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 evidencefrom experimental observations in animals, buttressed by human studies, suggest a deep-rooteddevelopmental 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 by the interaction of genetically determined hyperandrogenism and environmental factors (obesity), may have a significant role in the development © 2010 Middle East Fertility Society.