Abstract
- Polycystic ovary syndrome affects 6%-7% of reproductive-aged women, making it the most common endocrine disorder in this population. It is characterized by chronic anovulation and hyperandrogenism. Affected women may present with reproductive manifestations such as irregular menses or infertility, or cutaneous manifestations, including hirsutism, acne, or male-pattern hair loss. Over the past decade, several serious metabolic complications also have been associated with polycystic ovary syndrome including type 2 diabetes mellitus, metabolic syndrome, sleep apnea, and possibly cardiovascular disease and nonalcoholic fatty liver disease. In addition to treating symptoms by regulating menstrual cycles and improving hyperandrogenism, it is imperative that clinicians recognize and treat metabolic complications. Lifestyle therapies are first-line treatment in women with polycystic ovary syndrome, particularly if they are overweight. Pharmacological therapies are also available and should be tailored on an individual basis. This article reviews the diagnosis, clinical manifestations, metabolic complications, and treatment of the syndrome.
-
Keywords: Anovulation; Diabetes mellitus; Hirsutism; Insulin resistance; Polycystic ovary syndrome
Table 1.PCOS definitions 1990–20093
PCOS definition |
Clinical hyperandrogenism (Ferriman-Gallwey score ≥8) or biochemical hyperandrogenism (elevated total/free testosterone) |
Oligomenorrhea (less than 6–9 menses per year) or oligo-ovulation |
Polycystic ovaries on ultrasound (≥12 antral follicles in one ovary or ovarian volume ≥10cm3) |
NICHD(1990)7
|
Yes |
Yes |
No |
Rotterdam (2003)2
|
Yes |
Yes |
Yes |
|
|
2 of 3 criteria |
|
AE-PCOS Society8
|
Yes |
Yes |
Yes |
(2009) |
|
1 of 2 criteria |
|
Table 2.Posssible pathogenesis of polycystic ovary syndrome4
1. |
Hypothalamic-pituitary axis abnormalities cause abnormal secretion of gonadotropin releasing hormone and luteinizing hormone, resulting in increased ovarian androgen production. |
2. |
An enzymatic defect of ovarian (± adrenal) steroidogenesis favors excess androgen production. |
3. |
Insulin resistance drives the metabolic and reproductive abnormalities in polycystic ovary syndrome. |
Table 3.Laboratory testing to evaluate for metabolic complications of polycystic ovary syndrome1
Laboratory Test |
Evaluation for: |
Comment |
2-hr oral glucose tolerance |
Impaired glucose tolerance, |
Consider this in all women with polycystic ovary |
test |
type 2 diabetes |
syndrome, particularly those with a body mass |
|
|
index >25 kg/m2 or other risk factors for type 2 |
|
|
diabetes such as a positive family history. |
Fasting lipid profile |
Dyslipidemia |
Hypertriglyceridemia and decreased high-density |
|
|
lipoprotein are relatively common in women with |
|
|
polycystic ovary syndrome. Elevations in |
|
|
low-density lipoprotein have also been noted. |
|
|
Thus, periodic screening is recommended. |
Alanine aminotransferase |
Hepatic steatosis |
Consider checking transaminases in women with |
and aspartate |
|
other risk factors for nonalcoholic fatty liver |
aminotransferase |
|
disease. |
Table 4.Summary of recommendations for addressing reproductive, cosmetic, metabolic, and psychological complications of polycystic ovary syndrome1
|
Assess diabetes and cardiovascular disease risk |
Metabolic |
Assess risk for nonalcoholic fatty liver disease |
|
Discuss lifestyle therapies such as nutrition and physical activity |
|
Assess bleeding pattern and risk for endometrial hyperplasia |
Cycle control |
Provide therapies to prevent endometrial hyperplasia: estrogen-progestin therapy (oral |
|
contraceptives, patch, or vaginal ring) or cyclic progestin (every 1–3 months) |
|
Address body image and eating behaviors |
Psychosocial |
Screen for depression Discuss stress management |
|
Provide nonjudgmental support |
|
Discuss use of estrogen-containing oral contraceptives to suppress androgens if no |
|
contraindications |
Cosmetic |
Consider spironolactone 50–100 mg twice daily for refractory hirsutism or acne |
|
Discuss use of enflornithine hydrochloride 13.9% cream, laser therapy, and electrolysis |
|
Discuss over-the-counter topical minoxidil for male-pattern scalp hair loss |
|
Discuss fertility goals |
Ovulation |
Discuss therapies to increase ovulation frequency: weight loss, metformin |
|
Consider referral to Reproductive Endocrinology for assisted reproductive technologies |
Sleep apnea |
Screen for sleep apnea Refer for sleep study if indicated |
References
- 1. Setji TL, Brown AJ. Polycystic ovary syndrome: diagnosis and treatment. Am J Med 2007;120:128–32.ArticlePubMed
- 2. Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and longterm health risks related to polycystic ovary syndrome. Fertil Steril 2004;81:19–25.Article
- 3. Roe AH, Dokras A. The diagnosis of polycystic ovary syndrome in adolescents. Rev Obstet Gynecol 2011;4:45–51.PubMedPMC
- 4. American Association of Clinical Endocrinologists Polycystic Ovary Syndrome Writing Committee. American Association of Clinical Endocrinologists Position Statement on Metabolic and Cardiovascular Consequences of Polycystic Ovary Syndrome. Endocr Pract 2005;11:126–34.PubMed
- 5. Badawy A, Elnashar A. Treatment options for polycystic ovary syndrome. Int J Womens Health 2011;3:25–35.ArticlePubMedPMC
- 6. Lord JM, Flight IH, Norman RJ. Insulin-sensitising drugs (metformin, troglitazone, rosiglitazone, pioglitazone, D-chiro-inositol) for polycystic ovary syndrome. Cochrane Database Syst Rev 2003;CD003053.PubMed
- 7. Zimmermann S, Phillips RA, Dunaif A, Finegood DT, Wilkenfeld C, Ardeljan M, et al. Polycystic ovary syndrome: lack of hypertension despite profound insulin resistance. J Clin Endocrinol Metab 1992;75:508–13.ArticlePubMed
- 8. Azziz R, Carmina E, Dewailly D, Diamanti-Kandarakis E, Escobar-Morreale HF, Futterweit W, et al. The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report. Fertil Steril 2009;91:456–88.ArticlePubMed
Citations
Citations to this article as recorded by