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 estrogenprogestin 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.Polycystic ovary syndrome (PCOS) is the most common cause of chronic hyperandrogenic anovulation and the single most common cause of infertility in young women. 1 It is also a risk factor for metabolic syndrome-related comorbidities and for impaired wellbeing and mortality. 2 Considerable evidence suggests that PCOS has diverse causes, arising as a complex trait with contributions from both heritable and environmental factors that affect ovarian steroidogenesis. 3,4 Insulinresistant hyperinsulinism, in part related to coexistent obesity, is the most common nonsteroidogenic factor. The complex interactions generally mimic an autosomal dominant trait with variable penetrance: the disorder is correlated in identical twins 5 ; about half of sisters are hyperandrogenic, and half of these also have oligo-amenorrhea and thus PCOS 6,7 ; and polycystic ovaries appear to be inherited as an autosomal dominant trait. 7,8 Three percent to 35% of mothers have PCOS, 9,10 and metabolic syndrome prevalence is high in parents and siblings. 11-13 The syndrome was first described...