Polycystic ovarian syndrome is a common disorder causing androgen excess, ovulatory dysfunction and polycystic ovaries. PCOS can only be diagnosed if other potential causes of androgen excess are first ruled out (Congenital adrenal hyperplasia, Cushing’s, androgen tumors, etc) Thus, PCOS is a diagnosis of exclusion. In the developed world, PCOS is the most common endocrine disorder causing androgen excess and affects anywhere from 4-12% of all women. It appears to affect all races and nationalities.
In order to diagnose PCOS, the Rotterdam consensus of 2003 states that 2 out of the 3 criteria must be met: 1) elevated circulating androgens 2) oligo or anovulation 3) polycystic ovaries on ultrasound. Some controversy exists regarding the last criteria, since as many as 25% of females with normal androgen levels and regular menses may have polycystic ovaries.
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| Image from the Florida Department of Health webpage |
Most commonly, women with PCOS present with menstrual dysfunction. Other clinical manifestations of PCOS may include signs of virilization such as hirsutism, male pattern balding, oily skin and persistent acne. Women with PCOS appear to have a higher incidence of insulin resistance. Many such women also have metabolic syndrome: obesity and dyslipidemia. Approximately 30-40% of women with PCOS have impaired glucose tolerance and approximately 10% have type 2 diabetes based on 2 hour glucose challenge test results. In the long term, PCOS patients have increased risk of endometrial cancer, Type 2 Diabetes and cardiovascular disease.
Frequently, women with PCOS will present to the gynecologist with complaint of infertility. Although the precise mechanism in which PCOS causes anovulation is unknown, an understanding of the pathophysiology of PCOS will illuminate some aspects of its impact on normal ovulation. Disruptions of the pulsatile GnRH release leads to a relative increase of luteinizing hormones (LH) over follicle stimulating hormones (FSH). This imbalance creates excessive androgen production with decreased conversion of androgens to estradiol. FSH paucity leads to follicular atresia and subsequently anovulation. The LH:FSH ratio is elevated, and over 2 in 60% of women with PCOS. At present, insulin resistance is hypothesized to be another major factor in anovulation.
Most of these women are not infertile, but only sub-fertile. First line treatment and counseling should including weight loss, careful diet and nutrition, and regular exercise. If lifestyle modifications are initiated in earnest and weight loss is achieved, some women with PCOS can see resolution of hyperinsulinemia and ovulation dysfunction. For other patients, lifestyle modifications alone are not enough and may need to be started on medications such as clomiphene citrate and human menopausal gonadotropins and insulin sensitizing agents. For some women, the combination of metformin and clomiphene citrate works well in regulating ovulation and ultimately achieving fertility.PCOS remains a multi-factorial and complicated disorder. However, many different treatments and therapies are now available to resolve the clinical manifestations of this disease. Primary care physicians and gynecologists should be consulted first if one suspects PCOS. The appropriate referrals can then be made to reproductive endocrinology for more extensive workup.
For more information about PCOS as well as information about latest treatment guidelines and support groups, check out http://www.soulcysters.com/
and http://www.pcosupport.org/Common lab tests and treatment found here
Infertility resource center found here
Submitted by Emily Yen, Class of 2011, Women’s Health Pathway Student
References:
Legro, Richard., “Polycystic Ovary Syndrome, Hirsutism and other Androgenic Excess Disorders,” PRECIS: Reproductive Endocrinology, American College of Obstetricians and Gynecologists, 2002
Schorge JO, Schaffer JI, Halvorson LM, Hoffman BL, Bradshaw KD, Cunningham FG, "Chapter 17. Polycystic Ovarian Syndrome and Hyperandrogenism" (Chapter). Williams Gynecology: McGraw Hill Companies, 2008
