarkers for diagnosis and subtyping, and artificial intelligence (AI)-based methods, which can identify patterns in medical data and also classify patients into subgroups. Combining AI with omics might improve early diagnosis, risk prediction, personalised treatment, and long-term monitoring, though robust validation in large, diverse cohorts remains necessary.[16]

As of 2024, studies have successfully developed in vitro PMOS disease models through human embryonic stem cells (hESCs) and induced pluripotent stem cell technology (iPSC).[88] Both can be derived from individuals with PMOS and can differentiate into various cell types. Using adult somatic cells, iPSCs can reprogram the cells into a pluripotent state, which can then be specified to replicate PMOS-like traits. Furthermore, 3D "organoid" models of female reproductive tissue, such as the uterus and ovaries, produced from iPSCs, present a way to stimulate the development of reproductive disorders such as PMOS in vitro.[88]

Society and culture

edit

The direct economic costs of PMOS in the United States are estimated to be over $15 billion per year (in 2021 USD). This includes the costs of managing PMOS, treating its complications such as strokes, and its mental health costs.[89] Compared to arthritis and lupus—diseases with a similar or lower prevalence and similar severity—PMOS received lower NIH research funding between 2005 and 2015.[90] Australia likewise saw a low number of grants.[91] As of September 2024, no research on PMOS has been funded by the EU since 2020.[92] This possible underfunding reflects a gender bias in health care, where conditions mostly affecting women receive less research funding.[90]

There is substantial misinformation on PMOS in social media. For example, some health influencers promote restrictive diets, such as eliminating gluten or dairy, for which there is no evidence of effectiveness. Others recommend against intensive exercise, despite its usefulness.[93] Some social media influencers without medical qualifications, including those with large followings, have presented themselves as authorities on PMOS to promote their unproven treatments, taking advantage of the limited medical options available for treating the condition.[94]

Research has identified notable gaps in physician knowledge and education related to PMOS, which may contribute to challenges in timely diagnosis and treatment.[95] For instance, health care professionals in primary care, but also in gynecology and reproductive specialists, are often unfamiliar with the precise diagnostic criteria. In terms of management, many professionals have limited knowledge of associated metabolic conditions, recommended screening, and psychological impacts. Diagnosis is often delayed, and those with PMOS are usually dissatisfied with care.[5]

See also

edit

References

edit
  1. ↑ Kollmann M, Martins WP, Raine-Fenning N (2014). "Terms and thresholds for the ultrasound evaluation of the ovaries in women with hyperandrogenic anovulation". Human Reproduction Update. 20 (3): 463–4. doi:10.1093/humupd/dmu005. PMID 24516084.
  2. ↑ Sun H, Li D, Jiao J, Liu Q, Bian J, Wang X (1 January 2022). "A Potential Link Between Polycystic Ovary Syndrome and Asthma: a Meta-Analysis". Reproductive Sciences. 29 (1): 312–319. doi:10.1007/s43032-021-00662-8. ISSN 1933-7205. PMID 34811714.
  3. 1 2 3 4 5 6 7 8 9 "What are the symptoms of PCOS?". Eunice Kennedy Shriver National Institute of Child Health and Human Development. 21 August 2024. Archived from the original on 20 May 2025. Retrieved 28 June 2025.
  4. 1 2 "Is there a cure for PCOS?". Eunice Kennedy Shriver National Institute of Child Health and Human Development. 31 January 2017. Archived from the original on 9 October 2021. Retrieved 13 October 2021.
  5. 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 Joham AE, Norman RJ, Stener-Victorin E, Legro RS, Franks S, Moran LJ, et al. (September 2022). "Polycystic ovary syndrome". The Lancet Diabetes & Endocrinology. 10 (9): 668–680. doi:10.1016/S2213-8587(22)00163-2. PMID 35934017.
  6. 1 2 Goodarzi 2024, p. 16.
  7. 1 2 "Polycystic Ovary Syndrome (PCOS): Condition Information". National Institute of Child Health and Human Development. 21 August 2024. Archived from the original on 22 August 2025. Retrieved 7 September 2025.
  8. ↑ "Polycystic ovary syndrome: What else might it be?". CKS NICE. March 2025. Retrieved 26 July 2025.
  9. 1 2 "What are the treatments for PCOS?". Eunice Kennedy Shriver National Institute of Child Health and Human Development. 21 August 2024. Retrieved 24 July 2025.
  10. ↑ Goodarzi 2024, p. 3.
  11. 1 2 3 Teede HJ, Khomami MB, Morman R, Laven JS, Joham AE, Costello MF, et al. (May 2026). "Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: a multistep global consensus process". The Lancet. doi:10.1016/S0140-6736(26)00717-8. PMID 42119588.
  12. ↑ Piltonen TT, Kuusiniemi E, Teede H (11 May 2026). "Ovarian Cysts in Polycystic Ovary Syndrome". JAMA Internal Medicine. doi:10.1001/jamainternmed.2026.1370. PMC 13162137. PMID 42113530.
  13. 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 Stener-Victorin E, Teede H, Norman RJ, Legro R, Goodarzi MO, Dokras A, et al. (18 April 2024). "Polycystic ovary syndrome". Nature Reviews Disease Primers. 10 (1) 27. doi:10.1038/s41572-024-00511-3. PMID 38637590.
  14. ↑ CDC (15 May 2024). "Diabetes and Polycystic Ovary Syndrome (PCOS)". Diabetes and Polycystic Ovary Syndrome (PCOS). Retrieved 20 September 2024.
  15. ↑ Lentscher JA, Slocum B, Torrealday S (March 2021). "Polycystic Ovarian Syndrome and Fertility". Clinical Obstetrics and Gynecology. 64 (1): 65–75. doi:10.1097/GRF.0000000000000595. PMID 33337743. S2CID 229323594.
  16. 1 2 3 4 Helvaci N, Yildiz BO (April 2025). "Polycystic ovary syndrome as a metabolic disease". Nature Reviews Endocrinology. 21 (4): 230–244. doi:10.1038/s41574-024-01057-w. PMID 39609634.
  17. 1 2 Throwba H, Unnikrishnan L, Pangath M, Vasudevan K, Jayaraman S, Li M, et al. (2022). "The epigenetic correlation among ovarian cancer, endometriosis and PCOS: A review". Critical Reviews in Oncology/Hematology. 180 103852. doi:10.1016/j.critrevonc.2022.103852. PMID 36283585.
  18. ↑ Goodarzi 2024, p. 8.
  19. 1 2 3 4 5 Goodarzi 2024, p. 13.
  20. ↑ Carson SA, Kallen AN (2021). "Diagnosis and Management of Infertility: A review". JAMA. 326 (1): 65–76. Bibcode:2021JAMA..326...65C. doi:10.1001/jama.2021.4788. PMC 9302705. PMID 34228062.
  21. 1 2 "Polycystic ovary syndrome". NHS. 11 October 2022. Retrieved 27 June 2025.
  22. ↑ Loh HH, Yee A, Loh HS, Kanagasundram S, Francis B, Lim LL (September 2020). "Sexual dysfunction in polycystic ovary syndrome: a systematic review and meta-analysis". Hormones (Athens). 19 (3): 413–423. doi:10.1007/s42000-020-00210-0. PMID 32462512. S2CID 218898082. A total of 5366 women with PCOS from 21 studies were included. [...] Women with PCOS [...] [had higher] serum total testosterone level (2.34 ± 0.58 nmol/L vs 1.57 ± 0.60 nmol/L, p < 0.001) compared with women without PCOS. [...] PCOS is characterized by high levels of androgens (dehydroepiandrosterone, androstenedione, and testosterone) and luteinizing hormone (LH), and increased LH/follicle-stimulating hormone (FSH) ratio [52].
  23. 1 2 3 Stańczak NA, Grywalska E, Dudzińska E (2024). "The latest reports and treatment methods on polycystic ovary syndrome". Annals of Medicine. 56 (1) 2357737. doi:10.1080/07853890.2024.2357737. ISSN 0785-3890. PMC 11229724. PMID 38965663.
  24. ↑ Goodarzi 2024, p. 14.
  25. ↑ Goodarzi 2024, p. 67.
  26. ↑ Goodarzi 2024, p. 66.
  27. ↑ Chen H, Simons PI, Brouwers MC (May 2025). "Is cardiovascular disease in PCOS driven by MASLD?". Trends in Endocrinology & Metabolism. 36 (5): 389–391. doi:10.1016/j.tem.2024.10.005. PMID 39510952.
  28. ↑ Goodarzi 2024, p. 65.
  29. 1 2 Brutocao C, Zaiem F, Alsawas M, Morrow AS, Murad MH, Javed A (2018). "Psychiatric disorders in women with polycystic ovary syndrome: a systematic review and meta-analysis". Endocrine. 62 (2): 318–325. doi:10.1007/s12020-018-1692-3. ISSN 1559-0100. PMID 30066285.
  30. ↑ Pehlivan MJ, Sherman KA, Wuthrich V, Gandhi E, Zagic D, Kopp E, et al. (2 April 2024). "The effectiveness of psychological interventions for reducing poor body image in endometriosis, PCOS and other gynaecological conditions: a systematic review and meta-analysis". Health Psychology Review. 18 (2): 341–368. doi:10.1080/17437199.2023.2245020. PMID 37675797.
  31. ↑ Berni TR, Morgan CL, Berni ER, Rees DA (June 2018). "Polycystic Ovary Syndrome Is Associated With Adverse Mental Health and Neurodevelopmental Outcomes". The Journal of Clinical Endocrinology and Metabolism. 103 (6): 2116–25. doi:10.1210/jc.2017-02667. PMID 29648599.
  32. ↑ Pastoor H, Mousa A, Bolt H, Bramer W, Burgert TS, Dokras A, et al. (2024). "Sexual function in women with polycystic ovary syndrome: a systematic review and meta-analysis". Human Reproduction Update. 30 (3): 323–340. doi:10.1093/humupd/dmad034. ISSN 1460-2369. PMC 11063549. PMID 38237144.
  33. ↑ Teo P, Henry BA, Moran LJ, Cowan S, Bennett C (4 July 2022). "The role of sleep in PCOS: what we know and what to consider in the future". Expert Review of Endocrinology & Metabolism. 17 (4): 305–318. doi:10.1080/17446651.2022.2082941. PMID 35815469.
  34. ↑ Kulkarni S, Gupta K, Ratre P, Mishra PK, Singh Y, Biharee A, et al. (December 2023). "Polycystic ovary syndrome: Current scenario and future insights". Drug Discovery Today. 28 (12): 103821. doi:10.1016/j.drudis.2023.103821. PMID 37935329.{{cite journal}}: CS1 maint: article number as page number (link)
  35. ↑ Wang C, Wu W, Yang H, Ye Z, Zhao Y, Liu J, et al. (May 2022). "Mendelian randomization analyses for PCOS: evidence, opportunities, and challenges". Trends in Genetics. 38 (5): 468–482. doi:10.1016/j.tig.2022.01.005. PMID 35094873.
  36. ↑ Ozga M, Jurewicz J (23 April 2025). "Environmental exposure to selected non-persistent endocrine disrupting chemicals and polycystic ovary syndrome: a systematic review". International Journal of Occupational Medicine and Environmental Health. 38 (2): 98–121. doi:10.13075/ijomeh.1896.02551. ISSN 1896-494X. PMC 12064351. PMID 40200737.
  37. ↑ Su P, Chen C, Sun Y (2025). "Physiopathology of polycystic ovary syndrome in endocrinology, metabolism and inflammation". Journal of Ovarian Research. 18 (1) 34. doi:10.1186/s13048-025-01621-6. PMC 11841159. PMID 39980043.
  38. 1 2 Teede et al. 2023, p. 5.
  39. 1 2 Teede et al. 2023, p. 18.
  40. ↑ Chang S, Dunaif A (1 March 2021). "Diagnosis of Polycystic Ovary Syndrome: Which Criteria to Use and When". Endocrinology and Metabolism Clinics of North America. 50 (1): 11–23. doi:10.1016/j.ecl.2020.10.002. ISSN 1558-4410. PMC 7860982. PMID 33518179.
  41. 1 2 3 Teede et al. 2023, p. 232.
  42. 1 2 3 4 5 6 Teede et al. 2023, p. 233.
  43. ↑ Ghafari A, Maftoohi M, Samarin ME, Barani S, Banimohammad M, Samie R (1 March 2025). "The last update on polycystic ovary syndrome(PCOS), diagnosis criteria, and novel treatment". Endocrine and Metabolic Science. 17 100228. doi:10.1016/j.endmts.2025.100228. ISSN 2666-3961.
  44. ↑ Teede HJ, Tay CT, Laven JJ, Dokras A, Moran LJ, Piltonen TT, et al. (September 2023). "Recommendations From the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome". J Clin Endocrinol Metab. 108 (10): 2447–69. doi:10.1210/clinem/dgad463. PMC 10505534. PMID 37580314.
  45. ↑ Gyliene A, Straksyte V, Zaboriene I (1 January 2022). "Value of ultrasonography parameters in diagnosing polycystic ovary syndrome". Open Medicine. 17 (1): 1114–1122. doi:10.1515/med-2022-0505. ISSN 2391-5463. PMC 9210988. PMID 35799603.
  46. ↑ Amreen S (16 August 2022). "Ultrasound in Polycystic Ovarian Syndrome: What? When? How? Why? Who?". EMJ Radiology. doi:10.33590/emjradiol/22-00058.
  47. ↑ Markantes GK, Tsichlia G, Georgopoulos NA (2022). "Diet and exercise in the management of PCOS: Starting from the basics". Polycystic Ovary Syndrome. pp. 97–115. doi:10.1016/B978-0-12-823045-9.00010-9. ISBN 978-0-12-823045-9.
  48. ↑ Antoniou-Tsigkos A, Pastroma K, Memi E, Vrachnis N, Mastorakos G (2022). "Combined oral contraceptives: Why, when, where?". Polycystic Ovary Syndrome. pp. 135–152. doi:10.1016/B978-0-12-823045-9.00018-3. ISBN 978-0-12-823045-9.
  49. ↑ Ee C, Pirotta S, Mousa A, Moran L, Lim S (November 2021). "Providing lifestyle advice to women with PCOS: an overview of practical issues affecting success". BMC Endocrine Disorders. 21 (1) 234. doi:10.1186/s12902-021-00890-8. PMC 8609880. PMID 34814919.
  50. ↑ Teede et al. 2023, p. 100.
  51. ↑ Teede et al. 2023, p. 117.
  52. ↑ Teede et al. 2023, p. 118.
  53. ↑ NICE (December 2018). "Metformin Hydrochloride". National Institute for Care Excellence. NICE. Archived from the original on 10 June 2021. Retrieved 2 November 2017.
  54. ↑ Teede et al. 2023, p. 149.
  55. ↑ Teede et al. 2023, p. 116.
  56. ↑ Alesi S, Forslund M, Melin J, Romualdi D, Peña A, Tay CT, et al. (September 2023). "Efficacy and safety of anti-androgens in the management of polycystic ovary syndrome: a systematic review and meta-analysis of randomised controlled trials". eClinicalMedicine. 63 102162. doi:10.1016/j.eclinm.2023.102162. PMC 10424142. PMID 37583655.
  57. ↑ Teede et al. 2023, p. 240.
  58. ↑ Teede et al. 2023, p. 128.
  59. ↑ Duah J, Seifer DB (2025). "Medical therapy to treat obesity and optimize fertility in women of reproductive age: a narrative review". Reproductive Biology and Endocrinology. 23 (1): 2. doi:10.1186/s12958-024-01339-y. ISSN 1477-7827. PMC 11702155. PMID 39762910.
  60. ↑ Franik S, Le QK, Kremer JA, Kiesel L, Farquhar C (2022). "Aromatase inhibitors (letrozole) for ovulation induction in infertile women with polycystic ovary syndrome". The Cochrane Database of Systematic Reviews. 2022 (9) CD010287. doi:10.1002/14651858.CD010287.pub4. PMC 9514207. PMID 36165742.
  61. ↑ Sharpe A, Morley LC, Tang T, Norman RJ, Balen AH (December 2019). "Metformin for ovulation induction (excluding gonadotrophins) in women with polycystic ovary syndrome". The Cochrane Database of Systematic Reviews. 2019 (12) CD013505. doi:10.1002/14651858.CD013505. PMC 6915832. PMID 31845767.
  62. ↑ Teede et al. 2023, p. 153.
  63. 1 2 Bordewijk EM, Ng KY, Rakic L, Mol BW, Brown J, Crawford TJ, et al. (11 February 2020). "Laparoscopic ovarian drilling for ovulation induction in women with anovulatory polycystic ovary syndrome". The Cochrane Database of Systematic Reviews. 2 (2) CD001122. doi:10.1002/14651858.CD001122.pub5. ISSN 1469-493X. PMC 7013239. PMID 32048270.
  64. ↑ Teede et al. 2023, p. 154.
  65. 1 2 3 4 Polycystic Ovarian Syndrome~treatment at eMedicine
  66. 1 2 Teede et al. 2023, p. 156.
  67. ↑ Fraison E, Kostova E, Moran LJ, Bilal S, Ee CC, Venetis C, et al. (August 2020). "Metformin versus the combined oral contraceptive pill for hirsutism, acne, and menstrual pattern in polycystic ovary syndrome". The Cochrane Database of Systematic Reviews. 2020 (8) CD005552. doi:10.1002/14651858.CD005552.pub3. PMC 7437400. PMID 32794179.
  68. ↑ "Polycystic ovary syndrome - Treatment". nhs.uk. 11 October 2022. Retrieved 27 July 2025.
  69. ↑ Shirasath KR, Ahmed NZ, Kumar P, Alam S, Karwasra R, Goyal SN, et al. (November 2025). "Unraveling PCOS therapies: Pharmacotherapeutic strategies and emerging therapeutic targets". Pathology - Research and Practice. 275 156245. doi:10.1016/j.prp.2025.156245. PMID 41027241.
  70. ↑ Teede et al. 2023, p. 82.
  71. ↑ Teede et al. 2023, p. 83.
  72. ↑ Teede et al. 2023, p. 93.
  73. ↑ Teede et al. 2023, pp. 70–71.
  74. ↑ Teede et al. 2023, pp. 68.
  75. ↑ Guan C, Zahid S, Minhas AS, Ouyang P, Vaught A, Baker VL, et al. (May 2022). "Polycystic ovary syndrome: a "risk-enhancing" factor for cardiovascular disease". Fertility and Sterility. 117 (5): 924–935. doi:10.1016/j.fertnstert.2022.03.009. PMID 35512976.
  76. ↑ WHO (28 June 2023). "Polycystic ovary syndrome". World Health Organization- Polycystic Ovary Syndrome. Retrieved 20 September 2024.
  77. 1 2 Salari N, Nankali A, Ghanbari A, Jafarpour S, Ghasemi H, Dokaneheifard S, et al. (26 June 2024). "Global prevalence of polycystic ovary syndrome in women worldwide: a comprehensive systematic review and meta-analysis". Archives of Gynecology and Obstetrics. 310 (3): 1303–1314. doi:10.1007/s00404-024-07607-x. PMID 38922413.
  78. 1 2 Teede et al. 2023, p. 64.
  79. ↑ Liu M, Murthi S, Poretsky L (2020). "Polycystic Ovary Syndrome and Gender Identity". The Yale Journal of Biology and Medicine. 93 (4): 529–537. ISSN 1551-4056. PMC 7513432. PMID 33005117.
  80. ↑ Hanson AE (1975). "Hippocrates: Diseases of Women 1". Signs. 1 (2): 567–584. doi:10.1086/493243. JSTOR 3173068. PMID 21213645. ProQuest 1300109042.
  81. ↑ Kovacs GT, Norman R (22 February 2007). Polycystic Ovary Syndrome. Cambridge University Press. p. 4. ISBN 978-1-139-46203-7. Archived from the original on 16 June 2013. Retrieved 29 March 2013.
  82. 1 2 3 Adashi EY, Cibula D, Peterson M, Azziz R (2023). "The polycystic ovary syndrome: the first 150 years of study". F&S Reports. 4 (1): 2–18. doi:10.1016/j.xfre.2022.12.002. PMC 10028479. PMID 36959968.
  83. ↑ Imaging in Polycystic Ovary Disease at eMedicine
  84. 1 2 Myers SH, Forte G, Unfer V (1 September 2024). "Has the name PCOS run its course?". Archives of Gynecology and Obstetrics. 310 (3): 1761–1762. doi:10.1007/s00404-024-07571-6. ISSN 1432-0711. PMID 38836930.
  85. 1 2 Burge K (29 May 2025). "Name change for PCOS under discussion". NewsGP. Retrieved 26 July 2025.
  86. ↑ Taieb A, Asma G, Jabeur M, Fatma BA, Nassim BH, Asma BA (1 September 2024). "Rethinking the Terminology: A Perspective on Renaming Polycystic Ovary Syndrome for an Enhanced Pathophysiological Understanding". Clinical Medicine Insights: Endocrinology and Diabetes. 17 11795514241296777. doi:10.1177/11795514241296777. ISSN 1179-5514. PMC 11528641. PMID 39494232.
  87. 1 2 Azziz R (2014). "Polycystic ovary syndrome: what's in a name?". The Journal of Clinical Endocrinology and Metabolism. 99 (4): 1142–1145. doi:10.1210/jc.2013-3996. ISSN 1945-7197. PMC 3973784. PMID 24491161.
  88. 1 2 Khatun M, Lundin K, Naillat F, Loog L, Saarela U, Tuuri T, et al. (January 2024). "Induced Pluripotent Stem Cells as a Possible Approach for Exploring the Pathophysiology of Polycystic Ovary Syndrome (PCOS)". Stem Cell Reviews and Reports. 20 (1): 67–87. doi:10.1007/s12015-023-10627-w. ISSN 2629-3269. PMC 10799779. PMID 37768523.
  89. ↑ Yadav S, Delau O, Bonner AJ, Markovic D, Patterson W, Ottey S, et al. (3 August 2023). "Direct economic burden of mental health disorders associated with polycystic ovary syndrome: Systematic review and meta-analysis". eLife. 12 e85338. doi:10.7554/eLife.85338. ISSN 2050-084X. PMC 10471160. PMID 37534878.
  90. 1 2 Brakta S, Lizneva D, Mykhalchenko K, Imam A, Walker W, Diamond MP, et al. (1 December 2017). "Perspectives on Polycystic Ovary Syndrome: Is Polycystic Ovary Syndrome Research Underfunded?". The Journal of Clinical Endocrinology & Metabolism. 102 (12): 4421–4427. doi:10.1210/jc.2017-01415. ISSN 0021-972X. PMID 29092064.
  91. ↑ Rodgers RJ, Avery J, McAllister V (2019). "A new evidence-based guideline for assessment and management of polycystic ovary syndrome". Medical Journal of Australia. 210 (6): 285–285.e1. doi:10.5694/mja2.50054. ISSN 1326-5377. PMC 6850714. PMID 30835836.
  92. ↑ "'Patients feel unheard': PCOS experts call out lack of research". euronews. 12 September 2024. Retrieved 2 December 2025.
  93. ↑ Brinkhurst-Cuff C (22 June 2025). "I was diagnosed with PCOS – and was soon drowning in misinformation". The Guardian.
  94. ↑ Wakefield J (7 December 2024). "Influencers selling fake cures for polycystic ovary syndrome". BBC News.
  95. ↑ Dokras A, Saini S, Gibson-Helm M, Schulkin J, Cooney L, Teede H (2017). "Gaps in knowledge among physicians regarding diagnostic criteria and management of polycystic ovary syndrome". Fertility and Sterility. 107 (6): 1380–1386.e1. doi:10.1016/j.fertnstert.2017.04.011. PMID 28483503.

Cited sources

edit

Further reading

edit
edit
  • Wikimedia Commons logo Media related to Polyendocrine metabolic ovarian syndrome at Wikimedia Commons
Retrieved from "https://en.wikipedia.org/w/index.php?title=Polyendocrine_metabolic_ovarian_syndrome&oldid=1354718348"