Hirsutism, an excessive growth of androgen-responsive terminal hair in women, must be distinguished from hypertri-choses, excessive growth of vellus or non--androgen-responsive hair. Androgen-responsive terminal hairs are dark, thick and found in sex hormone--responsive areas such as the pubis, axilla, back, face, chest and abdomen. Sakiyama discusses the appropriate management of women with hirsutism.
Women with androgen-dependent hirsutism are either exposed to excessive androgens or have a heightened androgen-receptor sensitivity to normal circulating levels of androgen. Testosterone and other precursors are manufactured in the ovaries and the adrenal cortex. Measuring the level of sulfated dehydroepiandrosterone is the preferred plasma test of adrenal androgen production because of the consistency of the level throughout the day.
Causes of hirsutism can be classified as ovarian, adrenal, drug-related, idiopathic or genetic. Ovarian disorders include polycystic ovary syndrome and ovarian tumors. Adrenal disorders include congenital adrenal hyperplasia, Cushing's syndrome and adrenal tumors. Hirsutism may also result from ingestion of anabolic steroids or as a side effect of medications including cyclosporine, danazol, diazoxide, glucocorticoids, minoxidil and phenytoin.
Polycystic ovary syndrome is a nontumorous dysfunction of luteinizing hormone hypersecretion, with subsequent stimulation of thecal and stromal ovarian cells to produce androgens. The ratio of luteinizing hormone to follicle-stimulating hormone is frequently increased to 2.5 or greater in women with polycystic ovary syndrome. Total testosterone levels are elevated in 40 to 60 percent of these women. The major binding protein for testosterone is sex hormone--binding globulin, which is decreased in women with the polycystic ovary syndrome and accounts for elevated free testosterone levels despite normal total testosterone levels. Ovarian and adrenal tumors are uncommon causes of hirsutism. Elevations in sulfated dehydroepiandrosterone levels suggest an adrenal origin of androgen production, whereas greatly elevated testosterone levels indicate a possible ovarian or adrenal tumor. Idiopathic hirsutism is found in 50 percent of women evaluated for hirsutism. These patients show no sign of virilization and have slow progression of hirsutism.
Symptoms of polycystic ovary syndrome and idiopathic hirsutism develop between the ages of 15 and 25 years. Symptoms related to tumors or Cushing's syndrome generally begin later in life and progress rapidly. Virilization usually suggests a more serious disorder than polycystic ovary syndrome or idiopathic hirsutism.
Measurement of total serum testosterone and sulfated dehydroepiandrosterone levels are the two most important laboratory tests, with elevation of the former suggesting an androgen-secreting tumor of the ovary or adrenal gland, and elevations of the latter suggesting an adrenal tumor. Normal values exclude an androgensecreting tumor. Cushing's syndrome is diagnosed with a 24-hour free cortisol determination or a dexamethasone suppression test. Imaging studies may be helpful when searching for an adrenal or ovarian tumor.
Treatment includes mechanical removal of excess hair growth and therapy for the specific disorder diagnosed (see the accompanying table). Oral contraceptives can be used to suppress ovarian androgen production, keeping in mind the possible androgenic effects of the progestational component. Response to oral contraceptives varies but is more likely to occur in women with elevated testosterone levels. Gonadotropin-releasing hormone (GnRH) agonists can be used to suppress ovarian function in hirsute women and can be combined with oral contraceptives or conjugated estrogens and progestins.
Guidelines for the Treatment of Hirsutism
ACTH = adrenocorticotropic hormone; GnRH = gonadotropin-releasing hormone.
From Sakiyama R. Approach to patients with hirsutism. West J Med 1996;165:386-91. Used with permission.
Glucocorticoids, administered in the evening or at bedtime to suppress the nightly adrenocorticotropic hormone (ACTH) surge, can suppress ACTH-stimulated adrenal androgen production and are useful for patients with the nonclassic form of congenital adrenal hyperplasia. Finasteride, which blocks the conversion of testosterone to dihydrotestosterone, and spironolactone, an antiandrogen that inhibits the binding of testosterone and dihydrotestosterone to their respective receptors, may also be helpful. Both are contraindicated in pregnancy. Flutamide is another antiandrogen, but it is not recommended for routine treatment of hirsutism because of cost and possible toxic side effects.
The author concludes that initial therapy for women with idiopathic hirsutism or hirsutism caused by polycystic ovary syndrome should include spironolactone or oral contraceptives. Finasteride may be used in nonresponsive patients. GnRH agonists can be used in severe cases. Patients who do not respond to any of these treatments should be reevaluated for a serious underlying disorder.
COPYRIGHT 1997 American Academy of Family Physicians
COPYRIGHT 2004 Gale Group
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