Detecting polycystic ovarian syndrome in teens

September 1, 2008

PCOS is challenging to diagnose-and easy to miss-in teenagers especially because symptoms like acne and irregular periods are common in normal teens.

Polycystic ovarian syndrome (PCOS), an endocrine disorder characterized by hyperandrogenism and anovulation, begins at or before puberty.1 Even though this is well accepted, diagnosing the condition in adolescents remains challenging. That's because the relatively short duration of exposure to elevated androgens may be less likely to lead to the classic signs of androgen excess that are characteristically seen in adult women. Just how widespread is PCOS among reproductive-aged women? It's estimated at 5% to 10%.1,2 Our goal here is to provide gynecologists with a guide to diagnosing and managing PCOS in adolescents.

Diagnostic criteria

The most commonly accepted diagnostic guidelines for PCOS are the NIH 1990 and Rotterdam 2003 criteria. Previously, the NIH 1990 criteria specified that a diagnosis of PCOS could be made in women with (1) clinical hyperandrogenism and/or hyperandrogenemia, (2) chronic anovulation, and (3) exclusion of other known disorders that cause irregular menstrual cycles and androgen excess.3

Essentially, the more recent Rotterdam 2003 criteria expand the PCOS diagnosis to include women who may experience many, but not all of the signs and symptoms of ovarian dysfunction.

Pathophysiology

There are four distinct loci of disturbed endocrine functioning in women and adolescents with PCOS: (1) disordered gonadotropin secretion, (2) ovarian hyperandrogenemia, (3) adrenal hyperandrogenemia, and (4) insulin resistance. Furthermore, obesity may play a role in the pathophysiology of the disorder by aggravating or triggering insulin resistance.

(1) GnRH. The pulse frequency of hypothalamic gonadotropin-releasing hormone (GnRH) is increased in women and adolescents with PCOS when compared to women without the condition. Increased GnRH in turn increases the production and pulse frequency of LH.2,5,6

(2) Increased LH results in ovarian hyper–androgenemia through the stimulation of ovarian theca cells to produce increased amounts of androstenedione, 17-OH progesterone, and testosterone. Further, the granulosa cells of women with PCOS secrete smaller amounts of estrogen than granulosa cells from normal ovaries. A hormonal imbalance favoring androgen production thus exists within the ovaries.

(3) Generalized adrenal hyperresponsiveness in women with PCOS results in adrenal hyperandrogenemia with increased dehydroepiandrosterone, 17-OH progesterone, 17-hydroxypregnenolone, and androstenedione levels.

(4) Insulin also plays a role in the pathogenesis of PCOS. Not only does it enhance ovarian production of androgens by acting synergistically with LH,2 but insulin also increases adrenal responsiveness to ACTH. Further, it inhibits hepatic synthesis of sex hormone-binding globulin (SHBG). Normally, SHBG binds to testosterone and inactivates its androgenic effects. Therefore, decreased synthesis of this hormone increases the circulation of unbound, active testosterone, thereby further increasing the presence of hyperandrogenemia in PCOS.2,7