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 Alopecia: A Merck Manual of Patient Symptoms podcast
Alopecia is defined as loss of hair. Hair loss is often a cause of great concern to the patient for cosmetic and psychologic reasons, but it can also be an important sign of systemic disease.
Pathophysiology
Growth cycle:
Hair grows in cycles. Each cycle consists of a long growing phase (anagen), a brief transitional apoptotic phase (catagen), and a short resting phase (telogen). At the end of the resting phase, the hair falls out (exogen) and a new hair starts growing in the follicle, beginning the cycle again. Normally, about 50 to 100 scalp hairs reach the end of resting phase each day and fall out. When significantly more than 100 hairs/day go into resting phase, clinical hair loss (telogen effluvium) may occur. A disruption of the growing phase causing abnormal loss of anagen hairs is an anagen effluvium.
Classification:
Alopecia can be classified as focal or diffuse and by the presence or absence of scarring.
Scarring alopecia is the result of active destruction of the hair follicle. The follicle is irreparably damaged and replaced by fibrotic tissue. Several hair disorders show a biphasic pattern in which nonscarring alopecia occurs early in the course of the disease, and then scarring alopecia and permanent hair loss occurs as the disease progresses. Scarring alopecias can be subdivided further into primary forms, where the target of inflammation is the follicle itself, and secondary forms, where the follicle is destroyed as a result of nonspecific inflammation (see Table 1: Hair Disorders: Some Causes of Alopecia ).
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Table 1
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| Some Causes of Alopecia |
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Causes
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Examples
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Nonscarring diffuse hair loss
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Anagen effluvium (caused by agents that impair or disrupt the anagen cycle)
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Chemotherapeutic agents
Poisoning (eg, boric acid, mercury, thallium, other heavy metals)
Radiation (also causes scarring focal hair loss)
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Androgenetic alopecia (male-pattern or female-pattern hair loss)
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Androgens (eg, dihydrotestosterone)
Familial
Pathologic hyperandrogenism (virilization in females—see Hair Disorders: Hirsutism)
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Congenital disorders
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Congenital atrichia with papules
Ectodermal dysplasia
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Primary hair shaft abnormalities (trichodystrophies)
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Easy hair breakage (trichorrhexis nodosa)
Genetic disorders
Loose anagen hair syndrome
Overuse of hair dryers (bubble hair)
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Telogen effluvium (increased number of hairs entering resting phase)
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Drugs (eg, antimitotic chemotherapeutic agents, anticoagulants, retinoids, oral contraceptives, ACE inhibitors, β-blockers, lithium, antithyroid drugs, anticonvulsants, vitamin A excess)
Endocrine problems (eg, hyperthyroidism, hypothyroidism, menopause, postpartum)
Nutritional deficiencies (eg, zinc, biotin, or possibly iron deficiency)
Physiologic or psychologic stress (eg, surgery, systemic or febrile illness, pregnancy)
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Nonscarring focal hair loss
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Alopecia areata
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Hair loss that is most commonly focal but may be diffuse (alopecia totalis or alopecia universalis)
T-cell–mediated autoimmune disorders
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Other
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Hair loss due to compulsive hair pulling, twisting, or teasing (trichotillomania)
Lipedematous alopecia
Postoperative (pressure-induced) alopecia
Primary hair shaft abnormalities
Secondary syphilis
Temporal triangular alopecia
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Tinea capitis
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Microsporum audouinii
Microsporum canis
Trichophyton schoenleinii
Trichophyton tonsurans
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Traction alopecia
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Traction due to braids, rollers, or ponytails (occurs primarily at frontal and temporal hairlines)
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Scarring focal hair loss
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Acne keloidalis nuchae
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Folliculitis on the occipital scalp that results in scarring alopecia
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Chronic cutaneous lupus
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Discoid lupus lesions of the scalp
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Dissecting cellulitis of the scalp
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Boggy inflammatory nodules that coalesce with sinus tract formation
Part of the follicular occlusion tetrad
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Lichen planopilaris (lichen planus of the scalp)
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Secondary scarring alopecias
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Burns
Morphea
Progressive systemic sclerosis (scleroderma)
Radiation therapy (also causes nonscarring diffuse hair loss)
Sarcoidosis
Skin cancer
Superinfected kerion (due to severe primary syphilis or severe tinea capitis)
Trauma
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Nonscarring alopecia results from processes that reduce or slow hair growth without irreparably damaging the hair follicle. Disorders that primarily affect the hair shaft (trichodystrophies) also are considered nonscarring alopecia.
Etiology
The alopecias comprise a large group of disorders with multiple and varying etiologies (see Table 1: Hair Disorders: Some Causes of Alopecia).
The most common cause of alopecia is
Androgenetic alopecia is an androgen-dependent hereditary disorder in which dihydrotestosterone plays a major role.
Other common causes of hair loss are
Less common causes are primary hair shaft abnormalities, autoimmune diseases, heavy metal poisoning, and rare dermatologic conditions.
Evaluation
History:
History of present illness should cover the onset and duration of hair loss, whether hair shedding is increased, and whether hair loss is generalized or localized. Associated symptoms such as pruritus and scaling should be noted. Patients should be asked about typical hair care practices, including use of braids, rollers, and hair dryers, and whether they routinely pull or twist their hair.
Review of systems should include recent exposures to noxious stimuli (eg, drugs, toxins, radiation) and stressors (eg, surgery, chronic illness, fever, psychologic stressors). Symptoms of possible causes should be sought, including fatigue and cold intolerance (hypothyroidism) and, in women, hirsutism, deepening of the voice, and increased libido (virilization). Other features, including dramatic weight loss, dietary practices (including vegetarianism), and obsessive-compulsive behavior, should be noted. In women, a hormonal/gynecologic/obstetric history should be obtained.
Past medical history should note known possible causes of hair loss, including endocrine and skin disorders. Current and recent drug use should be reviewed for offending agents (see Table 1: Hair Disorders: Some Causes of Alopecia). A family history of hair loss should be recorded.
Physical examination:
Examination of the scalp should note the distribution of hair loss, the presence and characteristics of any skin lesions, and whether there is scarring. Part widths should be measured. Abnormalities of the hair shafts should be noted.
A full skin examination should be done to evaluate hair loss elsewhere on the body (eg, eyebrows, eyelashes, arms, legs), rashes that may be associated with certain types of alopecia (eg, discoid lupus lesions, signs of secondary syphilis or of other bacterial or fungal infections), and signs of virilization in women (eg, hirsutism, acne, deepening voice, clitoromegaly). Signs of potential underlying systemic disorders should be sought, and a thyroid examination should be done.
Red flags:
The following findings are of particular concern:
Interpretation of findings:
Hair loss that begins at the temples or vertex and spreads to diffuse thinning or nearly complete hair loss is typical of male-pattern hair loss. Hair thinning in the frontal, parietal, and crown regions is typical of female-pattern hair loss (see Fig. 1: Hair Disorders: Male- and female-pattern hair loss. ).
Hair loss that occurs 2 to 4 wk after chemotherapy or radiation therapy (anagen effluvium) can typically be ascribed to those causes. Hair loss that occurs 3 to 4 mo after a major stressor (pregnancy, febrile illness, surgery, medication change, or severe psychologic stressor) suggests a diagnosis of telogen effluvium.
Other findings help suggest alternative diagnoses (see Table 2: Hair Disorders: Interpreting Findings in Alopecia).
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Table 2
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| Interpreting Findings in Alopecia |
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Finding
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Possible Causes
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Asymmetric, bizarre, irregular hair loss pattern
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Trichotillomania
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Circular, discrete patches of loss; short, broken hairs; exclamation point hairs at periphery of patches
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Alopecia areata
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Patchy hair loss that appears moth-eaten
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Secondary syphilis
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Pruritus, erythema, and scaling
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Chronic cutaneous lupus
Tinea capitis (particularly if adenopathy present)
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Pustules
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Scarring dermatologic or infectious process (eg, dissecting cellulitis of the scalp, acne keloidalis nuchae)
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Scalp and body hair loss
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Alopecia universalis
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Unruly or unusually wooly hair
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Primary hair shaft abnormality
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Virilization
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Adrenal disorder or tumor
Polycystic ovary syndrome
Anabolic steroid use (sometimes surreptitious)
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Other than hair loss, scalp symptoms (eg, itching, burning, tingling) are often absent and, when present, are not specific to any cause.
Signs of hair loss in patterns other than those described above are nondiagnostic and may require microscopic hair examination or scalp biopsy for definitive diagnosis.
Testing:
Evaluation for causative disorders (eg, endocrinologic, autoimmune, toxic) should be done based on clinical suspicion.
Male-pattern or female-pattern hair loss usually requires no testing. When it occurs in young men with no family history, the physician should question the patient about use of anabolic steroids and other drugs. In addition to questions regarding prescription drug and illicit drug use, women with significant hair loss and evidence of virilization should have testosterone and dehydroepiandrosterone sulfate (DHEAS) levels measured (see Hair Disorders: Testing).
The pull test helps evaluate diffuse scalp hair loss. Gentle traction is exerted on a bunch of hairs (about 40) on at least 3 different areas of the scalp, and the number of extracted hairs is then counted and examined microscopically. Normally, < 3 telogen-phase hairs should come out with each pull. If ˃ 4 to 6 hairs come out with each pull, the pull test is positive and is suggestive of telogen effluvium.
The pluck test involves abruptly pulling out about 50 individual hairs (“by the roots”). The roots of the plucked hairs are examined microscopically to determine the phase of growth and thus help diagnose a defect of telogen or anagen or an occult systemic disease. Anagen hairs have sheaths attached to their roots; telogen hairs have tiny bulbs without sheaths at their roots. Normally, 85 to 90% of hairs are in the anagen phase, about 10 to 15% are in telogen phase, and < 1% are in catagen phase. Telogen effluvium shows an increased percentage of telogen-phase hairs on microscopic examination (typically > 20%), whereas anagen effluvium shows a decrease in telogen-phase hairs and an increased number of broken hairs. Primary hair shaft abnormalities are usually obvious on microscopic examination of the hair shaft.
Scalp biopsy is indicated when alopecia persists and diagnosis is in doubt. Biopsy may differentiate scarring from nonscarring forms. Specimens should be taken from areas of active inflammation, ideally at the border of a bald patch. Fungal and bacterial cultures may be useful; immunofluorescence studies may help identify SLE, lichen planopilaris, and systemic sclerosis.
Daily hair counts can be done by the patient to quantify hair loss when the pull test is negative. Hairs lost during the first morning combing or during washing are collected in clear plastic bags daily for 14 days. The number of hairs in each bag is then recorded. Scalp hair counts of > 100/day are abnormal except after shampooing, when hair counts of up to 250 may be normal. Hairs may be brought in by the patient for microscopic examination.
Treatment
Androgenetic alopecia:
Minoxidil (2% for women, 2% or 5% for men) prolongs the anagen growth phase and gradually enlarges miniaturized follicles (vellus hairs) into mature terminal hairs. Topical minoxidil 1 mL bid applied to the scalp is most effective for vertex alopecia in male-pattern or female-pattern hair loss. However, usually only 30 to 40% of patients experience significant hair growth, and minoxidil is generally not effective or indicated for other causes of hair loss except possibly alopecia areata. Hair regrowth can take 8 to 12 mo. Treatment is continued indefinitely because, once treatment is stopped, hair loss resumes. The most frequent adverse effects are mild scalp irritation, allergic contact dermatitis, and increased facial hair.
Finasteride inhibits the 5α-reductase enzyme, blocking conversion of testosterone to dihydrotestosterone, and is useful for male-pattern hair loss. Finasteride 1 mg po once/day can stop hair loss and can stimulate hair growth. Efficacy is usually evident within 6 to 8 mo of treatment. Adverse effects include decreased libido, erectile and ejaculatory dysfunction, hypersensitivity reactions, gynecomastia, and myopathy. There may be a decrease in prostate-specific antigen (PSA) levels in older men, which should be taken into account when this test is used for cancer screening. Common practice is to continue treatment for as long as positive results persist. Once treatment is stopped, hair loss returns to previous levels. Finasteride is not indicated for women and is contraindicated in pregnant women because it has teratogenic effects in animals.
Hormonal modulators such as oral contraceptives or spironolactone may be useful for female-pattern hair loss associated with hyperandrogenemia.
Surgical options include follicle transplant, scalp flaps, and alopecia reduction. Few procedures have been subjected to scientific scrutiny, but patients who are self-conscious about their hair loss may consider them.
Hair loss due to other causes:
Underlying disorders are treated.
Multiple treatment options for alopecia areata exist and include topical, intralesional, or, in severe cases, systemic corticosteroids, topical minoxidil, topical anthralin, topical immunotherapy (diphenylcyclopropenone or squaric acid dibutylester), or psoralen plus ultraviolet A (PUVA).
Treatment for traction alopecia is elimination of physical traction or stress to the scalp.
Treatment for tinea capitis is oral antifungals (see Fungal Skin Infections: Treatment)
Trichotillomania is difficult to treat, but behavior modification, clomipramine, or an SSRI (eg, fluoxetine, fluvoxamine, paroxetine, sertraline, citalopram) may be of benefit.
Scarring alopecia as seen in disorders such as dissecting cellulitis of the scalp and acne keloidalis nuchae is best treated by a long-acting oral tetracycline in combination with a potent topical corticosteroid.
Lichen planopilaris and chronic cutaneous lupus lesions may be treated with topical or oral drugs, such as antimalarials, corticosteroids, retinoids, or immunosuppressants.
Hair loss due to chemotherapy is temporary and is best treated with a wig; when hair regrows, it may be different in color and texture from the original hair. Hair loss due to telogen effluvium or anagen effluvium is usually temporary as well and abates after the precipitating agent is eliminated.
Key Points
Alopecia Areata
Alopecia areata is sudden patchy hair loss in people with no obvious skin or systemic disorder.
The scalp and beard are most frequently affected, but any hairy area may be involved. Hair loss may affect most or all of the body (alopecia universalis). Alopecia areata is thought to be an autoimmune disorder affecting genetically susceptible people exposed to unclear environmental triggers, such as infection or emotional stress. It occasionally coexists with autoimmune vitiligo or thyroiditis.
Diagnosis
Diagnosis is by inspection. Alopecia areata typically manifests as discrete circular patches of hair loss characterized by short broken hairs at the margins, which resemble exclamation points. Nails are sometimes pitted or display trachyonychia, a roughness of the nail also seen in lichen planus. Differential diagnosis includes tinea capitis, trichotillomania, cutaneous lupus, and secondary syphilis. If findings are equivocal (uncommon), further testing can be pursued with KOH preparation, fungal culture, lupus serology, screening for syphilis, or biopsy. Patients with clinical findings suggesting associated autoimmune diseases (particularly thyroid disease) are tested for those diseases.
Treatment
Intralesional corticosteroid injection is the treatment of choice in adults. Triamcinolone acetonide suspension (typically in doses of 0.1 to 3 mL of 2.5 to 5 mg/mL concentration q 4 to 8 wk) can be injected intradermally if the lesions are small. Potent topical corticosteroids (eg, clobetasol propionate 0.05% foam, gel, or ointment bid for about 4 wk) can be used; however, they often do not penetrate to the depth of the hair bulb where the inflammatory process is located. Oral corticosteroids are effective, but hair loss often recurs after cessation of therapy and adverse effects limit use. Topical anthralin cream (0.5 to 1% for 10 to 20 min daily, then washed off, contact time titrated as tolerated up to1 h/day) may be used to stimulate a mild irritant reaction. Minoxidil 5% solution may be helpful as an adjuvant to corticosteroid or anthralin treatment. Induction of allergic contact dermatitis using diphenylcyclopropenone or squaric acid dibutylester leads to hair growth due to unknown mechanisms, but this treatment is best reserved for patients with diffuse involvement who have not responded to other therapies.
Alopecia areata may spontaneously regress, become chronic, or spread diffusely. Risk factors for chronicity include extensive involvement, onset before adolescence, atopy, and involvement of the peripheral scalp (ophiasis).
Last full review/revision September 2012 by Wendy S. Levinbook, MD
Content last modified November 2012
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