Ontogeny of Polycystic Ovary Syndrome: A Creative Approach

Polycystic ovary syndrome (PCOS) is a common heterogeneous familial disorder characterized by hyperandrogenism, oligo/amenorrhea, infertility, and insulin resistance/hyperinsulinemia. Familial clustering of hyperandrogenism, insulin resistance, and hyperinsulinemia in this syndrome is well described (1–5). Both genetic and environmental factors contribute to the pathogenesis of PCOS. Affected women have a higher risk to develop impaired glucose tolerance and type 2 diabetes mellitus. Although controversy exists regarding extent of the risk for cardiovascular disease, increased carotid artery intima-media thickness, dyslipidemia, obesity, metabolic syndrome, and the presence of inflammatory markers have been described among women with PCOS (6). The clinical features of PCOS often develop during the peripubertal years; premature pubarche due to premature adrenarche is considered to represent the initial manifestation for some girls (7). Preventative care is a major aspect of pediatrics as illustrated by the development of vaccines to prevent childhood infectious diseases. Thus, premorbid identification of children at risk for PCOS and its associated disorders could be beneficial and enable therapeutic intervention(s). However, the earliest features of PCOS and its temporal progression are best characterized as murky. Prenatal factors such as maternal androgen excess, maternal hyperglycemia due to impaired glucose tolerance or gestational diabetes mellitus, or placental insufficiency may contribute to postnatal development of the metabolic derangements associated with PCOS. Another important factor involved in the pathogenesis of PCOS appears to be an inherent dysregulation of steroid biosynthesis (8).