Polycystic Ovarian Syndrome 

  • Author: Richard Scott Lucidi, MD; Chief Editor: Richard Scott Lucidi, MD   more...
 
Updated: Oct 25, 2011
 

Background

The major features of polycystic ovarian syndrome (PCOS) include menstrual dysfunction, anovulation, and signs of hyperandrogenism.[1] Although the exact etiopathophysiology is unclear, PCOS can result from abnormal function of the hypothalamic-pituitary-ovarian (HPO) axis. A key characteristic of PCOS is inappropriate gonadotropin secretion, which is more likely a result of, rather than a cause of, ovarian dysfunction. (See the image below.) (See Etiology and Workup.)

Longitudinal transabdominal ultrasonogram of an ovLongitudinal transabdominal ultrasonogram of an ovary. This image reveals multiple peripheral follicles.

Stein and Leventhal were the first to recognize an association between the presence of polycystic ovaries and signs of hirsutism and amenorrhea (eg, oligomenorrhea, obesity).[2] After women diagnosed with Stein-Leventhal syndrome underwent successful wedge resection of the ovaries, their menstrual cycles became regular, and they were able to conceive.[3] As a consequence, a primary ovarian defect was thought to be the main culprit, and the disorder came to be known as polycystic ovarian disease. (See Etiology and Treatment.)

Further biochemical, clinical, and endocrinologic studies revealed an array of underlying abnormalities; hence, the condition is now referred to as PCOS, although it may occur in women without ovarian cysts and ovarian morphology is no longer an essential requirement for diagnosis.

A woman is diagnosed with polycystic ovaries (as opposed to PCOS) if she has 12 or more follicles in at least 1 ovary, measuring 2-9 mm in diameter, or a total ovarian volume of greater than 10 cm3. (See Workup.)

Diagnostic criteria

A 1990 expert conference sponsored by National Institute of Child Health and Human Disease (NICHD) of the United States National Institutes of Health (NIH) proposed the following criteria for the diagnosis of PCOS:

  • Oligo-ovulation or anovulation manifested by oligomenorrhea or amenorrhea
  • Hyperandrogenism (clinical evidence of androgen excess) or hyperandrogenemia (biochemical evidence of androgen excess)
  • Exclusion of other disorders that can result in menstrual irregularity and hyperandrogenism

In 2003, the European Society for Human Reproduction and Embryology (ESHRE) and the American Society for Reproductive Medicine (ASRM) recommended that at least 2 of the following 3 features are required for PCOS to be diagnosed[4] :

  • Oligo-ovulation or anovulation manifested as oligomenorrhea or amenorrhea
  • Hyperandrogenism (clinical evidence of androgen excess) or hyperandrogenemia (biochemical evidence of androgen excess)
  • Polycystic ovaries (as defined on ultrasonography)

Patient education

For patient education information, see the Women's Health Center, as well as Ovarian Cysts, Amenorrhea, and Female Sexual Problems.

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Etiology

Women with polycystic ovarian syndrome (PCOS) have abnormalities in the metabolism of androgens and estrogen and in the control of androgen production. High serum concentrations of androgenic hormones, such as testosterone, androstenedione, and dehydroepiandrosterone sulfate (DHEA-S), may be encountered in these patients. However, individual variation is considerable, and a particular patient might have normal androgen levels.

PCOS is also associated with peripheral insulin resistance and hyperinsulinemia, and obesity amplifies the degree of both abnormalities. Insulin resistance in PCOS can be secondary to a postbinding defect in insulin receptor signaling pathways, and elevated insulin levels may have gonadotropin-augmenting effects on ovarian function.

In addition, insulin resistance in PCOS has been associated with adiponectin, a hormone secreted by adipocytes that regulates lipid metabolism and glucose levels; lean and obese women with PCOS have lower adiponectin levels than do women without PCOS.[5]

A proposed mechanism for anovulation and elevated androgen levels suggests that, under the increased stimulatory effect of luteinizing hormone (LH) secreted by the anterior pituitary, stimulation of the ovarian theca cells is increased. These cells, in turn, increase the production of androgens (eg, testosterone, androstenedione). Because of a decreased level of follicle-stimulating hormone (FSH) relative to LH, the ovarian granulosa cells cannot aromatize the androgens to estrogens, which leads to decreased estrogen levels and consequent anovulation. Growth hormone (GH) and insulin-like growth factor–1 (IGF-1) may also augment the effect on ovarian function.[6]

Hyperinsulinemia is also responsible for dyslipidemia and for elevated levels of plasminogen activator inhibitor-1 (PAI-1) in patients with PCOS. Elevated PAI-1 levels are a risk factor for intravascular thrombosis.

Polycystic ovaries are enlarged bilaterally and have a smooth, thickened capsule that is avascular. On cut sections, subcapsular follicles in various stages of atresia are seen in the peripheral part of the ovary. The most striking ovarian feature of PCOS is hyperplasia of the theca stromal cells surrounding arrested follicles. On microscopic examination, luteinized theca cells are seen.

Causes of PCOS

The cause of PCOS is unknown, although some evidence suggests that patients have a functional abnormality of cytochrome P450c17, the 17-hydroxylase, which is the rate-limiting enzyme in androgen biosynthesis.[5]

Cytochrome P450c17 is active in the adrenals and ovaries, and excess activity of this enzyme could explain the increased androgen production from both sources in PCOS.

PCOS is, in some cases, a familial disorder, but the genetic basis of the syndrome remains unclear.[6] Studies of family members with PCOS indicate that an autosomal dominant mode of inheritance, with premature male pattern baldness as the male phenotype, may occur. Full expression of the syndrome may require an insulin abnormality and a defect in androgen biosynthesis, but no gene (or genes) has been identified.

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Epidemiology

In the United States, polycystic ovarian syndrome (PCOS) is one of the most common endocrine disorders of women in the reproductive age group, with a prevalence of 4-12%.[7, 8] In various European studies, the prevalence of PCOS was 6.5-8%.[9, 10]

A great deal of ethnic variability in hirsutism is observed. For instance, Asian women have less hirsutism given the same serum androgen values as white women. On the other hand, southern Mediterranean women more often are hirsute.

PCOS affects premenopausal women, and the age of onset is most often perimenarchal (before bone age reaches 16 y). However, clinical recognition of the syndrome may be delayed by failure of the patient to become concerned by irregular menses, hirsutism, or other symptoms or by the overlap of PCOS findings with normal physiologic maturation during the 2 years after menarche.

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Prognosis

Evidence suggest that women with polycystic ovarian syndrome (PCOS) may be at increased for cardiovascular and cerebrovascular disease (women with hyperandrogenism have elevated serum lipoprotein levels similar to those of men).[11, 12, 13, 14]

Approximately 40% of patients with PCOS have insulin resistance that is independent of body weight. These women are at increased risk for type 2 diabetes mellitus and consequent cardiovascular complications compared with healthy women.

The American Association of Clinical Endocrinologists and the American College of Endocrinology recommend screening for diabetes by age 30 years in all patients with PCOS, including obese and nonobese women.[15] In patients at particularly elevated risk, testing before age 30 years may be indicated. Patients who initially test negative for diabetes should be periodically reassessed throughout their lifetime. Patients with PCOS are also at an increased risk for endometrial hyperplasia and carcinoma.[16] The chronic anovulation in PCOS leads to constant endometrial stimulation with estrogen and without progesterone and increases the risk of endometrial hyperplasia and carcinoma.

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Contributor Information and Disclosures
Author

Richard Scott Lucidi, MD  Associate Professor of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Virginia Commonwealth University School of Medicine

Richard Scott Lucidi, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists and American Society for Reproductive Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Robert J Ferry Jr, MD  Le Bonheur Chair of Excellence in Endocrinology, Professor and Chief, Division of Pediatric Endocrinology and Metabolism, Department of Pediatrics, University of Tennessee Health Science Center; Deputy Commander for Clinical Services, Texas Medical Command, Army National Guard

Robert J Ferry Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Medical Association, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research, and Texas Pediatric Society

Disclosure: Nutropin Speakers Bureau Honoraria Speaking and teaching; Genotropin Speakers Bureau Honoraria Speaking and teaching; Eli Lilly & Co. Grant/research funds Investigator; MacroGenics, Inc. Grant/research funds Investigator; Ipsen, S.A. (formerly Tercica, Inc.) Grant/research funds Investigator; NovoNordisk SA Grant/research funds Investigator; Diamyd Investigator

Lynne Lipton Levitsky, MD  Chief, Pediatric Endocrine Unit, Massachusetts General Hospital; Associate Professor of Pediatrics, Harvard Medical School

Lynne Lipton Levitsky, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Diabetes Association, American Pediatric Society, Endocrine Society, Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Pfizer Grant/research funds P.I.; Tercica Grant/research funds Other; Eli Lily Grant/research funds PI; NovoNordisk Grant/research funds PI

Phyllis W Speiser, MD  Chief, Division of Pediatric Endocrinology, Steven and Alexandra Cohen Children's Medical Center of New York; Professor of Pediatrics, Hofstra-North Shore LIJ School of Medicine at Hofstra University

Phyllis W Speiser, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, Endocrine Society, Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Specialty Editor Board

Jordan G Pritzker, MD, MBA, FACOG  Assistant Professor of Obstetrics/Gynecology and Women's Health, Women's Comprehensive Health Center, Hofstra University School of Medicine; Attending Physician, Department of Obstetrics and Gynecology, Long Island Jewish Medical Center

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

A David Barnes, MD, PhD, MPH, FACOG  Consulting Staff, Department of Obstetrics and Gynecology, Mammoth Hospital (Mammoth Lakes, California), Pioneer Valley Hospital (Salt Lake City, Utah), Warren General Hospital (Warren, Pennsylvania), and Mountain West Hospital (Tooele, Utah)

A David Barnes, MD, PhD, MPH, FACOG is a member of the following medical societies: American College of Forensic Examiners, American College of Obstetricians and Gynecologists, American Medical Association, Association of Military Surgeons of the US, and Utah Medical Association

Disclosure: Nothing to disclose.

Stephen Kemp, MD, PhD  Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Richard Scott Lucidi, MD  Associate Professor of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Virginia Commonwealth University School of Medicine

Richard Scott Lucidi, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists and American Society for Reproductive Medicine

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Kathy Silverman, DO, and Elizabeth Alderman, MD, to the development and writing of a source article.

References

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Longitudinal transabdominal ultrasonogram of an ovary. This image reveals multiple peripheral follicles.
 
 
 
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