Hypertrichosis and hirsutism

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106

Hypertrichosis and hirsutism

Shannon Harrison, Najwa Somani and Wilma F. Bergfeld

Evidence Levels: A Double-blind study B Clinical trial ≥ 20 subjects C Clinical trial < 20 subjects D Series ≥ 5 subjects E Anecdotal case reports

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Hirsutism is the excessive growth of terminal hairs in women in typically male androgen-dependent areas, such as the chin, upper lip, breasts, abdomen, and back, that can adversely affect quality of life. It is identified by a Ferriman–Gallwey (F-G) score of 8 or higher.

Hirsutism can result from endogenous androgens (ovaries or adrenal glands), exogenous androgens, or from increased hair follicle sensitivity to normal androgen levels. Polycystic ovarian syndrome (PCOS) and idiopathic hirsutism are the most common causes of hirsutism. Rarer causes are endocrinopathies, non-classical congenital adrenal hyperplasia, and androgen-secreting tumors.

Hypertrichosis is characterized by increased hair growth in an androgen-independent, non-sexual distribution. Hypertrichosis may be familial, or secondary to medications or an underlying systemic disorder.

Management strategy

A thorough history and physical examination should identify any underlying cause of hypertrichosis and hirsutism. Drugs causing hypertrichosis and androgenic medications known to cause hirsutism should be discontinued.

Most hirsute women will have raised circulating androgen levels. In idiopathic hirsutism, menstrual cycles appear normal and conventional testing does not detect androgen abnormalities. PCOS, HAIR-AN syndrome and ovarian hyperthecosis present with signs of hyperandrogenism and metabolic syndrome. Weight loss for obesity in women with PCOS can improve markers of the metabolic syndrome and reduce cardiovascular risk. BMI has also been shown to be the most important risk factor for the degree of hirsutism in women with PCOS.

Cushing’s disease, hyperprolactinemia, and acromegaly should be recognized and treatment initiated. Acute onset or rapid progression of hirsutism or virilization signs may indicate an adrenal or ovarian tumor. Tumor removal will reverse the hirsutism. In non-classical congenital adrenal hyperplasia, glucocorticoid therapy assists with ovulation induction, but hirsutism may also require systemic antiandrogen therapy. Glucocorticoid therapy for classical congenital adrenal hyperplasia manages ovulation induction and hirsutism.

Mechanical hair removal is the first-line treatment choice for hirsutism and hypertrichosis. Bleaching with hydrogen peroxide preparations can disguise dark facial hair, but can irritate. Painless depilatory methods remove hair shafts at the skin surface. Chemical depilatory creams are quick to use, but can irritate and skin folds should be avoided. Shaving is inexpensive, but is time-consuming and not acceptable to most women except for the axillae and legs. Shaving does not affect the diameter or rate of growth of hair.

Epilatory hair removal methods remove the entire hair including the root and are painful. Tweezing or plucking may be used in areas with fewer hairs. Waxing is also useful, but more expensive. Epilation with electrolysis can often achieve a permanent reduction in hair growth. A fine needle is inserted into the hair follicle and an electrical current applied damaging the hair follicle by direct current (galvanic electrolysis) or high frequency alternating current (thermolysis) or a combination of the two currents, the blend method. It is time-consuming, requiring multiple treatments and is operator dependent. It can be used on any skin or hair color. Side effects of all mechanical hair removal methods include erythema, folliculitis, pseudofolliculitis, infection, scarring, and dyspigmentation.

Photoepilation lasers include ruby (694 nm), alexandrite (755 nm), diode (800–810 nm), Nd : YAG (neodymium : yttrium-aluminum-garnet) laser (1064 nm) and IPL (intense pulsed light) non-coherent sources of 590–1200 nm. Lasers result in a partial short-term hair reduction up to 6 months and efficacy is improved with repeat treatments. IPL produces partial short-term hair reduction, improving with multiple sessions. No laser can achieve complete or persistent hair removal. Ideal candidates have fair skin and dark hair. Side effects include erythema, scarring, burns, dyspigmentation, and, rarely with IPL, a paradoxical increase in hair growth.

Twice daily eflornithine hydrochloride cream slows the rate of hair growth. Eflornithine irreversibly inhibits ornithine decarboxylase and is FDA approved to treat facial hirsutism. Benefits are reversed after 8 weeks of discontinuation. Side effects include acne, pseudofolliculitis barbae, irritant and allergic contact dermatitis. Efficacy may be improved when combined with hair removal laser.

Combined oral contraceptive pills (estrogen and progestin OCPs) reduce hyperandrogenism predominantly by suppressing ovarian androgen synthesis, increasing sex hormone binding globulin levels, and suppressing free plasma testosterone levels. Androgenic progestins should be avoided. Low androgenic progestins in oral contraceptives (desogesterol or norgestimate) and progestins with antiandrogenic properties (cyproterone acetate, drosperidone) should be used for hirsutism.

Spironolactone is an antiandrogen that inhibits androgen biosynthesis and blocks the androgen receptor. The usual dose for hirsutism is 100–200 mg daily. Side effects include hyperkalemia, hypotension, and irregular menses. Tumorigenicity has been shown in animals; the significance in humans is unknown. All antiandrogens including spironolactone have feminizing teratogenic potential and should be used with a reliable form of contraception. Hence, pharmacologic therapy for hirsutism should not be commenced in women planning pregnancy.

Table 106.1

Main causes of hirsutism

Ovarian

Polycystic ovarian syndrome (menstrual irregularities, infertility and metabolic syndrome^a)
HAIR-AN syndrome (hyperandrogenism, severe metabolic syndrome,^a acanthosis nigricans)
Hyperthecosis (menstrual irregularities and metabolic syndrome^a)
Ovarian tumors and hyperplasia (irregular menses, virilization symptoms)

Adrenal

Congenital adrenal hyperplasia – classical and non-classical types (irregular menses, primary amenorrhoea)
Cushing’s syndrome (striae, fat redistribution, fragile skin, proximal muscle weakness, mood disturbance, insulin resistance)
Adrenal tumors (virilization symptoms)

Pituitary^b

Cushing’s disease (striae, fat redistribution, fragile skin, proximal muscle weakness, mood disturbance, insulin resistance)
Acromegaly (coarse facies and enlarged hands)
Hyperprolactinemia (galactorrhea )

Idiopathic

Occult functional hyperandrogenism
Abnormalities in peripheral 5α-reductase or androgen receptor

Exogenous (androgenic medications)

Testosterone, adrenocorticotrophic hormone (ACTH), valproic acid, anabolic steroids, androgenic progestins

^a Metabolic syndrome: obesity, insulin resistance/diabetes mellitus type 2, lipid abnormalities, cardiovascular disease.

^b Pituitary tumors can also present with visual field disturbances.

Cyproterone acetate inhibits the androgen receptor and for hirsutism can be used in a sequential way for the first 10 days of the menstrual cycle (25–100 mg) with an OCP, or low dose (2 mg) in a combined OCP (Diane-35). It has similar side effects to the OCP.

Finasteride, a type II 5α-reductase inhibitor, has been used for hirsutism. It is pregnancy category X. No reports exist for dutasteride, a type I and II 5α-reductase inhibitor for the treatment of hirsutism.

Flutamide and insulin lowering drugs are not recommended for the treatment of routine hirsutism. Flutamide has significant risk of hepatotoxicity.

GnRH analogs are only recommended if oral contraceptives and antiandrogen treatments fail in the setting of severe hyperandrogenism. GnRH treatment reduces estrogen to menopausal levels causing hot flushes and osteoporosis risk. Cimetidine is ineffective in hirsutism. Ketoconazole has antiandrogenic properties, but has significant hepatotoxicity and drug interactions.