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Hirsutism is the excessive growth of thick or dark hair in women in locations that are more typical of male hair patterns (eg, mustache, beard, central chest, shoulders, lower abdomen, back, inner thigh). The amount of hair growth that is considered excessive may differ depending on ethnic background and cultural interpretation. Men vary significantly in amount of body hair, some being quite hairy, but rarely present for medical evaluation.

Hypertrichosis is a separate condition. It is simply an increase in the amount of hair growth anywhere on the body. Hypertrichosis may be generalized or localized.

Pathophysiology

Hair growth depends on the balance between androgens (eg, testosterone, dehydroepiandrosterone sulfate [DHEAS], dihydrotestosterone [DHT]) and estrogens. Androgens promote thick, dark hair growth, whereas estrogens slow hair growth or modulate it toward finer, lighter hairs.

When caused by increased androgen activity, hirsutism is often accompanied by virilization, which may manifest as loss of menses, increased muscle mass, voice deepening, and clitoral hypertrophy.

Etiology

There are a number of causes of hirsutism (see Table 3: Hair Disorders: Some Causes of Hirsutism). Overall, the most common causes are the following:

• Polycystic ovary syndrome
• Familial hirsutism

Table 3
Some Causes of Hirsutism Causes Examples Adrenal disorders Adrenal tumor Congenital or delayed-onset adrenal hyperplasia Cushing's syndrome Androgenic drugs Anabolic steroids Danazol Some Trade Names DANOCRINE Click for Drug Monograph Oral contraceptives (high-progesterone type) Ectopic hormone production Lung cancer and carcinoid tumors (ectopic ACTH secretion) Choriocarcinomas (β-human chorionic gonadotropin) Endocrine disorders that indirectly influence androgen balance Hyperinsulinemia Hypothyroidism Familial hirsutism May be secondary to a familial increased end-organ response to normal plasma androgen levels Ovarian disorders Ovarian hyperthecosis Ovarian tumors Polycystic ovary syndrome Pituitary disorder Cushing's disease Prolactin-secreting pituitary adenoma Acromegaly Drugs (phenothiazines)

Androgen excess: Hirsutism typically results from abnormally high androgen activity as a result of increased central production of androgens (eg, from ovarian or adrenal disorders) or increased peripheral conversion of testosterone to DHT by 5α-reductase. Free androgen levels also can increase as a result of decreased production of sex hormone–binding globulin, which can occur in a variety of conditions, including hyperinsulinemia and liver disease. However, the severity of hirsutism does not correlate with the level of circulating androgens because of individual differences in androgen sensitivity of the hair follicle.

No androgen excess: Hirsutism not associated with androgen excess may be physiologic (eg, postmenopausal, during pregnancy), the result of systemic nonandrogenic endocrine conditions, or a familial phenomenon, especially in people of Mediterranean or Middle Eastern ancestry.

Hypertrichosis involves nonandrogenic hair growth and is usually caused by a drug, systemic illness (see Table 4: Hair Disorders: Causes of Hypertrichosis), or paraneoplastic syndrome. It also occurs as part of a rare familial disorder.

Table 4
Causes of Hypertrichosis Causes Examples Disorders Acrodynia Anorexia CNS disorders Dermatomyositis Familial HIV infection if advanced Malnutrition Paraneoplastic syndromes Porphyria Pretibial myxedema Repeated skin trauma, friction, inflammation Systemic illness Traumatic brain injury Nonandrogenic drugs Acetazolamide Some Trade Names DIAMOX Click for Drug Monograph Benoxaprofen Cetuximab Some Trade Names ERBITUX Click for Drug Monograph Corticosteroids (systemic or topical) Cyclosporine Some Trade Names NEORAL SANDIMMUNE Click for Drug Monograph Diazoxide Some Trade Names PROGLYCEM Click for Drug Monograph Fenoterol Hexachlorobenzene Interferon-α Minoxidil Some Trade Names LONITEN ROGAINE Click for Drug Monograph Penicillamine Some Trade Names CUPRIMINE Click for Drug Monograph Phenytoin Some Trade Names DILANTIN Click for Drug Monograph Prostaglandin E1 Psoralen Streptomycin Some Trade Names No US trade name Click for Drug Monograph

Evaluation

History: History of present illness should cover the extent and acuity of hair growth as well as the age of onset.

Review of systems should seek signs of virilization (eg, deepening of the voice, increased libido) and review menstrual and fertility history. Symptoms of causative disorders should be sought, including cold intolerance, fatigue, and weight gain (hypothyroidism); polyuria (diabetes); bingeing and purging (eating disorders); and weight loss and fevers (cancer).

Past medical history should specifically seek known causative disorders such as endocrine disorders, adrenal or ovarian pathology, and cancer.

Family history should inquire about excess hair growth in family members. Drug history should review all prescribed drugs and specifically query for the surreptitious use of anabolic steroids.

Physical examination: The presence of excess coarse and dark hair growth should be assessed at multiple sites, including the face, chest, lower abdomen, back, buttocks, and inner thigh. Signs of virilization should be sought, including clitoromegaly, acne, male-pattern hair loss, breast atrophy, and increased muscle mass.

General physical examination should note signs of potentially causative disorders.

The eyes should be examined for extraocular movements, and the visual fields should be assessed.

The breasts should be examined for galactorrhea.

The abdomen (including pelvic examination) should be examined for masses.

The skin should be examined for velvety, black pigmentation on the axillae and neck and under the breasts (acanthosis nigricans); acne; and striae.

The general habitus should be examined for fat distribution (particularly a round face and accumulation of fat at the base of the neck posteriorly).

Red flags: The following findings are of particular concern:

• Virilization
• Abrupt appearance of hirsutism
• Pelvic or abdominal mass

Interpretation of findings: Excess hair growth beginning after use of an anabolic steroid or other causative drug (seeTable 3: Hair Disorders: Some Causes of Hirsutism and Table 4: Hair Disorders: Causes of Hypertrichosis) in an otherwise healthy female is likely due to that drug. Symptoms and signs sometimes point to a diagnosis (see Table 5: Hair Disorders: Some Symptoms and Signs for Diagnosis of Hirsutism).

Table 5
Some Symptoms and Signs for Diagnosis of Hirsutism Symptoms and Signs Possible Diagnosis Abrupt-onset hirsutism, pelvic mass on examination Adrenal or ovarian cancer Acanthosis nigricans Polycystic ovary syndrome or other hyperinsulinemic state Central obesity, moon facies, striae, hypertension, proximal muscle weakness Cushing's syndrome Galactorrhea, amenorrhea (with or without visual field deficits) Pituitary disorder causing hyperprolactinemia Irregular menses or amenorrhea, acne, obesity, hirsutism beginning after puberty Polycystic ovary syndrome Signs of malnutrition, poor dentition (particularly in adolescent females) Eating disorder Weight loss, fevers Paraneoplastic syndromes caused by occult cancer

Testing

Diagnostic testing in men with no other signs of illness is unnecessary.

Women should have laboratory measurement of serum hormone levels, including the following:

• Free and total testosterone
• DHEAS
• Follicle-stimulating hormone (FSH) and luteinizing hormone (LH)
• Androstenedione
• Thyroid-stimulating hormone (TSH)
• Prolactin

High levels of testosterone accompanied by a normal level of DHEAS indicate that the ovaries, and not the adrenal glands, are producing the excess androgen. High levels of testosterone accompanied by moderate elevations in DHEAS suggest an adrenal origin for the hirsutism.

Often, in women with polycystic ovary syndrome, LH levels are elevated and FSH levels are depressed, which results in elevated LH/FSH ratios (> 3 is common).

Imaging: Pelvic ultrasonography, CT, or both should be done to rule out pelvic or adrenal cancer, particularly when a pelvic mass is appreciated, when the total testosterone level is > 200 ng/dL (> 100 ng/dL in postmenopausal women), or when the DHEAS level is > 7000 ng/dL (> 4000 ng/dL in postmenopausal women). However, the majority of patients with elevated DHEAS have adrenal hyperplasia rather than adrenal carcinoma.

Patients with signs of Cushing's syndrome or an adrenal mass on imaging studies should have 24-h urine cortisol levels measured.

Treatment

The underlying disorder should be treated, including stopping or changing causative drugs. Treatment for hirsutism itself is unnecessary if the patient does not find the excess hair cosmetically objectionable.

Nonandrogen-dependent excess hair growth, such as hypertrichosis, is treated primarily with physical hair removal methods. Patients with androgen-dependent hirsutism require a combination of hair removal and medical antiandrogen therapy.

Hair removal: There are several techniques.

Depilatory techniques remove hair from the surface of the skin and include shaving and OTC depilatory creams, such as those containing barium sulfate and Ca thioglycolate.

Epilation involves removing intact hairs and the roots and can be achieved via mechanical means (eg, tweezing, plucking, or waxing) or home epilating devices. Permanent epilation techniques, including electrolysis, thermolysis, and laser epilation, can result in more long-term hair removal but often require multiple treatments.

As an alternative to hair removal, hair bleaching is inexpensive and works well when hirsutism is not excessive. Bleaches lighten the color of the hair, rendering it less noticeable. There are several types of commercial hair-bleaching products, most of which use hydrogen peroxide as the active ingredient.

Topical eflornithine Some Trade Names
VANIQA
Click for Drug Monograph
, applied twice/day, decreases hair growth and, with long-term use, may decrease the need to manually remove hair.

Hormonal treatment: Hirsutism resulting from androgen excess usually requires long-term therapy because the source of excess androgen rarely can be eliminated permanently. Hormonal treatments include

• Oral contraceptives
• Antiandrogenic drugs
• Sometimes other agents

Oral contraceptives in standard doses often are the initial treatment for hirsutism caused by ovarian hyperandrogenism. Oral contraceptives reduce ovarian androgen secretion and increase sex hormone–binding globulin, thereby decreasing free testosterone levels.

Antiandrogenic therapy is also used and can include finasteride Some Trade Names
PROPECIA
PROSCAR
Click for Drug Monograph
(5 mg po once/day), spironolactone Some Trade Names
ALDACTONE
Click for Drug Monograph
(25 to 100 mg po bid), or flutamide Some Trade Names
EULEXIN
Click for Drug Monograph
(125 mg po once/day or bid). These drugs are contraindicated during pregnancy as they may cause feminization of a male fetus.

Insulin sensitizers such as metformin Some Trade Names
GLUCOPHAGE
Click for Drug Monograph
decrease insulin Some Trade Names
HUMULIN
NOVOLIN
Click for Drug Monograph
resistance, causing a decline in testosterone levels. However, they are less effective than other antiandrogenic agents. Corticosteroids are used for adrenal suppression. Gonadotropin-releasing hormone agonists (eg, leuprolide Some Trade Names
LUPRON
Click for Drug Monograph
acetate, nafarelin Some Trade Names
SYNAREL
Click for Drug Monograph
, or triptorelin) can be used for severe forms of ovarian hyperandrogenism under the direction of a gynecologist or endocrinologist.

Key Points

• Hirsutism may be familial, and the degree of hair growth may vary with ethnicity.
• Polycystic ovary syndrome is the most frequent cause of hirsutism.
• Virilization suggests an androgenic disorder that requires further evaluation.
• Abrupt onset of hirsutism may indicate cancer.

Last full review/revision August 2008 by Wendy S. Levinbook, MD

Content last modified August 2008