The Diagnosis of Polycystic Ovary Syndrome in Adolescents

Abstract

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...

Diagnosis, Pathogenesis and Management of Polycystic Ovary Syndrome

“…In vitro fertilization studies found that PCOS patients have a lower oocyte implantation rate [32][33][34], due to oocytes which are exposed to high levels of androgens and other factors of abnormal levels, such as high insulin levels [3]. Gene chip analysis showed that abnormal endocrine and metabolic have a effects on the gene expression in PCOS oocyte, and most of the differentially expressed genes were upregulated in oocytes of PCOS patients [28,29,35].…”

Polycystic ovary syndrome: controversies and challenges

“…So this condition is very important. [1][2][3][4][5][6] It is known that PCOS is not characterized by the association of hyperandrogenism and chronic anovulation only, but also involves disorders of carbohydrate metabolism, with a focus on insulin resistance and increased risk of developing diabetes. The latter is higher with increases in weight and ultimately the appearance of obesity, leading to dyslipidemia, metabolic syndrome and increased possibility of malignancies such as endometrial carcinoma.…”

“…The latter is higher with increases in weight and ultimately the appearance of obesity, leading to dyslipidemia, metabolic syndrome and increased possibility of malignancies such as endometrial carcinoma. [1][2][3][4][5][6] Although the description of the clinical picture had been reported in the literature before the twentieth century, this syndrome was recognized by the work of two American surgeons, Stein e Leventhal, in 1935. 1 Since then, several publications have been made looking for a single agent to justify PCOS.…”

“…1 Since then, several publications have been made looking for a single agent to justify PCOS. [2][3][4][5] However, the interaction between genetic, environmental, behavioral and psychological factors is, to date, the best way to understand this condition and its various phenotypes.…”

“…Depending on the habits (sedentary lifestyle and poor diet), there could be worsened hyperinsulinemia and early pubarche, a clinical sign suggestive of greater chances of developing PCOS. [1][2][3][4][5][6][7] Other important factors are heredity (mothers with PCOS) and genetics. There are several genes that can serve as biomarkers, including GTF2A1L and LHCGR (plays a crucial role in luteinizing hormone [LH] receptors).…”