Valerie Robinson, DO
• Polycystic Ovarian Syndrome (PCOS) is a disorder that causes
menstrual and ovulation irregularities, androgen excess, and
infertility. Polycystic ovaries are found on ultrasound.
• PCOS is often found in an infertility work-up.
• Intraovarian androgen excess  excessive growth of small follicles and
hinders maturation of a dominant follicle  anovulation
• Other common findings include obesity and insulin resistance
• Prevalence is 6-8% in the general population
• Onset is usually during or soon after puberty
• Polycystic ovaries may not develop until two or more years after menarche
• Increased incidence is found in the following
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Use of anti-epileptic drugs - specifically valproate
Mexican-American
First degree family history – risk is 20-40%
History of premature adrenarche
Diabetes - type 1, type 2, or gestational
Infertility
• Risk factors
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First degree relative with polycystic ovaries
First degree relative with hyperandrogenism
Mother with PCOS
Father or Mother with metabolic syndrome
Congenital virilization (MCC is congenital adrenal hyperplasia)
Insulin resistance or hyperinsulinemia
• Menstrual dysfunction
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Oligo- or anovulation  Infertility
Oligo- or amenorrhea with irregular cycles
Adolescents may have delayed menarche
May begin regular menses and develop irregularity
Increased risk of endometrial hyperplasia/cancer. Oligoovulation results in
decreased progesterone secretion. Relative lack of progesterone leads to
chronic unopposed estrogen exposure.
• Ovarian abnormalities
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Multiple small antral and pre-antral follicles in the periphery
Follicle growth is arrested in antral stage
Increased thickness of stroma
Ovarian cortex is thickened and sclerotic
• Increased risk of metabolic syndrome
• Obesity, usually central
• Insulin resistance and hyperinsulinemia
• Acanthosis nigricans
• Pseudo-acromegaly
• Diabetes type 1 or 2
• Dyslipidemia
• Hyperandrogenism
• Hirsutism
• Acne
• Male-Pattern balding
• Hyperpituitarism
• Acromegaly
• Hyperprolactinemia
• Increased likelihood of depression and anxiety
• Increased risk of NASH
• Increased risk of CAD
• National Institutes of Health (NIH) 1990 criteria: irregular
menses, biochemical and/or clinical hyperandrogenism.
Other causes of hyperandrogenism excluded.
• Rotterdam 2003 criteria (requires two out of three of the
following): oligo- and/or anovulation, clinical and/or
biochemical hyperandrogenism, polycystic ovaries by ultrasound.
Other causes of hyperandrogenism excluded.
• Exclude congenital adrenal hyperplasias, androgen-secreting
tumors, Cushing's syndrome, hyperprolactinemia, steroid use.
• Menstrual history
• Physical exam
• Transvaginal Ultrasound
• 8-10 small follicles surrounding thickened stroma: “String of Pearls”
• Rotterdam Criteria: 12 or more follicles 2-9mm, or ovarian volume of >10mL
• As a lone finding, polycystic ovaries is insufficient for diagnosis
• Hormone abnormalities: non-diagnostic findings
• Some women may have increased LH, decreased FSH, increased prolactin
• Women with PCOS should be screened for depression, glucose
intolerance, dyslipidemia, HTN
• Serum HCG to rule out pregnancy in amenorrhea
• In high risk women or with virilization, testing may be needed to
rule out other uncommon causes of hyperandrogenism.
• Morning serum 17-hydroxyprogesterone in the follicular phase
• Serum testosterone
• Serum prolactin and TSH
• Obesity
• Weight loss: diet and exercise, bariatric surgery
• Insulin-lowering agents: metformin
• Hyperandrogenism
• Estrogen/Progesterone OCPs, also provide endometrial protection
• Antiandrogen after 6 months
• Spironolactone (if not planning conception), finasteride
• GnRH agonist (leuprolide) suppresses ovarian function
• Dyslipidemia
• Statins
• Fibrates
• NASH
• Weight loss
• Metformin
• Anovulation
• Weight loss
• Clomid
• Metformin
• Weight loss:
• Reduces androgenism, improves ovulation, and increases chance of planned pregnancy.
• Insulin-lowering agents
• Clomiphine
• Increases chances of ovulation
• Metformin
• Decreases insulin resistance and hyperinsulinemia, increases insulin sensitivity 
decreased androgens. May promote ovulation
• Aromatase inhibitor
• Induces ovulation
• Gonadotropins –
• Increases chances of ovulation
• Surgery
• We no longer use wedge resection
• We do occasionally use “ovarian drilling” to induce ovulation
+: usually effective; ±: marginally effective
• Ricardo Azziz, MD et al. “Epidemiology and pathogenesis of
the polycystic ovary syndrome in adults.” UpToDate. Updated
7/17/12
• Robert L Barbieri, MD, David A Ehrmann, MD et al. “Clinical
manifestations of polycystic ovary syndrome in adults.”
UpToDate. Updated 8/3/12.
• Robert L Barbieri, MD David A Ehrmann, MD et al. “ Diagnosis
of polycystic ovary syndrome in adults.” UpToDate. Updated
3/9/12.
• Robert L Barbieri, MD David A Ehrmann, MD et al. “Treatment
of polycystic ovary syndrome in adults.” UpToDate. Updated
9/20/12.
• Robert L Rosenfield, MD et al. “Clinical features and diagnosis
of polycystic ovary syndrome in adolescents.” UpToDate.
Updated 6/15/11.
• Robert L Rosenfield, MD et al. “Definition, pathogenesis, and
etiology of polycystic ovary syndrome in adolescents.”
UpToDate. Updated 6/15/11.
• Robert L Rosenfield, MD et al. “Treatment of polycystic ovary
syndrome in adolescents.” UpToDate. Updated 6/16/11.
• Figures http://www.advancedfertility.com
• Figures https://ufandshands.org/polycystic-ovary-syndrome