State of the Art Review: Emerging Therapies: The Use of Insulin Sensitizers in the Treatment of Adolescents with Polycystic Ovary Syndrome (PCOS)

Recognition of the highly prevalent association between PCOS and insulin resistance (IR) has stimulated research into the mechanism(s) behind this relationship, defining the metabolic, cardiovascular, and reproductive consequences of the IR, and evaluating therapies that target IR. Much of the current therapeutic paradigm incorporating insulin sensitization is derived from studies in adult women; application to the adolescent requires critical evaluation of the data supporting insulin sensitizer use in this age group. Although not intended as a comprehensive review of PCOS therapy, this report will discuss the options available for the treatment of adolescents with PCOS, with focus on the possible efficacy and costs of insulin sensitizing agents in comparison to more traditional therapies for PCOS.PCOS is a heterogeneous condition affecting 7-10% of women worldwide [1,2], irrespective of ethnic background [3], making it the most common endocrine disorder among reproductive-aged women. The 2003 Androgen Excess Society (AES) consensus required two of the following three criteria as necessary for the diagnosis: hyperandrogenism, ovarian dysfunction (oligo- or anovulation), and/or a polycystic ovary [4]. Summarizing the report of the recent 4th annual meeting of the Androgen Excess and PCOS Society [5], Yildiz and Azziz noted the difficulty in defining certain sub-phenotypes of PCOS, such as women with irregular menstrual cycling and polycystic ovarian morphology without evidence of hyperandrogenism (previously considered essential for the diagnosis).While hyperandrogenism is central to classically defined PCOS pathophysiology [6-8], and testosterone and DHEA-S are increased in up to 75% of PCOS patients, obesity and IR are frequently associated [9-11]. As many as 60% of women with PCOS have BMI values in the overweight or obese range [2] and 70% demonstrate IR and diabetes beyond that predicted by weight alone [12-14]. Hyperinsulinemia consequent to obesity and IR plac