Polycystic ovary syndrome (PCOS) is the most common endocrine disorder, affecting approximately 5%–18% of reproductive-age women worldwide. Both genetic and environmental factors play a role in the pathogenesis of the syndrome (1). The diagnosis can be established if two or more of the following criteria are met: oligo-amenorrhea, clinical or biochemical androgen excess, and polycystic ovaries (PCOs) as detected in ultrasonography, thus providing four different phenotypes that vary in their clinical manifestations (1). Women presenting with both hyperandrogenism and amenorrhea have the most severe phenotype in terms of an adverse metabolic profile (2,3). Other disorders and specific etiologies, such as congenital adrenal hyperplasia, Cushing’ s syndrome, thyroid hormone abnormalities, hyperprolactinemia, and ovarian or adrenal tumors, should also be excluded prior to diagnosis.