Learning Objectives:After participating in this continuing professional development activity, the provider should be better able to:
1. Describe the clinical presentation of polycystic ovary syndrome (PCOS) in the adolescent patient.
2. Apply adolescent-specific criteria to diagnose PCOS appropriately in this population.
3. Formulate evidence-based treatment plans, including pharmacologic and nonpharmacologic interventions, for managing adolescents with PCOS that optimize short- and long-term health outcomes.
Polycystic ovary syndrome (PCOS) is a chronic multisystem endocrinopathy characterized by hyperandrogenism and ovulatory dysfunction. The syndrome was first described in 1935 by Stein and Leventhal1 with a series of patients exhibiting a triad of oligomenorrhea or amenorrhea, hirsutism, the gross appearance of "polycystic ovaries," and "sterility." Today, PCOS is one of the most prevalent reproductive disorders worldwide, is the leading cause of anovulatory infertility, and is estimated to cost $8,000,000,000 annually in the United States alone.2,3
In adolescence, the clinical manifestations of PCOS may emerge, but diagnostic challenges arise. Many of the hallmark signs and symptoms of PCOS (menstrual irregularity, acne, and changes in hair growth patterns) occur during normal puberty. Obtaining a menstrual history can be difficult with adolescents who may not understand what constitutes "normal" and/or may be reluctant to discuss menstruation. Finally, the diagnostic criteria for PCOS are described differently by the National Institute of Health (NIH, 1990),4 the Rotterdam consensus in 2003,5 and most recently by the Androgen Excess Society in 2008.6 Until 2015, guidance for diagnosing PCOS in adolescents lacked specificity. In 2015, the first adolescent-specific PCOS guideline was published; this was updated in 2017 to include a robust discussion of the syndrome's pathophysiology.7,8 In 2018, the International PCOS Network published evidence-based guidelines for the assessment and management of PCOS, including adolescent-specific recommendations and input from consumer and patient representatives.9 Highlights from this 2018 publication are included throughout this review and will henceforth be referred to as "the guidelines."
PCOS has clinical features that are manifest throughout life involving multiple organ systems. Not only do the diagnostic criteria differ, the management of PCOS also varies. Two studies, in 2013 and 2018, compared the diagnosis and management of adolescents with PCOS across 3 specialties (adolescent medicine, pediatric endocrinology, and gynecology) at academic medical centers.10,11 Both studies reported considerable variability across specialties in the diagnosis and management of this disorder. Compared with other specialists, gynecologists were less likely to identify patients' weight concerns, recommend lifestyle modification, or screen for glucose, lipid, or liver abnormalities, or prescribe metformin. They were, however, more likely than other specialists to test estradiol levels, perform pelvic ultrasound, and prescribe hormonal contraception.
Failure to recognize PCOS in adolescents can negatively impact quality of life (QoL), short- and long-term health outcomes, and health care costs. More than a third of one group of adults with PCOS reported seeing 3 or more health professionals for 2 or more years before receiving a diagnosis; the majority felt dissatisfied with their health care experience and the information they received.12 Diagnostic experiences such as these may have lasting effects on patients' well-being and their lifetime approach to PCOS management. Although it remains unclear to what extent early treatment of PCOS impacts syndrome progression, benefits of timely recognition include reduction of distressing symptoms, deliberate surveillance for comorbidities, and improved patient experiences. Agreement over and adherence to best practices are important for optimal care. This review aims to close practice gaps for gynecologists in the diagnosis and management of adolescent PCOS.
Pathophysiology
PCOS is a clinically heterogeneous disorder with a range of phenotypes that likely develop through different pathways under the influence of incompletely understood genetic, epigenetic, and environmental factors. The syndrome disrupts ovarian, neuroendocrine, and metabolic function. By the time PCOS presents clinically, numerous aberrances have resulted in a dynamic imbalance of androgens, gonadotropins, and other signaling proteins such as anti-Mullerian hormone (AMH).
In a normally functioning ovary, endocrine, paracrine, and autocrine factors coordinate to promote cyclical follicle development and ovulation. Hypothalamic gonadotropin-releasing hormone (GnRH) acts on the anterior pituitary gland to release follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which induce ovarian production of estradiol and progesterone. These corticosteroid hormones participate in a negative feedback loop to regulate GnRH. Autocrine and paracrine growth factors are known to exert a major effect on ovarian androgenesis and folliculogenesis, which are driven by the hypothalamic-pituitary-ovarian endocrine axis.2 Ovarian theca cells secrete androgens, which are required for recruitment of quiescent primordial follicles into folliculogenesis. In each ovulatory cycle, multiple primordial follicles mature, and one emerges as "dominant," ultimately to be release an oocyte through ovulation, whereas the remaining follicles undergo atresia. Granulosa cells from growing follicles produce AMH, which provides negative feedback and inhibits further recruitment of primordial follicles. In PCOS, this normal ovarian process is disrupted and excess androgens are produced; sometimes adrenal function is similarly disrupted.
Rosenfield and Ehrmann2 proposed a functional classification of PCOS based on the source of androgen excess. According to their classification, 87% of PCOS cases are associated with primary functional ovarian hyperandrogenism (FOH), and of these, 25% have concomitant functional adrenal hyperandrogenism (FAH). The remaining cases are associated with isolated primary FAH (5%), or are deemed secondary to obesity or idiopathic (8%).
Regardless of the underlying androgen source, PCOS is exacerbated by insulin resistance (IR), which is present in approximately 50% of cases.2 In FOH, the primary issue is dysregulation of steroidogenesis, resulting in excess androgen at the level of the theca cell. Hyperandrogenism contributes to a disordered and self-perpetuating cycle; excess androgens beget more androgens. These excess androgens interrupt a number of regulatory processes including the ability of ovarian corticosteroid hormones to participate in a negative feedback loop with the hypothalamus, which causes a secondary rise in LH.2 Excess LH stimulates hypertrophy of testosterone-producing theca cells, further exacerbating hyperandrogenism. High intraovarian androgen levels stimulate excessive follicular recruitment and cause premature follicular arrest. Hyperandrogenemia suppresses sex-hormone-binding globulin concentration (SHBG), which elevates circulating free testosterone, which then may cause virilizing adverse effects. In FAH, the adrenal zona reticularis is hyperresponsive to adrenocorticotropic hormone, leading to excess dehydroepiandrosterone sulfate (DHEAS) and androstenedione secretion. Adipose tissue contributes to excess androgens via adipocyte conversion of androstenedione to testosterone.2
Although hyperinsulinemia does not appear to be the primary driver of PCOS, it contributes to hyperandrogenism and anovulation. Insulin directly stimulates ovarian and adrenal androgen secretion, and suppresses hepatic SHBG synthesis, thus increasing free testosterone. There is an apparent relationship between PCOS and intrinsic IR that is independent of obesity and androgen concentrations.13 The role of obesity in the pathogenesis and progression of PCOS is unclear. Obesity contributes to IR and hyperandrogenism, and can therefore influence the phenotypic expression of PCOS and contribute to more severe features.9
Diagnostic Criteria, Clinical Presentation, and Diagnostic Workup
Diagnostic Criteria
Over the last 3 decades, the Rotterdam diagnostic criteria have become the most universally accepted. This definition requires at least 2 of the following to be present to diagnose PCOS: oligomenorrhea and/or anovulation, clinical and/or biochemical signs of hyperandrogenism, and ultrasonic evidence of polycystic ovary morphology (PCOM).5 In 2012, the NIH Evidence-based Methodology Workshop on PCOS endorsed the Rotterdam criteria, and recommended classifying the syndrome as 1 of 4 phenotypes depending on the presence or absence of hyperandrogenism, ovulatory dysfunction, and/or PCOM.4
Before 2015, these adult diagnostic criteria were simply applied to adolescents. The 2015 guidelines, however, recommended against including PCOM for diagnosing adolescents. The change corresponds to the older 1990 NIH definition, referred to as the "classic" type, and has the strongest association with IR and metabolic disease.14 The change was made because finding multifollicular ovaries in those who had not reached "gynecologic maturity" (8 years post-menarche)9 is not sensitive or specific for PCOS. Codner et al estimated that 30% to 40% of adolescent females have PCOM but may not have anovulation, hyperandrogenism, or metabolic abnormalities.15,16
Adolescents with acne, hirsutism, menstrual irregularity, obesity, and IR but do not meet NIH criteria can be labeled as "at risk" for developing the syndrome. This includes those who demonstrated PCOS features before initiating hormonal contraception or within the first year after menarche. When diagnosis is unclear, the guidelines recommend engaging patients in a discussion around diagnostic uncertainty at this life stage, and informing them of their "at-risk" status for PCOS and associated comorbidities.9 At-risk patients should be counseled on healthy behaviors and reevaluated for PCOS at or before they reach gynecologic maturity.9
Clinical Presentation
Although heterogeneous, PCOS classically presents with acne, hirsutism, oligo- or sometimes amenorrhea, obesity, and IR. The presence and severity of signs and symptoms vary, especially in adolescents. Not all adolescents with acne, alterations in hair growth, or menstrual irregularity have underlying PCOS, and not all adolescents with underlying PCOS will have acne, hirsutism, and ovulatory dysfunction. Physicians must differentiate symptoms from the physiologically normal pubertal androgenic rise from those that result from pathologic hyperandrogenism. PCOS is ultimately a diagnosis of exclusion. Performing a thorough history, physical, and appropriate laboratory assessment to rule out other causes of hyperandrogenism and menstrual disturbances, including congenital adrenal hyperplasia, thyroid disorders, Cushing's disease, androgen-secreting tumors, hyperprolactinemia, hypo-gonadotropic hypogonadism, and drug-induced hyperandrogenism is essential.
Abnormal pubertal timing, such as early androgenization and menstrual irregularity, may indicate underlying PCOS. Premature pubarche (before age 8 in a genotypic female) and primary amenorrhea (no menarche by age 15 or 3 years after thelarche) warrant further evaluation and consideration of underlying pathology, including PCOS or increased risk for developing PCOS.9
Clinical Hyperandrogenism
Clinical hyperandrogenism is characterized by acne, hirsutism, and rarely, male-pattern alopecia. Acne vulgaris affects approximately 85% of adolescents.17 Increasing androgen levels after adrenarche stimulate sebaceous glands to produce sebum, which can block hair follicles and form acne. There are no validated assessment tools for scoring acne severity, but it is generally classified as mild, moderate, or severe, based on lesion quantity and quality (comedonal, inflammatory, and cystic). Mild acne is considered normal, whereas moderate or severe acne more likely reflects hyperandrogenism.8
Hirsutism is excessive, coarse, terminal hair growth that follows a male-pattern distribution. Greater than 80% of hirsutism is due to androgen excess, and 70% to 80% of individuals with hirsutism have PCOS.2,17 The modified Ferriman-Gallwey (mFG) system is a visual assessment tool to quantitate hair growth. A value between 0 (absent terminal hair) and 4 (extensive terminal hair) is assigned to each of 9 androgen-sensitive regions of the body (upper lip, chin, chest, upper abdomen, lower abdomen, thighs, back, arm, and buttocks). The guidelines define a score 4 or more to 6 (range is ethnicity dependent), as clinical evidence of hyperandrogenism. The hirsutism score is expected to increase with age, pubertal stage, and years elapsed since menarche.16 There are few data on how to quantitate hair growth in adolescents, and there is debate about whether or not an adolescent-specific cut-off should be used.7 PCOS is the most common cause of adolescent hirsutism; however, the overall prevalence of adolescent hirsutism is low. In a study of predominantly White adolescents with PCOS, most had mFG scores of 0, and 92% of subjects had scores less than 5, suggesting that hirsutism is specific, but not sensitive for PCOS.16
Biochemical Hyperandrogenism
Biochemical hyperandrogenism is excessive production and/or secretion of androgens as described by laboratory values. For females, there is no clearly defined "normal" testosterone level, as it varies with diurnal rhythms, menstrual phase, and pubertal stage.8 High-quality liquid chromatography-mass spectrometry and extraction/chromatography immunoassays are recommended for the most accurate assessment.9 Importantly, current or recent (within 12 weeks) use of hormonal contraceptives preclude accurate assessment of biochemical hyperandrogenism, as these medications affect gonadotropin-dependent androgen production and SHBG.
Ovulatory Dysfunction
Ovulatory dysfunction may manifest as primary or secondary amenorrhea, oligomenorrhea, and/or heavy menstrual bleeding. Menstrual irregularities can affect QoL. Defining menstrual abnormalities during adolescence is potentially difficult, as anovulation and varying cycle length are common with early menstrual cycles. The majority of people who menstruate develop ovulatory cycles of 20 to 45 days within the first 2 years after menarche; however, frequency of ovulation is related to both time since menarche and age at menarche. Regular ovulatory cycles may take up to 8 to 10 years to be established.9,18 Opinions conflict over the required symptom duration for a diagnosis of PCOS. Earlier guidelines recommend persistent menstrual abnormalities for a minimum of 2 years; the 2018 guidelines recommend a minimum of 1 year.7-9 The guidelines define "irregular" cycles as less than 21 or greater than 45 days when more than 1 or less than 3 years have elapsed since menarche, or, less than 21 or greater than 35 days, or less than 8 cycles per year more than 3 years from menarche.
Evaluation
Evaluation begins with a careful history and physical examination. History should specifically include age of thelarche, adrenarche, and menarche; menstrual cycle frequency and duration; presence and progression of symptoms, any cosmetic hair removal; other medical problems, any prescribed or nonprescribed drug use; and any family history of type 2 diabetes mellitus (T2DM) or PCOS.19 Physical examination includes blood pressure, weight, assessment for signs of hyperandrogenism (hirsutism, acne) and IR (acanthosis nigricans, skin tags). In a patient with signs of hyperandrogenism and irregular menstruation, the American College of Obstetricians and Gynecologists suggests testing LH, FSH, prolactin, thyroid-stimulating hormone, free and total testosterone, DHEAS, and 17-[alpha]-hydroxyprogesterone (17OHP).19 DHEAS and androstenedione are weak androgens that arise from the adrenal cortex. Although adrenal androgens are of limited utility for diagnosing PCOS, they can assess for adrenal causes of hyperandrogenism. Measurement of AMH is not recommended for evaluation of adolescent or adult PCOS.9 Ultrasound should not be used as PCOS diagnostic criteria for adolescents but can be used to evaluate for other ovarian pathology if indicated.
Management
Given the heterogeneity of PCOS, there is no "one-size fits all" therapy. Management is tailored to the individual to address weight, menstrual irregularity, and virilizing symptoms. Management of "at-risk" patients should target current symptoms and address risk factors for associated comorbidities. Treatment options for adolescents with PCOS include lifestyle interventions, combined oral contraceptive pills (COCPs), antiandrogens, insulin-sensitizing drugs, and dermatologic treatments.
Healthy eating and regular physical activity are recommended for all adolescents with PCOS to achieve and maintain a healthy weight and optimize general health, QoL, and lower levels of androgens and insulin.9 The guidelines recommend at least 60 minutes of moderate- to vigorous-intensity physical activity daily. Even for those with a normal weight, physical activity reduces the risk of metabolic syndrome, a significant risk factor for developing T2DM and cardiovascular disease.8
More than 50% of adolescents with PCOS have excess weight; approximately 25% have features of metabolic syndrome.11 Lifestyle interventions, including diet, behavioral modification, and exercise, are first-line therapy for overweight individuals.9,19 A combination of weight reduction and physical activity decreases androgen levels, normalizes menstrual cycles, and improves markers of cardiometabolic health.8 In Sebastian et al's study11 of 141 adolescent patients, less than 50% of overweight and obese patients with PCOS received weight management strategies from their gynecologist in the form of documented recommendation for lifestyle modification, referral to a comprehensive weight management program, or documented evidence that weight concerns were otherwise being managed by the pediatrician. This study may reflect a practice gap that is an easy area for improvement.
Pharmacotherapy
Although no medication is FDA approved to specifically treat adolescent PCOS, the androgen-lowering effects of COCPs, insulin-sensitizers, and antiandrogens are useful for managing acne, hirsutism, menstrual irregularity, and IR. Treatment should be offered to all adolescents with patient-important hirsutism or acne, regardless of whether they meet diagnostic criteria for PCOS.9,17 All guidelines recommend that a trial of at least 6 months of pharmacologic therapy be completed before making dose adjustments, adding a medication, or switching to a new medication.7-9,17,20
Combined Oral Contraceptive Pills
COCPs are the first-line agent for hyperandrogenism and menstrual irregularity. COCPs increase SHBG and suppress LH levels, resulting in lower bioavailable and total testosterone.17 The guidelines recommend any COCP with estrogen and progesterone (no specific formulation). There are 4 FDA-approved COCPs for moderate acne: ethinyl estradiol/norgestimate and ethinyl estradiol/norethindrone acetate/ferrous fumarate (for 15 years and older) and ethinyl estradiol/drospirenone and ethinyl estradiol/drospirenone/levomefolate (for 14 years and older).18
The choice of COCP should always be made with consideration of comorbid conditions or relative contraindications, in particular, PCOS-specific factors such as high body mass index (BMI), hyperlipidemia, and hypertension.8,9 Estrogen-containing medications are contraindicated in those with hypercoagulability or a history of blood clots, migraine with aura, and active liver disease. For patients who have acne but also have contraindications to estrogen, one can consider topical therapy (retinoids, benzoyl peroxide, and antibiotics), oral antibiotics, spironolactone, and/or isotretinoin. For those seeking control of irregular menstrual bleeding but are unable to take estrogen, progestin may be an option. In some cases, progestin may exacerbate acne if that is an associated problem. Many adolescents initiate COCPs for irregular menstrual cycles or acne without being assessed for PCOS, which potentially delays a PCOS diagnosis.
Metformin
Insulin affects androgen levels by stimulating ovarian and adrenal steroidogenesis, and decreasing hepatic synthesis of SHBG.2 Reducing insulin levels pharmacologically reduces hyperandrogenemia.17 Metformin, which inhibits gluconeogenesis and acts as an insulin sensitizer, is the most common insulin-lowering agent used to treat patients with PCOS. Compared with other specialists, gynecologists are less likely to prescribe metformin.10,11 Current evidence suggests that metformin is most effective when combined with lifestyle changes and COCPs.21 The guidelines indicate that metformin could be considered in adolescents with a clear diagnosis of PCOS or with symptoms of PCOS before the diagnosis is made, and, in combination with the COCP in adolescents with PCOS and a BMI 25 kg/m2 or more where COCP and lifestyle changes do not achieve desired goals.9
The short-term benefits of metformin on BMI and menstrual cycles are more pronounced in overweight and obese teens.21 A small trial of 36 obese adolescents demonstrated statistically significant reductions in central adiposity and total testosterone and increases in high-density lipoprotein when taking metformin, COCPs, and lifestyle compared with placebo, COCPs, and lifestyle.22 In adolescents with PCOS and hyperinsulinemia, metformin may produce ovulation and decreases serum androgens.8 Mild gastrointestinal distress is a significant adverse effect of metformin, which may affect adherence or long-term continuation.
Antiandrogens
The guidelines and the Endocrine Society recommend adding an antiandrogen if at least 6 months of COCPs have failed to acceptably resolve hirsutism.9,17 As antiandrogens may cause fetal undervirilization, they should only be used in combination with effective contraception. The guidelines do not comment on antiandrogens for acne; however, spironolactone, a potassium-sparing diuretic with antiandrogenic effects, is a popular acne treatment.23 Spironolactone reduces circulating free testosterone by blocking the androgen receptor, decreasing 5-[alpha]-reductase activity, and increasing SHBG. Daily doses of 50 to 100 mg of spironolactone have been shown to improve acne in 66% of women and are generally well tolerated.23 Adverse effects are dose-dependent. The most common symptoms are mild: diuresis, menstrual irregularities, and breast tenderness. Hyperkalemia can result when spironolactone is combined with other potassium-sparing agents, so this combination should be avoided.23
Hair Removal Therapy
As medication will not remove existing unwanted hair, bleaching, plucking, shaving, and waxing may be considered. Permanent hair reduction methods include photoepilation (laser hair removal), electrolysis, and topical eflornithine. The Endocrine Society offers guidance for selecting treatment based on hair color, skin color, and ethnicity.17 Photoepilation, which relies on the presence of melanin in the hair shaft to work, is recommended for the removal of auburn, brown, or black hair. Adverse effects of photoepilation are related to thermal injury of the epidermis and include pain, inflammation, burns, blisters, hypo- or hyperpigmentation, and scarring. Adverse effects are more likely to occur in people with higher melanin content; thus, using a long-wavelength, long-pulse-duration light source with appropriate skin cooling when treating people of color to minimize the risk of thermal injury is recommended.17 Mediterranean and Middle Eastern people are thought to have an increased risk of developing paradoxical hypertrichosis from photoepilation; thus, electrolysis is preferred for these ethnic groups. Electrolysis is also recommended for people with blonde or white hair, for whom melanin-dependent photoepilation will not be effective. Eflornithine, an amino acid derived from ornithine, inhibits follicular polyamine synthesis and slows hair growth. Topical eflornithine hydrochloride cream is recommended as monotherapy for those who are not candidates for photoepilation, or as an adjuvant treatment to photoepilation for laser-resistant facial hirsutism in patients 16 years or older.8
Ongoing Care/Addressing Comorbid Conditions
Monitoring serum androgens or other biomarkers is not recommended for patients with PCOS, as they do not reflect the severity or progression of the disorder.20 Ongoing care is tailored to the individual. The most common comorbidities associated with PCOS fall into 3 major categories-reproductive, metabolic, and psychosocial. Patients with or "at risk" for PCOS should have intentional changeovers of care, as they transition from pediatric to adult providers to address these needs.
Reproductive Concerns
Although a teen may not inquire specifically about reproduction, people with PCOS are at increased risk for infertility and pregnancy complications. A key feature of PCOS is ovulatory dysfunction, which results in prolonged time to conception and increased use of ovulation induction and in vitro fertilization. Patients may experience reduced embryo implantation rates and a greater risk of ovarian hyperstimulation syndrome when treated with ovulation-inducing agents. When pregnancy is achieved, PCOS is associated with increased risk of miscarriage, gestational diabetes mellitus, preeclampsia, preterm birth, and stillbirth.9 A cross-sectional study of adolescent girls demonstrated that those with PCOS were more concerned about fertility than their peers.24 Clinicians should educate adolescent patients about modifiable risk factors known to impact their future reproductive outcomes including weight, glucose control, nutrition, smoking cessation, and alcohol use. Of note, in some adolescents with or at risk for PCOS, normal ovulatory function may develop as they mature.8
PCOS has been associated with increased endometrial cancer risk, although it is unclear whether the risk is independent of comorbidities such as obesity and infertility. Chronic anovulation results in prolonged unopposed estrogen (ie, absence of progesterone exposure), which increases the risk of endometrial hyperplasia and endometrial carcinoma. Oral contraceptives help to mitigate this risk.9
Metabolic Concerns
Independent of weight, PCOS is associated with impaired glucose tolerance, T2DM, and metabolic syndrome. General pediatric guidelines recommend testing for "prediabetes" and T2DM in patients who are overweight with at least one of the following risk factors: non-White race, family history of T2DM, maternal gestational diabetes, and signs of or conditions associated with IR (including PCOS).25 "Prediabetes" refers to abnormally elevated glucose that is not high enough to meet criteria for diabetes, yet confers an increased risk of developing diabetes and cardiovascular disease. Gynecologists should ensure that metabolic comorbidities are adequately screened for and managed in their adolescent patients with or at risk for PCOS, as they are less likely than other specialists to test for glucose abnormalities, dyslipidemia, and liver disease.11
Psychosocial Concerns
PCOS is associated with an increased risk of anxiety, depression, eating disorders, psychosexual dysfunction, and low self-esteem-all of which can lower QoL.9 Inadequate symptom management, concern about long-term health consequences, and the stress of having a chronic disease can all negatively impact QoL in patients with PCOS. The guidelines recommend that adolescents be screened for anxiety and depression at the time of PCOS diagnosis.9 The PCOS QoL tool26 (to date validated for adults, but not adolescents) considers the domains of emotions, body hair, weight, infertility, and menstrual problems and thus can help clinicians understand which features are most distressing to an individual patient. Adolescents with PCOS score lower on QoL measures including general health perceptions, self-esteem, social emotional, physical and behavioral roles, and mental health.24,27 A 2020 review of the studies pertaining to QoL in adolescents with PCOS demonstrated that, in the majority of studies, weight issues were a major driver of lower QoL scores.28
Partnering With Patients
Education and empowerment are prominent themes in the guidelines.9 Adolescence is a particularly impressionable life phase, and medical experiences during this time may direct behaviors and choices throughout the life course that impact long-term health and well-being. Partnering with patients at the time of diagnosis and providing educational materials and reassurance about the potential for prevention of complications, providing close follow up, and assisting with transitions of care into adulthood may improve experiences and outcomes for people with PCOS.
Practice Pearls
* The diagnosis of PCOS in adolescents requires the presence of clinical and/or biochemical hyperandrogenism and ovulatory dysfunction.
* Polycystic ovarian morphology on ultrasound should not be considered in the diagnosis of PCOS in adolescents.
* Adolescents who have symptoms but do not meet the diagnostic criteria for PCOS should be labeled as "at risk" for developing PCOS and should be reevaluated at least at or before 8 years post-menarche. They should be educated and counseled on modifiable behaviors and outcomes, and screened for reproductive, metabolic, and psychological co-morbidities.
* Patients who meet clinical criteria for PCOS should be evaluated before initiating COCP or other hormonal medications.
* Spironolactone is an effective antiacne medication that is generally well tolerated in the setting of PCOS.
* Photoepilation, electrolysis, and/or topical eflornithine provide permanent hair removal. Choice of modality should be based on the patient's hair and skin color.
* Multimodal treatment plans that combine lifestyle interventions, COCPs, and metformin should be considered. Healthy eating and regular physical activity are recommended for all adolescent patients with PCOS to achieve and/or maintain a healthy weight, regulate androgen and insulin levels, and optimize general health and QoL.
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