ABSTRACT
The term ‘polycystic ovary’ (PCO)—formerly ‘Stein-Leventhal ovary’1-is now consistently used to describe the main phenotypic features of the clinical state known as polycystic ovarian syndrome (PCOS) in the human.2 Despite the accumulated literature and remarkable advances in the understanding of PCOS, the aetiology of the syndrome is still not clear and the primary mechanism is not known.3-5 Indeed, PCOS is a complex and heterogeneous disease,6,7 but the data obtained (mostly from clinical studies) and the many hypotheses and suggestions regarding its aetiology are largely conflicting and therefore contribute further to the complexity of the syndrome. Part of this complexity may be due to underestimation of the overall functioning of the ovaries. For example, treatment of patients with PCOS has always aimed to stimulate ovarian function, mainly follicular development, a strategy that may not be ideal to correct the syndrome. In fact, a PCO by definition contains numerous follicles most of which are healthy when compared with normal ovary.8,9 We believe that a new direction in research into the cause of PCOS and its treat-
concern. Molecular genetics techniques may prove valuable.
