Polycystic ovarian disease has a variety of biochemical and clinical features with great individual variation. In our clinical experience, oligo-ovulation, manifested as oligomenorrhea or frank amenorrhea, associated with an acyclic estrogen milieu, is a consistent finding. This may be associated with hyperandrogenemia, hirsutism, inappropriate gonadotropin levels, hyperprolactinemia, obesity, insulin resistance, and ultrasound evidence of multicystic enlarged ovaries. A common presentation is infertility or irregular menstruation secondary to oligo-ovulation and hirsutism secondary to altered androgen metabolism. A challenge in diagnosis is to differentiate polycystic ovarian disease from latent cases of congenital adrenal hyperplasia. Although the precise mechanism in the pathogenesis of polycystic ovarian disease remains undefined, altered function of the hypothalamic-pituitary-ovarian and adrenal axes is both involved and integrated. Results from clinical trials of ovulation induction using different agents have implicated one site or another as the major progenitor of the "vicious cycle" but with no definitive pathway established. Restoring fertility to these patients can be challenging in that not all patients with polycystic ovarian disease respond to clomiphene or do so satisfactorily. The use of glucocorticoid suppression, pituitary suppression with GnRH analogues, or the use of FSH alone may be of benefit in clomiphene treatment failures.