Abstract
INTRODUCTION It is estimated that approximately 50–70% of patients suffering from polycystic ovary syndrome (PCOS) present with cycle abnormalities and infertility1. Polycystic ovaries are enlarged and exhibit several classical characteristics, such as a greater number of follicles situated under the ovarian surface together with augmented and dense stroma. In the earlier days, diagnosis was based on morphology investigation. Since the early 1980s, these ovarian abnormalities can be diagnosed in a non-invasive way through the use of pelvic ultrasound. Initially, ovarian sonography has been performed through the transabdominal route2. Subsequent introduction of the transvaginal route has significantly improved visualization of ovaries. This new diagnostic tool has had a major impact on the diagnosis of this syndrome (for review see Fauser3 and Fox and Hull4) and once again has focused attention on the ovary in this heterogeneous disease. Variable underlying abnormalities may lead to a similar end-point, i.e. anovulation based on polycystic transformation of ovaries. Involved endocrine abnormalities include elevated serum luteinizing hormone (LH) or serum androgen concentration as well as insulin resistance. These factors may results in elevated intraovarian androgens which may in turn affect follicle development5. It should be stressed that serum levels of immunoreactive and bioactive (using the in vitro rat granulosa cell bioassay) follicle stimulating hormone (FSH)-the hormone primarily responsible for stimulation of follicle growth-are normal6.