Polycystic Ovary Syndrome (PCOS) affects 15%–20% of adolescents and women of childbearing age.
It is a result of androgen excess and leads to the progression of several endocrine, metabolic, cardiovascular, reproductive, and psychological disorders. The increased androgen levels may be due to the underlying hormonal imbalance and insulin resistance that is involved in PCOS.1
PCOS appears to be a congenital disorder with signs and symptoms starting as early as puberty. The primary cause of the excess androgen levels (male hormones) seen with PCOS is unknown; however, there appears to be recurrence in families. Many of these clinical manifestations occur in puberty and have a long-term impact on an adolescent’s or woman’s daily wellbeing and activities of daily living.2
Anti-Mullerian Hormone (AMH) increases in women with PCOS and affects follicogenesis. AMH levels should decrease when follicles enlarge, but when levels remain high, follicles do not mature and ovulation is affected. Increased androgen levels cause a decrease in progesterone and estrogen, leading to a hypersecretion of gonadotropic-releasing hormone (GnRH) and luteinizing hormone (LH) levels, which continues to stimulate immature follicles which do not mature and form cysts in the ovary.3
Most adolescents reported that primary symptoms associated with PCOS such as acne, obesity, hirsutism, infertility, and menstrual problems had the most negative impact on their lives. These symptoms caused mood fluctuations and affected personal relationships.4 Adolescents and women of childbearing age will visit numerous clinicians before being diagnosed with PCOS, and 50% to 75% of those adolescents and women will present to the primary care provider with already existing clinical manifestations of PCOS.5
Diagnosis of PCOS in adolescents is problematic because symptoms such as irregular menses, acne, and weight gain seen in adolescent girls are considered part of normal growth and development for this age group. For this age group, the most common diagnostic criteria used is increased androgen levels.5 In adolescents and women of child bearing age, the most common diagnostic criteria used for PCOS are evidence of increased androgen levels, anovulatory symptoms such as amenorrhea, menorrhagia, oligomenorrhea, infertility, and/or polycystic ovaries.
Other clinical features that alert clinicians to the possibility of PCOS include:
- Androgenic alopecia (hair loss);
- and Acanthosis Nigricans.
Early pubarche in girls (8.73 vs. 10.73 years) and early thelarche (breast development 8.76 vs. 10.27 years) were early indicators of increased androgen levels and an increased likelihood of having PCOS. The most common disorders linked to PCOS include diabetes, cardiovascular disorders, reproductive disorders, cancer risks, and psychological disorders. PCOS is a heterogeneous disorder (not all patients show all symptoms of the disease.1
More than 50 percent of women with PCOS in the United States are obese (body mass index > 30 kg/m3), a similar rate to that of obesity in the United States.7 Most of these women have an increased amount of adipose tissue in the central body region. Obesity in women with PCOS causes increased androgen levels, insulin resistance, cardiovascular risks, and infertility. Insulin resistance and abnormal glucose metabolism seen in these women can lead to the development of type 2 diabetes.
At least 10% of women with PCOS will develop diabetes, a risk attributed to obesity, which increases glucose intolerance and insulin resistance over time.8 Insulin resistance occurs in about 50% to 80% of obese women with PCOS. Lean women with PCOS have lessened insulin resistance.9
In addition to diabetes risk, women with PCOS have increased cardiovascular risk. These women have increased clinical and subclinical markers for atherosclerosis such as increased coronary artery calcification and carotid plaque, which is exacerbated by obesity.10 Women with PCOS are four times more likely to develop metabolic syndrome than women who do not have PCOS. Metabolic syndrome involves physical and biochemical abnormalities that include elevated blood pressure (>or = 130/85), increased waist circumference (> or = 35 inches), elevated fasting glucose levels (> or = 100 mg/mg/dl), decreased high density lipoprotein cholesterol levels (< or = 50 mg/d), and elevated triglyceride levels (> or = 150 mg/dl). This syndrome is linked to an increased risk of cardiovascular disease and stroke.11
PCOS is the most common cause of anovulation and infertility in women. Central abdominal obesity causes increased androgen levels and insulin resistance, inhibiting ovarian follicle development and maturation leading to anovulation symptoms such as menstrual irregularities and infertility. As little as 5% weight loss can lower androgen levels and resume menses.13 PCOS accounts for 90% to 95% of women attending infertility clinics due to anovulatory symptoms. About 60% of these women are fertile (able to conceive in 12 months). Most women with PCOS and infertility will need assisted reproductive technologies to successfully achieve pregnancy. Pregnancy causes perinatal complications such as spontaneous abortion, gestational diabetes, and preterm birth.14
Long-term anovulation and increased unopposed estrogen lead to uterine hyperplasia over time. The increased unopposed estrogen occurs because the ovarian follicles do not mature and are not released to form progesterone to oppose high levels of estrogen. Estrogen levels remain high and lead to irregular menses, or prolonged bleeding from a buildup of the uterine lining by all the estrogen. Some of the excess estrogen is converted to testosterone which can cause increased appetite levels and lead to obesity.15 Women with PCOS have a significantly higher risk of developing endometrial and ovarian cancer compared to women who do not have PCOS.16
In addition to biological and physical problems, women with PCOS have increased risk for psychological problems as well. Documented psychological problems include:
- Poor self-esteem
- Psychosexual dysfunction
- Bipolar disorder
These psychological problems could be attributed to clinical features such as hirsutism, obesity, acne, and infertility, which can negatively affect mood and psychological well-being.17 Women with PCOS had a 4- fold increase in depressive scores compared to the control group.18
Treatment for women with PCOS can be complex. The first step in treating these women is to schedule a consultation with a primary care physician experienced with the condition or a reproductive endocrinologist. Weight reduction in obese women is a commonly supported intervention. Women are advised to reduce caloric intake and exercise to achieve at least a 5 percent weight loss. Weight reduction is most beneficial to those women showing signs of metabolic syndrome. In addition, these women will need insulin-sensitizing agents, such as metformin and lipid-lowering agents such as statins as needed. Bariatric surgery may be prescribed for those that are morbidity obese.19,20
Treatment of high androgen related symptoms include oral contraceptive pills, antiandrogens (spironolactone), acne treatments, and laser hair removal treatments. Progestin-only contraceptives may be prescribed to prevent uterine hyperplasia, but may cause abnormal bleeding. Women with PCOS and infertility should be referred to a reproductive endocrinologist to discuss treatment options to achieve pregnancy. Risks associated with the various ovulatory induction medications should be discussed such as ovarian hyperstimulation and multiple births. Clomid is the first-line ovulation induction medication that is prescribed. Second-line ovulatory medication is injectable gonadotropins. Laparoscopic ovarian surgery (ovarian drilling) is a surgical treatment option that can regulate menses and trigger ovulation in women with PCOS. This procedure involves use of a laser fibre or electromagnetic needle to puncture the ovary four to ten times.19
- Stirmans, S.M., Pate, K.A. Epidemiology, diagnosis, and management of polycystic ovary syndrome. Clinical Epidemiology. 2013; 1: 1-13.
- Buggs, C., Rosenfield, R.L. Polycystic ovary syndrome in adolescence. Endocrinology and Metabolism Clinics of North America. 2005; 34: 667-705.
- Pellatt, L., Rice, S., Mason, H.D. Anti-Müllerian hormone and polycystic ovary syndrome: a mountain too high? Reproduction. (2010); 139 (5): 825–833.
- Jones G.L., Hall J.M., Lashen H.L., Balen A.H., Ledger W.L. Health-related quality of life among adolescents with polycystic ovary syndrome. Journal of Obstetrics, Gynecology and Neonatal Nursing. 2011; 40 (5): 577-588.
- March, W.A., Moore, V.M., Wilson, K.J., Phillips, D.J., Norman, R.J., Davies, MJ. The prevalence of polycystic ovary syndrome in a community sample assessed under contrasting diagnostic criteria. Human Reproduction. 2010; 24: 541-544.
- Hassan, A., Gordon, C.M. Polycystic ovary syndrome in adolescence. Current Opinion in Pediatrics. 2007; 19 (4): 389-397.
- Stankiewicz, M., Norman, R. Diagnosis and management of polycystic ovary syndrome. Drugs. 2006; 66: 903-912.
- Cosar E, Ucok K, Akgun L, Koken G, Sahin FK, Arioz DT, Bas O. Body fat composition and distribution in women with polycystic ovary syndrome. Gynecological Endocrinology. 2008; 24: 428-432.
- Moran L.J, & Teede H. Metabolic features of the reproductive phenotypes of polycystic ovary syndrome. Human Reproductive Update. 2009; 15: 477-488.
- Ehrmann D.A, Liljenquist D.R, Kasza K, et al. Prevalence and predictors of the metabolic syndrome in women with polycystic ovary syndrome. Journal of Clinical Endocrinology and Metabolism. 2006; 91: 48-53.
- Grundy, S.M., Cleeman J.I., Daniels, S.R. Diagnosis and management of the metabolic syndrome: an American heart, lung, and blood institute scientific statement: executive summary. Critical Pathways in Cardiology. 2005; 4 (4): 198-203.
- Pasquali, R., & Gambineri, A. (2006). Polycystic ovary syndrome: a multifaceted disease from adolescence to adult age. Annals of New York Academic of Sciences. 2006; 1092: 158-174.
- Brassard M., AinMelk Y., Baillargeon J.P. Basic infertility including polycystic ovary syndrome. Medical Clinics of North America. 2008; 92: 1163-1192.
- De Franca Neto, A.H., Rogatto, S., Amorim, M.M., Tamanaha, S., Aoki, T., Aldrighi, J.M. Oncological repercussions of polycystic ovary syndrome. Gynecological Endocrinology. 2010; 26 (10): 701-711.
- Chittenden, B.G., Fullerton, G., Maheshwari, A., Bhattacharya, S. Polycystic ovary syndrome and the risk of gynecological cancer: a systematic review. Reproductive Biomedicine Online. 2009; 19 (3): 398-405.
- Deeks A.A., Gibson-Helm M.E., Teede H.J. (2010). Anxiety and depression in polycystic ovary syndrome: a comprehensive investigation. Fertility and Sterility. 2010; 93: 2421-2423
- Dokras, A., Clifton, S., Futterweit, W., Wild, R. Increased risk for abnormal depression scores in women with polycystic ovary syndrome. Obstetrics and Gynecology. 2011; 117 (1):145-152.
- American College of Obstetricians and Gynecologists (ACOG). ACOG practice bulletin. Polycystic ovary syndrome, 2009. Obstetrics and Gynecology. 2009; 114 (4): 936-949.
- Badawy, A., Elnashar, A. Treatment options for polycystic ovary syndrome. International Journal of Women’s Health. 2011; 3: 25-35.