Polycystic ovary syndrome in obese adolescents.

PURPOSE OF REVIEW

As the prevalence of pediatric obesity escalates, polycystic ovary syndrome is an increasingly common morbidity for adolescent females. This review describes recent insights into the pathophysiology and treatment of polycystic ovary syndrome, with special attention given to the relationship between polycystic ovary syndrome and obesity.

RECENT FINDINGS

Recent research has elucidated three key concepts in our understanding of polycystic ovary syndrome. First, patients may enter the hyperandrogenism-hyperinsulinism cycle of polycystic ovary syndrome via several pathways, including genetic polymorphisms that affect androgen synthesis, fetal programming that alters lipid and glucose metabolism, and obesity accompanied by insulin resistance. Second, obesity plays a significant role in the pathophysiology of polycystic ovary syndrome by increasing free androgen concentrations through multiple mechanisms. Finally, just as the etiology of polycystic ovary syndrome is multifactorial, successful treatment will probably require a combination of lifestyle modification and therapeutic interventions.

SUMMARY

Obesity contributes to the pathophysiology of polycystic ovary syndrome and increases the likelihood of associated metabolic and cardiovascular morbidities.