Hirsutism is excessive hair growth in androgen-dependent hair patterns (i.e., face, chest, areolae, linea alba, lower back, buttocks, inner thighs, and external genitalia) secondary to increased androgenic activity.
Causes of Hirsutism
- Androgens promote conversion of vellus hairs to terminal hairs in androgen-sensitive hair follicles (pubis, axillae, back, face, chest, abdomen).
- 5α-Dihydrotestosterone, derived from conversion of testosterone by 5α-reductase at the hair follicle, is the hormonal stimulus for hair growth.
- 50 to 70% of circulating testosterone in normal women is derived from precursors, androstenedione, and DHEA; the rest is secreted directly, mostly by the ovaries. In hyperandrogenic women, a greater percentage of androgens may be secreted directly.
- In women, adrenal glands secrete androstenedione, DHEA, DHEA sulfate, and testosterone; ovaries secrete mainly androstenedione and testosterone.
Symptoms of Hirsutism
The signs and symptoms which are indicative of hirsutism are hair growth on the abdomen, breasts and upper lip; irregular menstrual period, loss of feminine body shape and formation of masculine traits such as a deep voice, frontal balding, enlarged shoulders and muscles among others.
Treatment
Cosmetic Shaving, waxing, electrolysis, hydrogen peroxide bleaching. Removal with laser, effective and the best method.
Systemic Antiandrogen Therapy Cyproterone Acetate (CPA) Potent progestogen (not available in the United States). Both antiandrogen and inhibitor of secretion of gonadotropin. Decreases androgen production. Increases testosterone clearance. Decreases 5α-reductase activity. Administered with cyclical estrogens to maintain regular menstruation.
Regimen: 50 to 100 mg CPA for 10 days percycle.
Side effects: weight gain, fatigue, loss of libido, mastodynia, nausea, H/A, depression.
Contraindications: smoking, obesity, hypertension.
SpironolactoneAn antihypertensive diuretic. Decreases testosterone biosynthesis. Binds to androgen receptor. Decreases 5α-reductase activity.
Regimen: begin at 50 mg bid from day 4 through day 22 of each menstrual cycle; dose can be given as high as 100 mg bid.
Cimetidine Histamine-2 receptor antagonist; competes for target tissue binding with androgens; less effective than spironolactone.
Glucocorticoid First-line therapy for classic CAH. Regimen: 1 mg dexamethasone qhs. For late-onset, nonclassic CAH, use antiandrogens or oral contraceptives.
Oral Contraceptives Suppress ovarian and adrenal androgen production by decreasing LH and FSH. Recommend an oral contraceptive with the lowest tolerable dose of ethinyl estradiol (30 to 35 µg) and a low dose of a progestin with low androgenic potential (less than 1 mg of norethindrone, norgestimate, desogestrel, ethynodiol diacetate).
Avoid levonorgestrel, norgestrel, and high doses of norethindrone acetate.
References