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Alopecia has
multiple causes. Diagnosis of cause can sometimes be made by gross
and microscopic examination of hair. Treatment is of underlying
cause.
Most alopecia is a concern for cosmetic and psychologic reasons, but it is occasionally the primary sign of an important systemic disease.
Etiology
Alopecia can be nonscarring and diffuse, nonscarring and focal, or scarring and focal.
Nonscarring diffuse
loss:
Causes include male-pattern baldness, female-pattern baldness, telogen effluvium, anagen effluvium, primary hair shaft abnormalities, and congenital disorders.
Male-pattern baldness (androgenetic alopecia) is common, familial, and androgenetic. Hair loss begins at the temples and/or vertex and can spread to diffuse thinning or nearly complete loss. Female-pattern baldness is hair thinning in the frontal, parietal, and crown regions. This too is androgenetic.
Telogen effluvium refers to loss of scalp hair caused by synchronicity of hair cycle so that many hairs enter the resting or telogen phase at once. At the end of this resting phase, usually several months after the inciting event, a significant increase in hair shedding is noticed. Drugs are a common cause, especially antiproliferative chemotherapeutic agents, warfarin , H2-blockers, oral contraceptives, ACE inhibitors, β-blockers, and lithium . Other drugs that can precipitate telogen effluvium are fluorobutyrophenone, clofibrate , bezafibrate , trimethadione , valproate , captopril , penicillamine , ibuprofen , interferon, ranitidine , sulindac , tamoxifen , terfenadine, and thiamphenicol. Telogen effluvium is also common with nutritional deficiencies, after physiologic or psychologic stress (surgery, systemic illness), and with pathologic (hypothyroidism or hyperthyroidism) or physiologic (postpartum, menopause) endocrine changes.
Anagen effluvium refers to loss of scalp hair in its growth (or anagen) phase. Radiation and chemotherapeutic agents are the most common causes, but it can occur with mercury, thallium, boric acid, and vitamin A poisoning.
Primary hair shaft abnormalities (trichodystrophies) include a variety of disorders that lead to unruly or unusually wooly hair or to fractures of the hair shaft. In trichorrhexis invaginata, hairs have a ball and cup invagination (bamboo hair). This hair abnormality can occur in association with ichthyosis in the rare autosomal recessive Netherton syndrome. Bubble hair, in which bubbles are seen in the hair shaft, may occur with excessive use of hair dryers. Trichonodosis or knotting of hair occurs with excess rubbing or scratching. Monilethrix is an uncommon autosomal dominant condition that causes beaded and very brittle hair.
Other congenital disorders of the hair include wooly hair nevus (tightly coiled hair over all or portions of the scalp), the uncombable hair syndrome (scalp hair that resists all efforts to comb or brush it), trichorrhexis nodosa (hair shafts break easily and broken stumps are present over large portions of the scalp), and trichothiodystrophy (brittle hair from a defect in sulfur metabolism).
Nonscarring focal
loss:
Common causes include traction alopecia, tinea capitis, trichotillomania, and alopecia areata (see Hair Disorders: Alopecia Areata). Uncommon causes include syphilis and primary hair shaft abnormalities.
Traction alopecia is hair loss primarily at the frontal and/or temporal hairline due to traction from braids, rollers, or ponytails. Tinea capitis, hair shaft infection with Trichophyton
tonsurans, is discussed in Fungal Skin Infections: Tinea Capitis; other less common causes of tinea capitis include Microsporum canis
, M. audouinii, and T. schoenleinii. Trichotillomania—focal hair loss due to hair pulling, twisting, or teasing—is symptomatic of an obsessive-compulsive disorder (see Anxiety Disorders: Obsessive-Compulsive Disorder (OCD)).
Late secondary syphilis causes hair loss ranging from localized patches to total alopecia. It may follow the distribution of the preceding exanthem. The serology is always positive. Examination reveals focal yellow-red areas with a moth-eaten appearance.
Scarring
focal loss:
Scarring refers to obliteration of the hair follicle with fibrosis. Scarring loss is most often due to unusual primary disorders, such as lichen planopilaris (lichen planus of the scalp), folliculitis decalvans (an idiopathic scarring alopecia associated with pustules and intact hairs clumped in a “tufted” pattern), and pseudopelade of Brocq (a particular pattern of scarring alopecia). Other causes include burns, trauma, radiation therapy, severe primary (kerion) or secondary (syphilis) infections, sarcoidosis, lupus erythematosus, and skin malignancy.
Symptoms,
Signs, and Diagnosis
Symptoms, other than hair loss, are often absent and, when present (eg, itching, burning, tingling), are not specific to any cause. Except in alopecia areata (see Hair Disorders: Alopecia Areata), some cases of infection (kerion, syphilis), lichen planus, and dissecting cellulitis of the scalp (folliculitis abscedens et suffodiens), signs of hair loss are nondiagnostic. If scarring is noted, examination should include the entire skin surface and mucous membranes to detect lesions associated with systemic disease.
Male-pattern baldness generally requires no testing. When it occurs in young males without a family history, the physician should question the patient about anabolic steroid use and other drugs. In women with significant hair loss and evidence of virilization, testosterone and dehydroepiandrosterone sulfate levels should be measured.
The “pull” test helps evaluate diffuse scalp hair loss; gentle traction is exerted on 40 to 60 hairs on at least 3 areas of the scalp, and the number of extracted hairs is counted and examined microscopically. Normally, < 6 telogen-phase hairs should come out. Extraction of > 6 hairs in telogen phase is abnormal and suggestive of telogen effluvium.
The “pluck” test is similar except that hairs are abruptly, painfully extracted. The pluck test helps diagnose a defect of telogen or anagen or an occult systemic disease.
Microscopic examination of hair from either test or from hair cuttings is almost always helpful. 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 hairs, whereas anagen effluvium shows a decrease in telogen hairs and easy breakage. A high percentage of hairs in the catagen phase (a transitional phase between growth and rest) and trichomalacia are pathognomonic for trichotillomania. Primary hair shaft abnormalities, such as trichorrhexis invaginata and monilethrix, are usually obvious on microscopic evaluation 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 an area of active inflammation, ideally at the border of a bald patch. Fungal and bacterial cultures may be useful; immunofluorescence studies may help identify lupus erythematosus, lichen planopilaris, and systemic sclerosis.
Daily hair counts can be performed by the patient to quantify hair loss when the pull test is negative. Scalp hair counts of > 100 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 of hair shafts and bulbs.
Treatment
Male-pattern
baldness:
Most treatments for hair loss have been developed for male-pattern baldness because it is so prevalent.
Minoxidil prolongs the anagen phase and may increase blood flow to the follicle; 1 mL of 2% or 5% topical drug applied bid to the scalp is most effective for vertex alopecia in male-pattern baldness affecting men or women. However, at most 30 to 40% of patients experience significant hair growth, and minoxidil is generally not effective or indicated for other causes except possibly alopecia areata. Hair growth may not be seen until 6 to 9 mo; common practice is to continue treatment as long as positive results persist.
Finasteride inhibits 5-α reductase enzyme, blocking conversion of testosterone to dihydrotestosterone, and is useful for male-pattern baldness. Finasteride 1 mg po once/day stimulates scalp hair growth. Adverse effects include decreased libido, erectile dysfunction, ejaculation disorder, and decreased ejaculate volume in about 1% of patients. The drug is not indicated for women and is contraindicated in pregnant women. Hair growth may not be seen until 6 mo; common practice is to continue treatment for 24 mo as long as positive results persist. Once treatment is discontinued, hair loss returns to previous levels.
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.
Other causes:
Underlying causes are treated. Treatment for traction alopecia is elimination of physical traction or stress to the scalp. Treatment for tinea capitis is topical or oral antifungals (see Fungal Skin Infections: Diagnosis and Treatment). Trichotillomania is difficult to treat, but behavior modification, clomipramine 25 to 250 mg po once/day in adults or 3 mg/kg (up to 100 mg maximum) in children, and/or fluoxetine 20 to 40 mg po once/day may be of benefit.
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.
Alopecia
Areata
Alopecia areata
is sudden patchy hair loss in people with no obvious skin disorder
or systemic disease.
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 disease affecting genetically susceptible people exposed to unclear environmental triggers, such as infection or emotional stress. It occasionally coexists with autoimmune vitiligo or thyroiditis.
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, discoid lupus, and secondary syphilis. Measures of TSH, vitamin B12, and autoantibodies are indicated only when coexisting disease is suspected.
Treatment is with corticosteroids. Triamcinolone acetonide suspension (in doses not to exceed 0.1 mL per injection site, eg, 10 mg/mL concentration to deliver 1 mg) can be injected intradermally if the lesions are small. Potent topical corticosteroids (such as betamethasone 0.05% bid) 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 recurs after cessation of therapy and adverse effects limit use. Topical anthralin (0.5 to 1% for 10 to 20 min daily, then washed off, frequency titrated as tolerated up to 30 min bid) and/or minoxidil may be used. Induction of allergic contact dermatitis using diphencyprone or squaric dibutylester leads to hair growth due to unknown mechanisms, but this intervention is best reserved for patients with diffuse involvement who are refractory 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 November 2005
Content last modified November 2005
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