H&P + Diagnosis
PCOS is a clinical syndrome, not a single d/o. It is defined by hyperandrogenism, ovulatory dysfunction, & polycystic ovaries.
Dx is made w/ the Rotterdam criteria. The patient needs 2 of 3 criteria + exclude phenotypically similar androgen excess disorders.
Menstrual hx: amenorrhea/oligomenorrhea? Onset & freq. of menses?
S/sx of hyperandrogenism (acne, hirsutism, seborrhea, pattern baldness, clitoromegaly)?
S/sx of hyperinsulinemia (acanthosis nigricans, skin tags)?
Check BP, BMI, waist circumference.
Exam: thyroid exam, breast exam (presence of galactorrhea), and pelvic exam (for size & contour of ovaries).Risk Factors:
Differential diagnosis.
Diagnostic algorithm (AFP 2016)
Diagnostic tests:
–Beta-HCG (Pregnancy test); TSH; Prolactin; 17-hydroxyprogesterone (draw in the AM, especially during the follicular phase).
–A1C, Fasting Lipid Panel, CMP (to eval DM, HLD, NAFLD, and metabolic syndrome, which are complications of PCOS)
-2-hour oral GTT. Give Glucola and draw both glucose and insulin 2hrs after the Glucola. ***Oral GTT with 75 grams is recommended for all PCOS patients. It is preferable to a fasting blood sugar.
-DHEAS (to r/o adrenal androgen-secreting tumor)
-Total testosterone level (to r/o ovarian androgen-secreting tumor. Also if moderate to severe hirsutism is noted)
-LH, FSH, as needed.
-Pelvic ultrasound, as needed (esp. in women w/ normal cycles).
-Endometrial sampling (if history indicates)
-Overnight dexamethasone suppression test (if signs or symptoms of hypercortisolism i.e.Cushing’s syndrome)
-Will consider idiopathic hirsutism and severe insulin resistance syndrome depending on workup results.
Treatment
Tx of PCOS involves treating the individual components of the syndrome – hyperandrogenism (hirsutism, acne), ovulatory dysfunction (oligomenorrhea/amenorrhea, infertility), obesity, and insulin resistance – in accordance w/ the patient’s goals esp. about pregnancy.
Pts can bed divided into Women not pursuing pregnancy vs. Women pursuing pregnancy.
Lifestyle changes (exercise, diet, and weight loss) treats high BMI (overweight/obesity), decreases insulin resistance, decreases progression from pre-DM to DM, and increases ovulation rate.
Metformin 850 -1000 mg PO bid helps with metabolic/glycemic abnormalities but also improves menstrual abnormalities (even though OCPs better).
COCs (low-dose) are the 1st-line tx for hyperandrogenism (hirsutism, acne ) and menstrual dysfunction in pts who also desire contraception. OCPs also decrease hyperandrogenism and the risk for endometrial hyperplasia. Evaluate these pts risks for OCPs like you would any other pts w/o PCOS. If unable to take COCs, use intermittent progestin therapy.
Spironolactone 50-200 mg daily is 2nd-line for treating hirsutism if 6 mo tx with COCs hasn’t produced satisfactory results. Pt must cont. COCs b/c spironolactone is teratogenic.
Clomiphene / Letrozole is 1st-line therapy for infertility. These drugs induce ovulation. Also, IVF (in-vitro fertilization is an option).
Evaluate and treat long-term metabolic complications of PCOS: Metabolic syndrome, OSA, depression, HTN, labs for DM, HLD, NAFLD. Consider screening for endometrial hyperplasia in pts w/ longstanding PCOS & anovulation.
Refer to a reproductive specialist if the patient desires fertility or pregnancy.
managing hyperandrogenism and menstrual dysfunction
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Key Points
- Clinical features associated with hyperandrogenism.
- Low-dose combined OCPs frequently used to reduce the risk of endometrial cancer in patients with chronic anovulation and the resulting unopposed estrogen secretion.
- Algorithm from AAP for Diagnosing PCOS.
- PCOS is a risk for endometrial carcinoma.
- PCOS is not a specific endocrine disorder but rather is a syndrome represented by a collection of signs and symptoms. No one sign, symptom or test is diagnostic. Diagnosis is is clinical, based on history and physical exam.
- “Management of polycystic ovary syndrome is typically aimed at addressing patient symptoms, as well as irregular menses and the risk of endometrial hyperplasia. Infertility may become a therapeutic target for women who desire pregnancy at some point in their lives. In this patient, who needs contraception and hopes to address her hirsutism, combined oral contraceptives are most likely to address both concerns. In addition to suppressing ovulation they also suppress gonadotropin and ovarian androgen production. The estrogen component increases hepatic production of sex hormone binding globulin, thus decreasing androgen bioavailability. Progestin-only pills and the levonorgestrel IUD protect against pregnancy but will not improve hirsutism. Cyclic progesterone every 1–3 months can be used to prevent endometrial hyperplasia but will not provide contraception or address hirsutism. Spironolactone is an androgen receptor antagonist that can decrease hair growth, but it will not provide contraception.” ABFM
- Ultrasound criteria for PCOS: 12 or more subcapsular follicle cysts measuring 2-8 mm in diameter. Increased ovarian stroma and volume.
- Diagnostic tests explained: Workup to exclude of phenotypically similar androgen excess disorders such as congenital adrenal hyperplasia (CAH), androgen-secreting tumors, Cushing syndrome, thyroid dysfunction, and hyperprolactinemia, etc.
- The Endocrine Society recommends screening for depression and obstructive sleep apnea (OSA) in overweight/obese patients with PCOS.
- Metformin is beneficial for metabolic/glycemic abnormalities and for improving menstrual irregularities, but it has limited or no benefit in treating hirsutism, acne, or infertility. And it shouldn’t given the MOA of Metformin.
Labs explained
–Beta-HCG (pregnancy test) to r/o pregnancy.
-Prolactin to r/o hyperprolactinemia
-TSH to r/o thyroid dysfunction.
-17-hydroxyprogesterone to r/o nonclassical CAH. Patient to draw lab in the morning, especially during the follicular phase.
-DHEAS (to r/o adrenal androgen-secreting tumor)
-Total testosterone level (to r/o ovarian androgen-secreting tumor. Also if moderate to severe hirsutism is noted)
–Fasting lipid panel – to evaluate for metabolic syndrome.
-2-hour oral GTT. Give Glucola and draw both glucose and insulin 2hrs after the Glucola. ***Oral GTT with 75 grams is recommended for all PCOS patients. It is preferable to a fasting blood sugar.
Women with PCOS have:
an increase in serum LH (increase in LH pulse frequency and amplitude)
decreased FSH levels.
from an increase in GnRH pulse frequency
from negative feedback of elevated estrone.
Increased Inhibin B
Insulin Resistance
Increased LH and Insulin increase Androgens and lower SHBG
Obesity aggravates
Genetic and Environmental Factors
Populations with an increased incidence of CAH: Ashkenazi Jewish, Yupik Eskimo, Slavic, Mediterranean, Hispanics, and if hirsutism at menarche or pre-). 10% of Israeli, Indian, Jordanian hirsute women have CAH.
References:
The Journal of Clinical Endocrinology & Metabolism, Volume 98, Issue 12, 1 December 2013, Pages 4565–4592. Diagnosis and Treatment of Polycystic Ovary Syndrome: An Endocrine Society Clinical Practice Guideline. https://www.ncbi.nlm.nih.gov/pubmed/24151290
N Engl J Med 2016;375(1):54-64. Polycystic ovary syndrome.
Am Fam Physician. 2016 Jul 15;94(2):106-113.Diagnosis and Treatment of Polycystic Ovary Syndrome. http://www.aafp.org/afp/2016/0715/p106.html
Presentation by Dr. Maher Abdallah, FACOG at UCR Palm Springs in November 2016