Polycystic ovary syndrome (PCOS) is the most common endocrinopathy among reproductive-aged women; the prevalence is about 5% to 10%.1 Like women with PCOS, affected adolescents often present with irregular menses, hirsutism, and acne. However, despite widespread agreement that the metabolic derangements of PCOS arise during puberty, the condition is diagnosed more often in adults than in adolescents.
Diagnosis of PCOS in adolescence is complicated by the following challenges:
•Signs of PCOS, including acne and oligomenorrhea, are common among healthy teenaged girls.
•Puberty is a dynamic state, and the syndrome may take time to fully evolve.
•No formal criteria exist for diagnosing PCOS in adolescents.
Adolescents with PCOS are at risk for such sequelae as dyslipidemia, hypertension, type 2 diabetes mellitus, infertility, and (potentially) coronary artery disease. Prompt diagnosis is essential to optimize therapy, establish healthy diet and exercise habits, and prevent potential health risks.
This is the first of 2 articles on PCOS. Here the focus is on diagnosis. After a brief review of the pathophysiology, we review current diagnostic criteria and differential diagnostic considerations. In Part 2 Polycystic Ovary Syndrome: Update on the Pros and Cons of Treatment Options, we discuss treatment options.
In a future issue, we will detail the various treatment options for PCOS. We will also discuss screening for—and monitoring of—the long-term associated risks.
Although the basic pathophysiology of PCOS is unknown, several cardinal endocrine derangements have been identified:
•Insulin resistance and resultant hyperinsulinism.
•Dysfunctional secretion of gonadotropin-releasing hormone (GnRH).
•Increased production of androgens primarily by the ovary.
Insulin resistance and resultant hyperinsulinism are central to the pathophysiology of PCOS. Insulin acts on ovarian theca cells to promote androgen secretion both independently and synergistically with luteinizing hormone (LH). Hyperinsulinism also increases levels of bioavailable androgen by reducing the amount of sex hormone-binding globulin (SHBG) produced by the liver.2
Increased production of GnRH from the hypothalamus is thought to be responsible for the hypersecretion of LH in PCOS. Excess LH acts on theca cells in the ovary to augment androgen production.1 The reason for the more frequent secretion of GnRH in patients with PCOS remains unknown; it is possible that there is an intrinsic defect in the GnRH pulse generator or a lack of feedback inhibition of GnRH caused by chronically low progesterone(Drug information on progesterone) levels.3,4
Obesity is not a cause of the syndrome; however, it exacerbates many of the symptoms. Like hyperinsulinemia, obesity reduces SHBG production by the liver, which increases levels of active testosterone in the circulation. In addition, obesity worsens insulin resistance and hyperinsulinism, thereby increasing ovarian androgen production.5,6
Obesity alone, however, does not entirely explain the degree of insulin resistance seen in adolescents with PCOS. PCOS has been shown to compound the degree of insulin resistance found in persons with obesity alone.6 Furthermore, lean patients with PCOS are more insulin-resistant than those without PCOS.