Consensus has recently been reached by international pediatric subspecialty societies that otherwise unexplained persistent hyperandrogenic anovulation using age- and stage-appropriate standards are appropriate diagnostic criteria for polycystic ovary syndrome (PCOS) in adolescents. The purpose of this review is to summarize these recommendations and discuss their basis and implications. Anovulation is indicated by abnormal uterine bleeding, which exists when menstrual cycle length is outside the normal range or bleeding is excessive: cycles outside 19 to 90 days are always abnormal, and most are 21 to 45 days even during the first postmenarcheal year. Continued menstrual abnormality in a hyperandrogenic adolescent for 1 year prognosticates at least 50% risk of persistence. Hyperandrogenism is best indicated by persistent elevation of serum testosterone above adult norms as determined in a reliable reference laboratory. Because hyperandrogenemia documentation can be problematic, moderate-severe hirsutism constitutes clinical evidence of hyperandrogenism. Moderate-severe inflammatory acne vulgaris unresponsive to topical treatment is an indication to test for hyperandrogenemia. Treatment of PCOS is symptom-directed. Cyclic estrogen-progestin oral contraceptives are ordinarily the preferred first-line medical treatment because they reliably improve both the menstrual abnormality and hyperandrogenism. First-line treatment of the comorbidities of obesity and insulin resistance is lifestyle modification with calorie restriction and increased exercise. Metformin in conjunction with behavior modification is indicated for glucose intolerance. Although persistence of hyperandrogenic anovulation for ≥2 years ensures the distinction of PCOS from physiologic anovulation, early workup is advisable to make a provisional diagnosis so that combined oral contraceptive treatment, which will mask diagnosis by suppressing hyperandrogenemia, is not unnecessarily delayed.
Skip Nav Destination
Article navigation
December 2015
State-of-the-Art Review Article|
State-of-the-Art Review Article|
December 01 2015
The Diagnosis of Polycystic Ovary Syndrome in Adolescents
Robert L. Rosenfield, MD
Professor Emeritus of Pediatrics and Medicine, The University of Chicago Pritzker School of Medicine, Chicago, Illinois
Address correspondence to Robert L. Rosenfield, MD, Section of Adult and Pediatric Endocrinology, Metabolism, and Diabetes, University of Chicago Medical Center, 5841 S. Maryland Ave (MC-5053), Chicago, IL 60637. E-mail: robros@peds.bsd.uchicago.edu
Search for other works by this author on:
Address correspondence to Robert L. Rosenfield, MD, Section of Adult and Pediatric Endocrinology, Metabolism, and Diabetes, University of Chicago Medical Center, 5841 S. Maryland Ave (MC-5053), Chicago, IL 60637. E-mail: robros@peds.bsd.uchicago.edu
FINANCIAL DISCLOSURE: The author has indicated he has no financial relationships relevant to this article to disclose.
Pediatrics (2015) 136 (6): 1154–1165.
Article history
Accepted:
June 25 2015
Citation
Robert L. Rosenfield; The Diagnosis of Polycystic Ovary Syndrome in Adolescents. Pediatrics December 2015; 136 (6): 1154–1165. 10.1542/peds.2015-1430
Download citation file:
Sign in
Don't already have an account? Register
Pay-Per-View Access
$25.00
Combined oral contraceptive (COC) treatment is ordinarily recommended as first-line treatment of polycystic ovary syndrome (PCOS) because it more reliably corrects hyperandrogenemia and more reliably normalizes menstrual/endometrial cycling than does dietary modification/behavioral counseling with or without metformin, as reviewed.1 Dyslipidemia is one aspect of metabolic syndrome, which variably results from the interaction of obesity, insulin resistance, and age.1 In our experience with a predominantly obese/overweight group of adolescent PCOS patients (n=36) that had an approximately 25% prevalence of metabolic syndrome, only a minority had dyslipidemia: 31% had low serum high-density lipoprotein cholesterol, 20% had elevated triglycerides.2 Dyslipidemia prevalence by standard measures or by advanced lipid testing in adolescent PCOS is generally unremarkable for the degree of obesity.3,4 We agree that dietary modification--a high fiber, low glycemic index, low saturated fat, lower calorie diet--coupled with behavioral counseling for weight loss, is the foundation of dyslipidemia management and metformin may provide additive benefit. Rarely are statins required, and while they improve low-density lipoprotein cholesterol and lower serum testosterone slightly, alone they have little impact on the clinical manifestations or insulin resistance of PCOS.5 Use of COCs with a low estrogen dose and a low androgenicity progestin (such as 20-30 mcg ethinyl estradiol plus 3 mg drospirenone or 0.25 mg norgestimate) minimizes the COC impact on insulin resistance and hence on lipid levels.5
References
1. Rosenfield RL. The diagnosis of polycystic ovary syndrome in adolescents. Pediatr 2015;136:1154-65.
2. Leibel NI, Baumann EE, Kocherginsky M, Rosenfield RL. Relationship of adolescent polycystic ovary syndrome to parental metabolic syndrome. J Clin Endocrinol Metab 2006;91:1275-83.
3. Hart R, Doherty DA, Mori T, et al. Extent of metabolic risk in adolescent girls with features of polycystic ovary syndrome. Fertil Ster 2011;95:2347-53, 53 e1.
4. Gourgari E, Lodish M, Shamburek R, et al. Lipoprotein particles in adolescents and young women with PCOS provide insights into their cardiovascular risk. J Clin Endocrinol Metab 2015;100:4291-8.
5. Goodman NF, Cobin RH, Futterweit W, Glueck JS, Legro RS, Carmina E. American Association of Clinical Endocrinologists, American College of Endocrinology, and Androgen Excess and Pcos Society Disease State Clinical Review: Guide to the Best Practices in the Evaluation and Treatment of Polycystic Ovary Syndrome - Part 2. Endocr Pract 2015;21:1415-26.
I am a lipidologist and have been treating pcos patients for 15 years through the lens of advanced lipid testing which helps detect insulin resistance in setting of normal glucose. Most adolescents with pcos will not have abnornal glucose as they have good pancreatic compensation with resultant hyperinsulinemia. In my opinion Dietary modification with low glycemic load higher fiber higher good fat diet and possibly metformin should be considered prior to initiating ocp which has many other metabolic consequences.
Tara Dall MD