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 Hirsutism: A Merck Manual of Patient Symptoms podcast
Hirsutism is the excessive growth of thick or dark hair in women in locations that are more typical of male hair growth 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, acne, androgenic alopecia, and clitoromegaly.
Etiology
There are a number of causes of hirsutism (see Table 3: Hair Disorders: Some Causes of Hirsutism ). Overall, the most common cause is the following:
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Table 3
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| Some Causes of Hirsutism |
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Causes
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Examples
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Adrenal disorders
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Adrenal tumor
Congenital or delayed-onset adrenal hyperplasia
Cushing syndrome
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Androgenic drugs
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Anabolic steroids (including danazol)
Oral contraceptives (high-progesterone type)
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Ectopic hormone production
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Lung cancer and carcinoid tumors (ectopic ACTH secretion)
Choriocarcinomas (β-human chorionic gonadotropin)
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Systemic disorders that indirectly influence androgen balance
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Hyperinsulinemia
Liver disease
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Familial hirsutism
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May be secondary to a familial increased end-organ response to normal plasma androgen levels
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Ovarian disorders
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Ovarian hyperthecosis
Ovarian tumors
Polycystic ovary syndrome
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Pituitary disorders
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Acromegaly
Cushing disease
Drugs
Prolactin-secreting pituitary adenoma
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Androgen excess
Hirsutism typically results from abnormally high androgen activity as a result of increased central production of androgens (eg, due to 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, South Asian, 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 in rare familial disorders called congenital hypertrichosis.
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Table 4
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| Causes of Hypertrichosis |
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Causes
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Examples
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Disorders
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Acrodynia
Anorexia
CNS disorders
Dermatomyositis
Familial
HIV infection if advanced
Paraneoplastic syndromes
Porphyria
Pretibial myxedema
Repeated skin trauma, friction, and/or inflammation (eg, after removal of a cast)
Systemic illness
Traumatic brain injury
Undernutrition
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Nonandrogenic drugs
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Acetazolamide
Benoxaprofen
Cetuximab
Corticosteroids (systemic or topical)
Cyclosporine
Diazoxide
Fenoterol
Hexachlorobenzene
Interferon alfa
Minoxidil
Penicillamine
Phenytoin
Prostaglandin E1
Psoralen
Streptomycin
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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 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:
Interpretation of findings
Excess hair growth beginning after use of an anabolic steroid or other causative drug (see Table 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: Interpreting Findings in Hirsutism).
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Table 5
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| Interpreting Findings in Hirsutism |
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Finding
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Possible Causes
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Abrupt-onset hirsutism, flank or pelvic mass
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Adrenal or ovarian cancer
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Acanthosis nigricans
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Polycystic ovary syndrome or other hyperinsulinemic states
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Central obesity, moon facies, striae, hypertension, proximal muscle wasting and weakness
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Cushing syndrome
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Galactorrhea, amenorrhea (with or without visual field deficits)
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Pituitary disorder causing hyperprolactinemia
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Irregular menses or amenorrhea, acne, obesity, hirsutism beginning after puberty
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Polycystic ovary syndrome
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Signs of undernutrition, poor dentition (particularly in adolescent females)
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Eating disorder
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Weight loss, fevers
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Paraneoplastic syndromes caused by occult cancer
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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:
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 for polycystic ovary syndrome).
Imaging
Pelvic ultrasonography, CT, or both should be done to rule out pelvic or adrenal cancer, particularly when a pelvic mass is suspected, 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 syndrome or an adrenal mass on imaging studies should have urine cortisol levels measured for 24 h.
Treatment
The underlying disorder should be treated, including stopping or changing causative drugs. Treatment for hirsutism itself is necessary only if the patient finds 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 with their roots and can be achieved via mechanical means (eg, tweezing, plucking, 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, applied twice daily, slows the rate of hair growth and, with long-term use, may increase the amount of time between hair removal treatments.
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 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 (5 mg po once/day), spironolactone (25 to 100 mg po bid), or flutamide (125 mg po once/day or bid). These drugs are contraindicated during pregnancy because they may cause feminization of a male fetus.
Insulin sensitizers such as metformin decrease insulin resistance, causing a decline in testosterone levels. However, they are ineffective or less effective than other antiandrogenic drugs. Corticosteroids are used when necessary to suppress adrenal androgen production. Gonadotropin-releasing hormone agonists (eg, leuprolide acetate, nafarelin, triptorelin) can be used for severe forms of ovarian hyperandrogenism under the direction of a gynecologist or endocrinologist.
Key Points
Last full review/revision September 2012 by Wendy S. Levinbook, MD
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