Policystic Ovary Syndrome and Hirsutism

Stein and Leventhal: first report of seven amenorrheic women with smooth, enlarged ovaries, who ovulated following wedge polycistic ovary syndrome

The advent of radioimmunoassay

Clinical Features

Obesity: seen in at least 50% of women with polycistic ovary syndrome (PCO).

Upper body obesity is frequently characteristic

Oligomenorrhea or amenorrhea

Hirsutism 1. Not always present 2. Hirsutism is a function of both target tissue response and hyperandrogenism

Premenarchal onset of symptoms

Infertility

Acne

Biochemical Features

Increased free testosterone: if not present, the diagnosis is suspect; the most reliable biochemical indicator of the disorder

Decreased sex hormone-binding globulin polycystic ovary syndrome, hirsutism (SHBG): a consequence of both elevated androgen secretion and obesity

Increased luteinizing hormone (LH): not always present, and may vary from time to time polycystic ovary syndrome

D. Normal follicle-stimulating hormone (FSH)

E. Prolactin occasionally elevated

F. Dehydroepiandrosterone sulfate often elevated: no longer viewed as evidence of intrinsic adrenal dysfunction

G. Insulin resistance

1. Seen even in lean subjects

2. Subsequent risk for type II diabetes mellitus may be increased

IV. DIFFERENTIAL DIAGNOSIS

A. Simple obesity

B. Congenital adrenal hyperplasia

C. Hyperprolactinemia

D. Hypothyroidism

E. Severe insulin resistance syndromes

A. The "vicious cycle" theory

1. Originally proposed by Yen

2. No longer considered viable in toto in light of clinical experience with

gonadotropin-releasing hormone (GnRH) analogs

B. The role of hyperinsulinism: data indicating ability of insulin to stimulate ovarian androgen production is very suggestive