Polycystic ovary syndrome and impact on health
Abstract
Polycystic ovary syndrome (PCOS) is a multifactorial, heterogeneous, complex genetic, endocrine and metabolic disorder, diagnostically characterized by chronic anovulation, polycystic ovaries and biochemical and clinical manifestations of hyperandrogenism. It has a tremendous negative impact on the physiology and metabolism of the body as it may evolve into a metabolic syndrome with insulin resistance, hyperinsulinemia, abdominal obesity, hypertension and dyslipidemia presenting as frequent metabolic traits and culminating in serious long-term consequences, such as type 2 diabetes mellitus, endometrial hyperplasia and cardiovascular disease. The key endocrine abnormalities include dysregulation of the gonadotropin-releasing hormone (GnRH) pulse generator to feedback inhibition by ovarian steroids, resulting in luteinizing hormone (LH) hypersecretion, and decreased follicle-stimulating hormone (FSH), and ovarian stromal–thecal hyperactivity, resulting in ovarian hyperandrogenism, all of which may lead to significant biochemical, reproductive and metabolic dysfunction. Though it is detected in approximately 5–10% of women of reproductive age, recent evidence from experimental observations in animals, buttressed by human studies, suggest a deep-rooted developmental origin of PCOS, the pathophysiology of which progresses from infancy to adulthood. In utero fetal programming or dysregulation of the hypothalamic–pituitary–gonadotropic axis at crucial developmental stages, mediated…
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