The Polycystic Ovary Syndrome
Pediatric and adult endocrinologists may encounter PCOS as a mildly virilizing state since it is the most frequent cause of hyperandrogenism in female teenagers and in adult women.
Pathophysiology: Puberty and PCOS
The observation that menstrual disturbances and hirsutism commonly originate in puberty and that many of the endocrine alterations of PCOS look like an exaggeration of those that accompany puberty (see above) suggests a pathogenetic link. Among these features, hyperinsulinism may be the clue factor.
This metabolic defect may even pre-date the PCOS since it is most likely genetic in nature, although it remains to be proven that this is the case in all patients. An increased body of evidence suggests that it has a role in causing and/or propagating the disease. Hyperinsulinism may interfere early with the pubertal maturation process at the hypothalamic, pituitary, ovarian and adrenal levels, leading to a ‘hyperpubertal state’. This may trigger a selfperpetuating process causing the outcome of puberty to be PCOS in genetically susceptible young women.
Nevertheless, in lean and normoinsulinemic women, other still unknown factors, either genetic or environmental, may be basic for the development of PCOS. Many studies have been conducted to characterize the dysregulation of LH secretion and to elucidate whether a primary hypothalamic abnormality could explain the onset of PCOS in normoinsulinemic adolescents. So far, however, no data have clearly indicated that this dysregulation does not simply result from the long-term effects of ovarian steroid abnormalities or other peripheral influence.
Revision date: June 21, 2011
Last revised: by Andrew G. Epstein, M.D.