Polycystic ovary syndrome

"PCOS" redirects here. For the Colombian political party, see Comunitarian Party Option Seven.
Polycystic ovary syndrome
Synonyms hyperandrogenic anovulation (HA),[1] Stein–Leventhal syndrome[2]
A polycystic ovary shown on an ultrasound image.
Classification and external resources
Specialty Gynecology
ICD-10 E28.2
ICD-9-CM 256.4
OMIM 184700
MedlinePlus 000369
eMedicine med/2173 ped/2155 radio/565
Patient UK Polycystic ovary syndrome
MeSH D011085

Polycystic ovary syndrome (PCOS) is a set of symptoms due to elevated androgens (male hormones) in women.[3][4] Signs and symptoms of PCOS include irregular or no menstrual periods, heavy periods, excess body and facial hair, acne, pelvic pain, difficulty getting pregnant, and patches of thick, darker, velvety skin.[5] Associated conditions include type 2 diabetes, obesity, obstructive sleep apnea, heart disease, mood disorders, and endometrial cancer.[3]

PCOS is due to a combination of genetic and environmental factors.[6] Risk factors include obesity, not enough physical exercise, and a family history of someone with the condition.[7] Diagnosis is based on two of the following three findings: no ovulation, high androgen levels, and ovarian cysts.[3] Cysts may be detectable by ultrasound. Other conditions that produce similar symptoms include adrenal hyperplasia, hypothyroidism, and hyperprolactinemia.[8]

PCOS has no cure.[9] Treatment may involve lifestyle changes such as weight loss and exercise. Birth control pills may help with improving the regularity of periods, excess hair growth, and acne. Metformin and anti-androgens may also help. Other typical acne treatments and hair removal techniques may be used.[10] Efforts to improve fertility include weight loss, clomiphene, or metformin. In vitro fertilization is used by some in whom other measures are not effective.[11]

PCOS is the most common endocrine disorder among women between the ages of 18 and 44.[12] It affects approximately 2% to 20% of this age group depending on how it is defined.[7][13] It is one of the leading causes of poor fertility.[3] The earliest known description of what is now recognized as PCOS dates from 1721 in Italy.[14]

Signs and symptoms

Common signs and symptoms of PCOS include the following:

Asians affected by PCOS are less likely to develop hirsutism than those of other ethnic backgrounds.[19]


PCOS is a heterogeneous disorder of uncertain cause.[15][20][21] There is some 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.[6][20][21]

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.[21][22][23][24] 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.[22][24] The phenotype appears to manifest itself at least partially via heightened androgen levels secreted by ovarian follicle theca cells from women with the allele.[23] The exact gene affected has not yet been identified.[6][21][25] In rare instances, single-gene mutations can give rise to the phenotype of the syndrome.[26] Current understanding of the pathogenesis of the syndrome suggests, however, that it is a complex multigenic disorder.[27]

The severity of PCOS symptoms appears to be largely determined by factors such as obesity.[6][12]

PCOS has some aspects of a metabolic disorder, since its symptoms are partly reversible. Even though considered as a gynecological problem, PCOS consists of 28 clinical symptoms.

Even though the name suggests that the ovaries are central to disease pathology, cysts are a symptom instead of the cause of the disease. Some 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 the ovaries being the primary organ affected. However, recent insights show a multisystem disorder, with the primary problem lying in hormonal regulation in the hypothalamus, with the 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.[28]

PCOS may be related to or worsened by exposures during the prenatal period, epigenetic factors, environmental impacts (especially industrial endocrine disruptors[29] such as bisphenol A and certain drugs) and the increasing rates of obesity.[29][30][31][32][33][34][35]


Not everyone with PCOS has polycystic ovaries (PCO), nor does everyone with ovarian cysts have PCOS; although a pelvic ultrasound is a major diagnostic tool, it is not the only one.[36] The diagnosis is straightforward using the Rotterdam criteria, even when the syndrome is associated with a wide range of symptoms.


Two definitions are commonly used:


In 1990 a consensus workshop sponsored by the NIH/NICHD suggested that a person has PCOS if they have all of the following:[37]
  1. oligoovulation
  2. signs of androgen excess (clinical or biochemical)
  3. exclusion of other disorders that can result in menstrual irregularity and hyperandrogenism


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, in the absence of other entities that might cause these findings[12][38][39]
  1. oligoovulation and/or anovulation
  2. excess androgen activity
  3. polycystic ovaries (by gynecologic ultrasound)

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.[40][41]

Androgen Excess PCOS Society
In 2006, the Androgen Excess PCOS Society suggested a tightening of the diagnostic criteria to all of the following:[12]
  1. excess androgen activity
  2. oligoovulation/anovulation and/or polycystic ovaries
  3. exclusion of other entities that would cause excess androgen activity

Standard diagnostic assessments

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 women with PCOS. Common cut-offs to designate abnormally high LH/FSH ratios are 2:1[50] or 3:1[46] as tested on Day 3 of the menstrual cycle. The pattern is not very sensitive; a ratio of 2:1 or higher was present in less than 50% of women with PCOS in one study.[50] There are often low levels of sex hormone-binding globulin,[46] in particular among obese or overweight women.

Anti-Müllerian hormone (AMH) is increased in PCOS, and may become part of its diagnostic criteria.[51][52]

Associated conditions

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.[12][39][46]


Polycystic ovaries develop when the ovaries are stimulated to produce excessive amounts of androgenic hormones, in particular testosterone, by either one or a combination of the following (almost certainly combined with genetic susceptibility[23]):

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.

Women with PCOS experience an increased frequency of hypothalamic GnRH pulses, which in turn results in an increase in the LH/FSH ratio.[54]

A majority of women 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,[15] decreased follicular maturation, and decreased SHBG binding. Furthermore, excessive insulin, acting through its cognate receptor in the presence of component cAMP signalling, upregulates 17α-hydroxylase activity via PI3K, 17α-hydroxylase activity being responsible for synthesising androgen precursors.[55] The combined effects of hyperinsulinemia contribute to an increased risk of PCOS.[56] Insulin resistance is a common finding among women with a normal weight as well as overweight women.[12][18]

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).[57]

PCOS may be associated with chronic inflammation,[15][58] with several investigators correlating inflammatory mediators with anovulation and other PCOS symptoms.[59][60] Similarly, there seems to be a relation between PCOS and increased level of oxidative stress.[61]

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.[62]

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.[63]

Transgender men may experience a higher than expected rate of PCOS due to increased testosterone, if they choose to take hormone therapy as part of their gender presentation.[64][65]


The primary treatments for PCOS include: lifestyle changes, medications and surgery.[66]

Goals of treatment may be considered under four categories:

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.[67]


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.[68] 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.[68] Vitamin D deficiency may play some role in the development of the metabolic syndrome, so treatment of any such deficiency is indicated.[69] As of 2012, interventions using dietary supplements to correct metabolic deficiencies in people with PCOS had been tested in small, uncontrolled and nonrandomized clinical trials; the resulting data is insufficient to recommend their use.[70]


Medications for PCOS include oral contraceptives and metformin. The oral contraceptives increase sex hormone binding globulin production, which increases binding of free testosterone. This reduces the symptoms of hirsutism caused by high testosterone and regulates return to normal menstrual periods. Metformin is a drug commonly used in type 2 diabetes to reduce insulin resistance, and is used off label (in the UK, US, AU and EU) to treat insulin resistance seen in PCOS. In many cases, metformin also supports ovarian function and return to normal ovulation.[15][69][71] Spironolactone can be used for its antiandrogenic effects, and the topical cream eflornithine can be used to reduce facial hair. A newer insulin resistance drug class, the thiazolidinediones (glitazones), have shown equivalent efficacy to metformin, but metformin has a more favorable side effect profile.[72][73] 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.[74][75] Metformin may not be effective in every type of PCOS, and therefore there is some disagreement about whether it should be used as a general first line therapy.[76] The use of statins in the management of underlying metabolic syndrome remains unclear.[77]

It can be difficult to become pregnant with PCOS because it causes irregular ovulation. Medications to induce fertility when trying to conceive include the ovulation inducer clomiphene or pulsatile leuprolide. Metformin improves the efficacy of fertility treatment when used in combination with clomiphene.[78] Metformin is thought to be safe to use during pregnancy (pregnancy category B in the US).[79] A review in 2014 concluded that the use of metformin does not increase the risk of major birth defects in women treated with metformin during the first trimester.[80]


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 gonadotropins, hyperandrogenemia and hyperinsulinemia.[81] 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.

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 those women that after weight loss still are anovulatory or for anovulatory lean women, then the ovulation-inducing medications clomiphene citrate[69] and FSH are the principal treatments used to promote ovulation.[15] Previously, the anti-diabetes medication metformin was recommended treatment for anovulation,[15] but it appears less effective than clomiphene.[82]

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).

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[69] or ovulations after adjuvant treatment with clomiphene or FSH. (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.[69]

Hirsutism and acne

For more details on this topic, see Hirsutism.

When appropriate (e.g., in women of child-bearing age who require contraception), a standard contraceptive pill is frequently effective in reducing hirsutism.[15][69] Progestogens such as norgestrel and levonorgestrel should be avoided due to their androgenic effects.[69]

Other drugs with anti-androgen effects include flutamide,[83] and spironolactone,[15][69] which can give some improvement in hirsutism. 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.[69] 5-alpha reductase inhibitors (such as finasteride and dutasteride) may also be used;[84] 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[69]), 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.

Menstrual irregularity

If fertility is not the primary aim, then menstruation can usually be regulated with a contraceptive pill.[15][69] 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.[85] If menstruation occurs less often or not at all, some form of progestogen replacement is recommended.[84] An alternative is oral progestogen taken at intervals (e.g., every three months) to induce a predictable menstrual bleeding.[15]

Alternative medicine

There is not enough evidence to conclude any beneficial effect from D-chiro-inositol.[86] Based on a systematic review, myo-inositol supplementation, however, appears to be effective in improving several of the hormonal disturbances of PCOS.[87] There is also not evidence to support the use of acupuncture for treatment of ovulation disorders in women with PCOS.[88]


A diagnosis of PCOS suggests an increased risk of the following:

Early diagnosis and treatment may reduce the risk of some of these, such as type 2 diabetes and heart disease.[15]

The risk of ovarian cancer and breast cancer is not significantly increased overall.[89]


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).[100] 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.[12]

One study in the United Kingdom concluded that the risk of PCOS development was higher in lesbian women than in heterosexuals.[101] However, two subsequent studies of women with PCOS have not replicated this finding.[102][103] Ultrasonographic findings of polycystic ovaries are found in 8-25% of normal women.[104][105][106][107] 14% women on oral contraceptives are found to have polycystic ovaries.[105] Ovarian cysts are also a common side effect of intrauterine devices (IUDs).[108]


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.[36][37]

The earliest published description of a person with what is now recognized as PCOS was in 1721 in Italy.[14] Cyst-related changes to the ovaries were described in 1844.[14]


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 women with all the symptoms of amenorrhea with infertility, hirsutism, and enlarged polycystic ovaries.[36]

Most common names for this disease derive from a typical finding on medical images, called a polycystic ovary.[15] A polycystic ovary has an abnormally large number of developing eggs visible near its surface,[36] looking like many small cysts[109] or a string of pearls.

See also


  1. Kollmann M, Martins WP, Raine-Fenning N (2014). "Terms and thresholds for the ultrasound evaluation of the ovaries in women with hyperandrogenic anovulation". Hum. Reprod. Update. 20 (3): 463–4. doi:10.1093/humupd/dmu005. PMID 24516084.
  2. "USMLE-Rx". MedIQ Learning, LLC. 2014. Stein-Leventhal syndrome, also known as polycystic ovary syndrome (PCOS), is a disorder characterized by hirsutism, obesity, and amenorrhea because of luteinizing hormone-resistant cystic ovaries.
  3. 1 2 3 4 "Polycystic Ovary Syndrome (PCOS): Condition Information". http://www.nichd.nih.gov/. 2013-05-23. Retrieved 13 March 2015. External link in |website= (help)
  4. "Polycystic ovary syndrome (PCOS) fact sheet". Womens Health. December 23, 2014. Retrieved 11 August 2016.
  5. "What are the symptoms of PCOS?" (05/23/2013). http://www.nichd.nih.gov. Retrieved 13 March 2015. External link in |website= (help)
  6. 1 2 3 4 Diamanti-Kandarakis E, Kandarakis H, Legro RS (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.
  7. 1 2 "How many people are affected or at risk for PCOS?". http://www.nichd.nih.gov. 2013-05-23. Retrieved 13 March 2015. External link in |website= (help)
  8. "How do health care providers diagnose PCOS?". http://www.nichd.nih.gov/. 2013-05-23. Retrieved 13 March 2015. External link in |website= (help)
  9. "http://www.nichd.nih.gov". Is there a cure for PCOS?. 2013-05-23. Retrieved 13 March 2015. External link in |title= (help)
  10. "Treatments to Relieve Symptoms of PCOS". http://www.nichd.nih.gov/. 2014-07-14. Retrieved 13 March 2015. External link in |website= (help)
  11. "Treatments for Infertility Resulting from PCOS". http://www.nichd.nih.gov/. 2014-07-14. Retrieved 13 March 2015. External link in |website= (help)
  12. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 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 (1): 41. doi:10.1186/1741-7015-8-41. PMC 2909929Freely accessible. PMID 20591140.
  13. editor, Lubna Pal, (2013). "Diagnostic Criteria and Epidemiology of PCOS". Polycystic Ovary Syndrome Current and Emerging Concepts. Dordrecht: Springer. p. 7. ISBN 9781461483946.
  14. 1 2 3 Kovacs, Gabor T.; Norman, Robert (2007-02-22). Polycystic Ovary Syndrome. Cambridge University Press. p. 4. ISBN 9781139462037. Retrieved 29 March 2013.
  15. 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 Mayo Clinic Staff (4 April 2011). "Polycystic Ovary Syndrome – All". MayoClinic.com. Mayo Clinic. Retrieved 15 November 2011.
  16. 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.
  17. 1 2 Huang A, Brennan K, Azziz R (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 2859983Freely accessible. PMID 19249030.
  18. 1 2 Nafiye Y, Sevtap K, Muammer D, Emre O, Senol K, Leyla M (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.
  19. Carmina E, Koyama T, Chang L, Stanczyk FZ, Lobo RA (1992). "Does ethnicity influence the prevalence of adrenal hyperandrogenism and insulin resistance in polycystic ovary syndrome?". Am. J. Obstet. Gynecol. 167 (6): 1807–12. doi:10.1016/0002-9378(92)91779-a. PMID 1471702.
  20. 1 2 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". Hum. Reprod. Update. 17 (6): 829–47. doi:10.1093/humupd/dmr033. PMC 3191938Freely accessible. PMID 21896560.
  21. 1 2 3 4 Legro RS, Strauss JF (2002). "Molecular progress in infertility: polycystic ovary syndrome". Fertil. Steril. 78 (3): 569–76. doi:10.1016/S0015-0282(02)03275-2. PMID 12215335.
  22. 1 2 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.
  23. 1 2 3 Strauss JF (2003). "Some new thoughts on the pathophysiology and genetics of polycystic ovary syndrome". Ann. N. Y. Acad. Sci. 997: 42–8. Bibcode:2003NYASA.997...42S. doi:10.1196/annals.1290.005. PMID 14644808.
  24. 1 2 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.
  25. Amato P, Simpson JL (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.
  26. Draper; et al. (2003). "Mutations in the genes encoding 11β-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase interact to cause cortisone reductase deficiency". Nature Genetics. 34: 434–439. doi:10.1038/ng1214. PMID 12858176.
  27. Ehrmann David A (2005). "Polycystic Ovary Syndrome". N Engl J Med. 352: 1223–1236. doi:10.1056/NEJMra041536.
  28. Dunaif A, Fauser BC (2013). "Renaming PCOS--a two-state solution". J. Clin. Endocrinol. Metab. 98 (11): 4325–8. doi:10.1210/jc.2013-2040. PMID 24009134.
  29. 1 2 Palioura E, Diamanti-Kandarakis E (2013). "Industrial endocrine disruptors and polycystic ovary syndrome". J. Endocrinol. Invest. 36 (11): 1105–11. doi:10.1007/bf03346762. PMID 24445124.
  30. Hoeger KM (2014). "Developmental origins and future fate in PCOS". Semin. Reprod. Med. 32 (3): 157–158. doi:10.1055/s-0034-1371086. PMID 24715509.
  31. Harden CL (2005). "Polycystic ovaries and polycystic ovary syndrome in epilepsy: evidence for neurogonadal disease". Epilepsy Curr. 5 (4): 142–6. doi:10.1111/j.1535-7511.2005.00039.x. PMC 1198730Freely accessible. PMID 16151523.
  32. Rasgon N (2004). "The relationship between polycystic ovary syndrome and antiepileptic drugs: a review of the evidence". J Clin Psychopharmacol. 24 (3): 322–34. doi:10.1097/01.jcp.0000125745.60149.c6. PMID 15118487.
  33. Hu X, Wang J, Dong W, Fang Q, Hu L, Liu C (2011). "A meta-analysis of polycystic ovary syndrome in women taking valproate for epilepsy". Epilepsy Res. 97 (1-2): 73–82. doi:10.1016/j.eplepsyres.2011.07.006. PMID 21820873.
  34. Abbott DH, Barnett DK, Bruns CM, Dumesic DA (2005). "Androgen excess fetal programming of female reproduction: a developmental aetiology for polycystic ovary syndrome?". Hum. Reprod. Update. 11 (4): 357–74. doi:10.1093/humupd/dmi013. PMID 15941725.
  35. Rutkowska A, Rachoń D (2014). "Bisphenol A (BPA) and its potential role in the pathogenesis of the polycystic ovary syndrome (PCOS)". Gynecol. Endocrinol. 30 (4): 260–5. doi:10.3109/09513590.2013.871517. PMID 24397396.
  36. 1 2 3 4 Marrinan, Greg (20 April 2011). Lin, Eugene C, ed. "Imaging in Polycystic Ovary Disease". eMedicine. eMedicine. Retrieved 19 November 2011.
  37. 1 2 3 4 5 6 7 8 Richard Scott Lucidi (25 October 2011). "Polycystic Ovarian Syndrome". eMedicine. Retrieved 19 November 2011.
  38. Azziz R (2006). "Controversy in clinical endocrinology: diagnosis of polycystic ovarian syndrome: the Rotterdam criteria are premature". J. Clin. Endocrinol. Metab. 91 (3): 781–5. doi:10.1210/jc.2005-2153. PMID 16418211.
  39. 1 2 "Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS)". Hum. Reprod. 19 (1): 41–7. 2004. doi:10.1093/humrep/deh098. PMID 14688154.
  40. Carmina E (2004). "Diagnosis of polycystic ovary syndrome: from NIH criteria to ESHRE-ASRM guidelines". Minerva Ginecol. 56 (1): 1–6. PMID 14973405.
  41. Hart R, Hickey M, Franks S (2004). "Definitions, prevalence and symptoms of polycystic ovaries and polycystic ovary syndrome". Best Pract Res Clin Obstet Gynaecol. 18 (5): 671–83. doi:10.1016/j.bpobgyn.2004.05.001. PMID 15380140.
  42. Pedersen SD, Brar S, Faris P, Corenblum B (2007). "Polycystic ovary syndrome: validated questionnaire for use in diagnosis". Can Fam Physician. 53 (6): 1042–7, 1041. PMC 1949220Freely accessible. PMID 17872783.
  43. 1 2 Dewailly D, Lujan ME, Carmina E, Cedars MI, Laven J, Norman RJ, Escobar-Morreale HF (2013). "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.
  44. O'Brien, William T. (1 January 2011). Top 3 Differentials in Radiology. Thieme. p. 369. ISBN 978-1-60406-228-1. Retrieved 30 August 2014. Ultrasound findings in PCOS include enlarged ovaries with peripheral follicles in a "string of pearls" configuration.
  45. Somani N, Harrison S, Bergfeld WF (2008). "The clinical evaluation of hirsutism". Dermatol Ther. 21 (5): 376–91. doi:10.1111/j.1529-8019.2008.00219.x. PMID 18844715.
  46. 1 2 3 4 5 6 7 8 "Polycystic Ovarian Syndrome Workup". eMedicine. 25 October 2011. Retrieved 19 November 2011.
  47. Sharquie KE, Al-Bayatti AA, Al-Ajeel AI, Al-Bahar AJ, Al-Nuaimy AA (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.
  48. Robinson S, Rodin DA, Deacon A, Wheeler MJ, Clayton RN (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.
  49. Li X, Lin JF (2005). "[Clinical features, hormonal profile, and metabolic abnormalities of obese women with obese polycystic ovary syndrome]". Zhonghua Yi Xue Za Zhi (in Chinese). 85 (46): 3266–71. PMID 16409817.
  50. 1 2 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.
  51. 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.
  52. Broer SL, Broekmans FJ, Laven JS, Fauser BC (2014). "Anti-Müllerian hormone: ovarian reserve testing and its potential clinical implications". Hum. Reprod. Update. 20 (5): 688–701. doi:10.1093/humupd/dmu020. PMID 24821925.
  53. 1 2 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/jcem.84.1.5393. PMID 9920077.
  54. Lewandowski KC, Cajdler-Łuba A, Salata I, Bieńkiewicz M, Lewiński A (2011). "The utility of the gonadotrophin releasing hormone (GnRH) test in the diagnosis of polycystic ovary syndrome (PCOS)". Endokrynol Pol. 62 (2): 120–8. PMID 21528473.
  55. Munir, Iqbal; Yen, Hui-Wen; Geller, David H.; Torbati, Donna; Bierden, Rebecca M.; Weitsman, Stacy R.; Agarwal, Sanjay K.; Magoffin, Denis A. (January 2004). "Insulin Augmentation of 17α-Hydroxylase Activity Is Mediated by Phosphatidyl Inositol 3-Kinase But Not Extracellular Signal-Regulated Kinase-1/2 in Human Ovarian Theca Cells". Endocrinology. 145 (1): 175–183. doi:10.1210/en.2003-0329.
  56. Diamanti-Kandarakis, Evanthia; Dunaif, Andrea (December 2012). "Insulin Resistance and the Polycystic Ovary Syndrome Revisited: An Update on Mechanisms and Implications". Endocrine Reviews. 33 (6): 981–1030. doi:10.1210/er.2011-1034.
  57. Kumar Cotran Robbins: Basic Pathology 6th ed. / Saunders 1996
  58. Sathyapalan T, Atkin SL (2010). "Mediators of inflammation in polycystic ovary syndrome in relation to adiposity". Mediators Inflamm. 2010: 1–5. doi:10.1155/2010/758656. PMC 2852606Freely accessible. PMID 20396393.
  59. 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.
  60. 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.
  61. 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): 268–88. doi:10.1093/humupd/dms059. PMID 23303572.
  62. Kelly CJ, Stenton SR, Lashen H (2010). "Insulin-like growth factor binding protein-1 in PCOS: a systematic review and meta-analysis". Hum. Reprod. Update. 17 (1): 4–16. doi:10.1093/humupd/dmq027. PMID 20634211.
  63. Gleicher N, Weghofer A, Lee IH, Barad DH (2010). "FMR1 genotype with autoimmunity-associated polycystic ovary-like phenotype and decreased pregnancy chance". PLoS ONE. 5 (12): e15303. Bibcode:2010PLoSO...515303G. doi:10.1371/journal.pone.0015303. PMC 3002956Freely accessible. PMID 21179569.
  64. http://www.obgyn.net/articles/transgenderpcos[]
  65. http://www.cancer-network.org/cancer_information/transgender_gender-nonconforming_people_and_cancer/transgender_men_and_ovarian_cancer.php[]
  66. Lim DC, Chen W, Cheng LN, Xue CC, Wong FW, O'Sullivan AJ, Liu JP (2011). "Acupuncture for polycystic ovarian syndrome". Cochrane Database Syst Rev (8): CD007689. doi:10.1002/14651858.CD007689.pub2. PMID 21833961.
  67. Veltman-Verhulst SM, Boivin J, Eijkemans MJ, Fauser BJ (2012). "Emotional distress is a common risk in women 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.
  68. 1 2 Moran LJ, Ko H, Misso M, Marsh K, Noakes M, Talbot M, Frearson M, Thondan M, Stepto N, Teede HJ (2013). "Dietary composition in the treatment of polycystic ovary syndrome: a systematic review to inform evidence-based guidelines". Hum. Reprod. Update. 19 (5): 432. doi:10.1093/humupd/dmt015. PMID 23727939.
  69. 1 2 3 4 5 6 7 8 9 10 11 "Polycystic Ovarian Syndrome Treatment & Management". eMedicine. 25 October 2011. Retrieved 19 November 2011.
  70. Huang, G; Coviello, A (December 2012). "Clinical update on screening, diagnosis and management of metabolic disorders and cardiovascular risk factors associated with polycystic ovary syndrome.". Current opinion in endocrinology, diabetes, and obesity. 19 (6): 512–9. doi:10.1097/med.0b013e32835a000e. PMID 23108199.
  71. 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 259161Freely accessible. PMID 14576245.
  72. Li, X.-J.; Yu, Y.-X.; Liu, C.-Q.; Zhang, W.; Zhang, H.-J.; Yan, B.; Wang, L.-Y.; Yang, S.-Y.; Zhang, S.-H. (2011-03). "Metformin vs thiazolidinediones for treatment of clinical, hormonal and metabolic characteristics of polycystic ovary syndrome: a meta-analysis". Clinical Endocrinology. 74 (3): 332–339. doi:10.1111/j.1365-2265.2010.03917.x. ISSN 1365-2265. PMID 21050251. Check date values in: |date= (help)
  73. Grover, Anjali; Yialamas, Maria A. (2011-03). "Metformin or thiazolidinedione therapy in PCOS?". Nature Reviews Endocrinology. 7 (3): 128–. doi:10.1038/nrendo.2011.16. ISSN 1759-5029. Retrieved 2015-05-24. Check date values in: |date= (help)
  74. National Institute for Health and Clinical Excellence. 11 Clinical guideline 11 : Fertility: assessment and treatment for people with fertility problems . London, 2004.
  75. Balen A (December 2008). "Metformin therapy for the management of infertility in women with polycystic ovary syndrome" (PDF). Scientific Advisory Committee Opinion Paper 13. Royal College of Obstetricians and Gynaecologists. Retrieved 2009-12-13.
  76. Leeman L, Acharya U (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.
  77. Legro, RS; Arslanian, SA; Ehrmann, DA; Hoeger, KM; Murad, MH; Pasquali, R; Welt, CK; Endocrine, Society (December 2013). "Diagnosis and treatment of polycystic ovary syndrome: an Endocrine Society clinical practice guideline.". The Journal of Clinical Endocrinology and Metabolism. 98 (12): 4565–92. doi:10.1210/jc.2013-2350. PMID 24151290.
  78. Nestler, John E.; Jakubowicz, Daniela J.; Evans, William S.; Pasquali, Renato (1998-06-25). "Effects of Metformin on Spontaneous and Clomiphene-Induced Ovulation in the Polycystic Ovary Syndrome". New England Journal of Medicine. 338 (26): 1876–1880. doi:10.1056/NEJM199806253382603. ISSN 0028-4793. PMID 9637806. Retrieved 2015-05-24.
  79. Feig, Denice S.; Moses, Robert G. (2011-10-01). "Metformin Therapy During Pregnancy Good for the goose and good for the gosling too?". Diabetes Care. 34 (10): 2329–2330. doi:10.2337/dc11-1153. ISSN 0149-5992. PMID 21949224. Retrieved 2015-05-24.
  80. Cassina M, Donà 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". Hum. Reprod. Update. 20 (5): 656–69. doi:10.1093/humupd/dmu022. PMID 24861556.
  81. Qiao J, Feng HL (2010). "Extra- and intra-ovarian factors in polycystic ovary syndrome: impact on oocyte maturation and embryo developmental competence". Hum. Reprod. Update. 17 (1): 17–33. doi:10.1093/humupd/dmq032. PMC 3001338Freely accessible. PMID 20639519.
  82. 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.
  83. "Polycystic ovary syndrome – Treatment". United Kingdom: National Health Service. 17 October 2011. Retrieved 19 November 2011.
  84. 1 2 Richard Scott Lucidi (25 October 2011). "Polycystic Ovarian Syndrome Medication". eMedicine. Retrieved 19 November 2011.
  85. "What are the health risks of PCOS?". Verity – PCOS Charity. Verity. 2011. Retrieved 21 November 2011.
  86. Galazis N, Galazi M, Atiomo W (2011). "D-Chiro-inositol and its significance in polycystic ovary syndrome: a systematic review". Gynecol. Endocrinol. 27 (4): 256–62. doi:10.3109/09513590.2010.538099. PMID 21142777.
  87. Unfer V, Carlomagno G, Dante G, Facchinetti F (2012). "Effects of myo-inositol in women with PCOS: a systematic review of randomized controlled trials". Gynecol. Endocrinol. 28 (7): 509–15. doi:10.3109/09513590.2011.650660. PMID 22296306.
  88. Lim, Chi Eung Danforn; Ng, Rachel WC; Xu, Ke; Cheng, Nga Chong Lisa; Xue, Charlie CL; Liu, Jian Ping; Chen, Nini (3 May 2016). "Acupuncture for polycystic ovarian syndrome". Cochrane Database of Systematic Reviews. John Wiley & Sons, Ltd. doi:10.1002/14651858.cd007689.pub3.
  89. 1 2 Barry JA, Azizia MM, Hardiman PJ (2014). "Risk of endometrial, ovarian and breast cancer in women with polycystic ovary syndrome: a systematic review and meta-analysis". Hum. Reprod. Update. 20 (5): 748–758. doi:10.1093/humupd/dmu012. PMID 24688118.
  90. New MI (1993). "Nonclassical congenital adrenal hyperplasia and the polycystic ovarian syndrome". Ann. N. Y. Acad. Sci. 687: 193–205. Bibcode:1993NYASA.687..193N. doi:10.1111/j.1749-6632.1993.tb43866.x. PMID 8323173.
  91. Hardiman P, Pillay OC, Atiomo W (2003). "Polycystic ovary syndrome and endometrial carcinoma". Lancet. 361 (9371): 1810–2. doi:10.1016/S0140-6736(03)13409-5. PMID 12781553.
  92. Mather KJ, Kwan F, Corenblum B (2000). "Hyperinsulinemia in polycystic ovary syndrome correlates with increased cardiovascular risk independent of obesity". Fertil. Steril. 73 (1): 150–6. doi:10.1016/S0015-0282(99)00468-9. PMID 10632431.
  93. Moran LJ, Misso ML, Wild RA, Norman RJ (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.
  94. Barry JA, Kuczmierczyk AR, Hardiman PJ (2011). "Anxiety and depression in polycystic ovary syndrome: a systematic review and meta-analysis". Hum. Reprod. 26 (9): 2442–51. doi:10.1093/humrep/der197. PMID 21725075.
  95. Rocha MP, Maranhão RC, Seydell TM, Barcellos CR, Baracat EC, Hayashida SA, Bydlowski SP, Marcondes JA (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.
  96. 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". Hum. Reprod. Update. 17 (4): 495–500. doi:10.1093/humupd/dmr001. PMID 21335359.
  97. Goldenberg N, Glueck C (2008). "Medical therapy in women with polycystic ovarian syndrome before and during pregnancy and lactation". Minerva Ginecol. 60 (1): 63–75. PMID 18277353.
  98. Boomsma CM, Fauser BC, Macklon NS (2008). "Pregnancy complications in women with polycystic ovary syndrome". Semin. Reprod. Med. 26 (1): 072–084. doi:10.1055/s-2007-992927. PMID 18181085.
  99. Troischt MJ, Mehlman TR, and Nield LS (November 1, 2008). "Polycystic Ovary Syndrome: An Intriguing Diagnosis". Consultant for Pediatricians.
  100. Vos T, Flaxman AD, et al. (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.
  101. 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". Fertil. Steril. 82 (5): 1352–7. doi:10.1016/j.fertnstert.2004.04.041. PMID 15533359.
  102. De Sutter P, Dutré T, Vanden Meerschaut F, Stuyver I, Van Maele G, Dhont M (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.
  103. 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.
  104. Polson DW, Adams J, Wadsworth J, Franks S (1988). "Polycystic ovaries--a common finding in normal women". Lancet. 1 (8590): 870–2. doi:10.1016/s0140-6736(88)91612-1. PMID 2895373.
  105. 1 2 Clayton RN, Ogden V, Hodgkinson J, Worswick L, Rodin DA, Dyer S, Meade TW (1992). "How common are polycystic ovaries in normal women and what is their significance for the fertility of the population?". Clin. Endocrinol. (Oxf). 37 (2): 127–34. doi:10.1111/j.1365-2265.1992.tb02296.x. PMID 1395063.
  106. Farquhar CM, Birdsall M, Manning P, Mitchell JM, France JT (1994). "The prevalence of polycystic ovaries on ultrasound scanning in a population of randomly selected women". Aust N Z J Obstet Gynaecol. 34 (1): 67–72. doi:10.1111/j.1479-828X.1994.tb01041.x. PMID 8053879.
  107. van Santbrink EJ, Hop WC, Fauser BC (1997). "Classification of normogonadotropic infertility: polycystic ovaries diagnosed by ultrasound versus endocrine characteristics of polycystic ovary syndrome". Fertil. Steril. 67 (3): 452–8. doi:10.1016/S0015-0282(97)80068-4. PMID 9091329.
  108. Hardeman J, Weiss BD (2014). "Intrauterine devices: an update.". Am Fam Physician. 89 (6): 445–50. PMID 24695563.
  109. "What is Polycystic Ovary Syndrome (PCOS)?". Verity – PCOS Charity. Verity. 2011. Retrieved 21 November 2011.
Wikimedia Commons has media related to Polycystic ovary syndrome.
This article is issued from Wikipedia - version of the 11/28/2016. The text is available under the Creative Commons Attribution/Share Alike but additional terms may apply for the media files.