Chapter 172 Polycystic Ovary Syndrome
INTRODUCTION
Description: Polycystic ovary syndrome (PCOS) consists of amenorrhea, hirsutism, insulin resistance, and obesity in association with enlarged, multicystic ovaries.
Prevalence: Up to 5% of women, 30% of secondary amenorrhea. The most common hormonal disorder among women of reproductive age.
ETIOLOGY AND PATHOGENESIS
Causes: The exact pathophysiology of polycystic ovary syndrome is not well established, but increased amplitude of gonadotropin-releasing hormone (GnRH) pulsation and abnormal secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) during puberty are thought to result in androgen excess. Elevated levels of LH persist and may be used to help establish the diagnosis. Insulin resistance is a prominent aspect of this syndrome.
DIAGNOSTIC APPROACH
Differential Diagnosis
• Cushing’s disease (truncal obesity, facial rounding, cervicodorsal fat deposition [buffalo hump], and red or purple striae are often not fully developed)
Workup and Evaluation
Laboratory: Elevated levels of luteinizing hormone may be used to help establish the diagnosis. (A two-to-one ratio of luteinizing hormone to follicle-stimulating hormone is considered diagnostic.) Evaluation for possible virilizing process (prolactin, follicle-stimulating hormone, thyroid screening). (Patients suspected of having adrenal sources of hyperandrogenicity may be screened by measuring 24-hour urinary-free cortisol, by performing adrenocorticotropin hormone [ACTH] stimulation tests, or an overnight dexamethasone suppression test.) Serum testosterone (total) is generally 70 to 120 ng/mL and androstenedione is 3 to 5 ng/mL. Dehydroepiandrosterone sulfate (DHEA-s) is elevated in approximately 50% of patients.
Imaging: Ultrasonography (abdominal or transvaginal) may identify ovarian enlargement or the presence of multiple small follicles. Magnetic resonance imaging (MRI) or computed tomography (CT) may be used to evaluate the adrenal glands.
