Polycystic Ovarian Syndrome

The polycystic ovarian syndrome (PCOS) is a common dysfunction that appears in women at reproductive age. The etiology of this syndrome is still unknown. The PCOS reproductive manifestations include hyperandrogenism, impaired ovulation, amenorrhea, polycystic ovaries and are generally associated with metabolic alterations like insulin resistance, obesity, dyslipemia and a high risk of cardiovascular disease. Therefore, consensus about the main clinic manifestations is needed to diagnose the PCOS, since this syndrome has many associated phenotypes. A recent scientific meeting suggested that the PCOS diagnosis should exclude other hyperandrogenic disorders, thyroid disease or another related disorder. Furthermore, PCOS diagnosis should have at least two of the following three criteria: oligo/anovulation, hyperandrogenism (clinical or biochemical) or polycystic ovary on ultrasonography. There are many phenotypes of this syndrome and the discovery of the DNA genome has allowed the association between the clinical and the genetic basis of the PCOS. This syndrome is associated with genes involved in the biosynthetic pathway of androgens in adrenal and ovarian glands, in the androgen receptor expression and in LH and FSH regulation. The metabolic characteristics of this syndrome may be associated with the expression of metabolic genes, for example, the insulin gene. Nevertheless, the evidence is not enough for a monogenic association; it suggests that PCOS is a polygenic syndrome. The basic research of the PCOS is based on animal models. The neonatal or fetal administration of steroids can affect the metabolic and reproductive axis of the rodents, and scientist can study the basis of the syndrome. Furthermore, for a better approximation at human physiology, there are other models in rhesus monkeys. These researches can study the characteristics of women with PCOS during adulthood with an early modification in hormone levels; it allows us to study the target tissue of hyperandrogenism. Finally, PCOS etiology may include a polygenetic basis that modifies the reproductive and metabolic physiology when it interacts with a specific environment such as fetal hyperandrogenism or insulin resistance.

Bibliography:
“Review: Fetal Programming of PCOS by androgen Excess: Evidence from experimental, clinical and genetics association studies” Xita, 2006, J. of Clinical Endocrinology and Metabolism.

“Insulin resistance, dyslipemia, and metabolic syndrome in women with PCOS” El-Mazny, 2010, International Journal of Gynecology and Obstetrics