Hirsutism: Implications, etiology, and management

Abstract

Hirsutism usually results from a subtle excess of androgens. As such, it is a clue to possible endocrine disturbance in addition to presenting cosmetic problems. We use the term hirsutism to mean male-pattern hirsutism--excessive growth of hair in areas where female subjects normally have considerably less than male subjects. An elevation of the plasma free (unbound) testosterone level is the single most consistent endocrinologic finding in hirsutism. The plasma free testosterone level is sometimes elevated when the total level of plasma testosterone is normal because testosterone-estradiol--binding globulin (TEBG) levels are often depressed in hirsute women. Frequent blood sampling is sometimes necessary to demonstrate subtle hyperandrogenic states since androgen levels in the blood are pulsatile and seemingly reflect episodic ovarian and adrenal secretion. The source of hyperandrogenemia can usually be determined from dexamethasone suppression testing. Those patients whose plasma free androgen levels do not suppress normally usually have functional ovarian hyperandrogenism (polycystic ovary syndrome variants). Very high plasma androgen levels or evidence of hypercortisolism, which is not normally suppressible by dexamethasone, should lead to the search for a tumor or Cushing's syndrome. Those patients in whom hyperandrogenemia is suppressed normally by dexamethasone have a form of the adrenogenital syndrome, a prolactinoma, obesity, or idiopathic hyperandrogenemia. In such patients, glucocorticoid therapy may reduce hirsutism and acne and normalize menses. The treatment of hirsutism resulting from functional ovarian hyperandrogenism is not as satisfactory; estrogen-progestin treatment is the most useful adjunct to cosmetic approaches to hirsutism in this country. However, other manifestations of polycystic ovary syndrome, such as infertility, may take precedence over hirsutism when an optimal therapeutic program is designed for many patients.