Polycystic ovary syndrome: a vitamin deficiency? Floating a new pathogenesis hypothesis.

摘要

Polycystic ovary syndrome (PCO'S) is a medical condition that causes irregular menstrual cycle, chronic anovulation most often manifested as oligo-amenorrhea, and androgen excess with the typical ovarian ultrasound features1. It is the most common cause of ovulatory disorders and female infertility and affects approximately 6-10% of women in childbearing age2. However, its pathogenesis is still poorly understood.Recently many investigators focused both on impaired glucose tolerance, that affects 30 to 40% of patients with PCO'S3, and insulin resistance, that is manifested in a significant proportion of women with PCO'SInsulin plays a direct role in the pathogenesis of hyperandrogenemia in the polycystic ovary syndrome, acting synergistically with luteinizing hormone to enhance the androgen production of theca cell4. Since the report by Burghen et al5 in 1980 where PCOS was associated with hyperin-sulinemia, it has become clear that this syndrome has major metabolic as well as reproductive morbidities. The recognition of this association has also instigated extensive investigation on the relationship between insulin and gonadal function. An inositol phosphoglycan molecule containing D-chiro-inositol is known to have a role in activating enzymes that control glucose metabolism6. A defect in tissue availability or utilisation of D-chiro-inositol (DCI) or inositolphosphoglycan (IPG) mediators mav contribute to insulin resistance.