Alopecia
(Hair Loss; Baldness)
Alopecia is defined as loss of hair from the body. 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.
(See also Alopecia Areata.)
Pathophysiology
Growth cycle
Hair grows in cycles. Each cycle consists of phases:
At the end of the resting phase, the hair falls out (exogen). Normally, about 50 to 100 scalp hairs reach the end of resting phase each day and fall out. When a new hair starts growing in the follicle, the cycle begins again.
Disorders of the growth cycle include
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: Some Causes of Alopecia).
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.
Some Causes of Alopecia
Alopecia Disorder |
Causes or Descriptions |
Nonscarring diffuse hair loss |
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Anagen effluvium (caused by agents that impair or disrupt the anagen cycle) |
Chemotherapeutic agents Poisoning (eg, thallium, arsenic, other metals) Radiation (also causes scarring focal hair loss) |
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Androgenetic alopecia (male-pattern or female-pattern hair loss) |
Androgens (eg, dihydrotestosterone) Familial Pathologic hyperandrogenism (virilization in females—see Hirsutism and Hypertrichosis) |
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Congenital disorders |
Congenital atrichia with papules Ectodermal dysplasia |
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Primary hair shaft abnormalities |
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) |
Drugs (eg, antimitotic chemotherapeutic agents, anticoagulants, retinoids, oral contraceptives, angiotensin-converting enzyme inhibitors, beta-blockers, lithium, antithyroid drugs, anticonvulsants, vitamin A excess) Endocrine problems (eg, hyperthyroidism, hypothyroidism) Nutritional deficiencies (eg, zinc, biotin, or possibly iron deficiency) Physiologic or psychologic stress (eg, surgery, systemic or febrile illness, pregnancy) |
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Diffuse loss of scalp hair (less common form of alopecia areata) Alopecia totalis (complete scalp hair loss) Alopecia universalis (complete scalp and body hair loss) |
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Nonscarring focal hair loss |
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Patchy loss of scalp hair (most common form of alopecia areata) Ophiasis (band pattern hair loss along periphery of temporal and occipital scalp) Sisaipho (central hair loss, sparing the hairs at the margin of the scalp) |
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Other |
Hair loss due to compulsive hair pulling, twisting, or teasing (trichotillomania) Lipedematous alopecia Postoperative (pressure-induced) alopecia Primary hair shaft abnormalities Secondary syphilis Systemic lupus erythematosus (typically causes scarring discoid lesions, but can also cause nonscarring diffuse alopecia) Temporal triangular alopecia |
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Microsporum audouinii Microsporum canis Trichophyton schoenleinii Trichophyton tonsurans |
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Traction alopecia |
Traction due to braids, rollers, or ponytails (occurs primarily at frontal and temporal hairlines) |
Scarring hair loss (focal or diffuse) |
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Acne keloidalis nuchae |
Folliculitis on the occipital scalp that results in scarring alopecia |
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Central centrifugal cicatricial alopecia |
Progressive scarring alopecia on the crown or vertex of the scalp Most common cause of alopecia in black patients, typically occurring in women of African descent |
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Chronic cutaneous lupus |
Discoid lupus lesions of the scalp |
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Dissecting cellulitis of the scalp |
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)‡ |
Typically perifollicular erythema and follicular hyperkeratosis |
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Secondary scarring alopecias |
Burns Morphea (localized scleroderma) Progressive systemic sclerosis (scleroderma) Radiation therapy (also causes nonscarring diffuse hair loss) Superinfected kerion (due to severe primary syphilis or severe tinea capitis) Trauma |
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* Tinea capitis can cause scarring if the follicle is sufficiently damaged. † The follicular occlusion tetrad (also called acne inversa) is acne conglobata, hidradenitis suppurativa, dissecting cellulitis of the scalp, and pilonidal sinus—disorders that have follicular hyperkeratinization in common. ‡ Frontal fibrosing alopecia is a localized variant of lichen planopilaris. |
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Etiology
The alopecias comprise a large group of disorders with multiple and varying etiologies (see Table: 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. This form of alopecia may eventually affect up to 80% of white men by the age of 70 (male-pattern hair loss) and about half of all women (female-pattern hair loss).
Other common causes of hair loss are
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Drugs (including chemotherapeutic agents)
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Infection (eg, tinea capitis, kerion)
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Systemic disorders (disorders that cause high fever, systemic lupus erythematosus, endocrine disorders, and nutritional deficiencies)
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Trauma
Traumatic causes include trichotillomania, traction alopecia, central centrifugal cicatricial alopecia, burns, radiation, and pressure-induced (eg, postoperative) hair loss.
Less common causes are
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 (eg, fatigue and cold intolerance [hypothyroidism] and, in women, hirsutism, deepening of the voice, and increased libido [virilization]) should be sought. Other features, including dramatic weight loss, dietary practices (including various restrictive diets), 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: 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
Interpretation of findings
Hair loss that begins at the temples and/or crown (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 Figure: Male- and female-pattern hair loss (androgenetic alopecia)). In androgenetic alopecia, the central part width is wider on the crown of the scalp than it is on the occipital scalp.
Hair loss that occurs 2 to 4 weeks after chemotherapy or radiation therapy (anagen effluvium) can typically be ascribed to those causes. Hair loss that occurs 3 to 4 months after a major stressor (pregnancy, major febrile illness, surgery, medication change, or severe psychologic stressor) suggests a diagnosis of telogen effluvium.
Other findings help suggest alternative diagnoses (see Table: Interpreting Physical Findings in Alopecia).
Interpreting Physical Findings in Alopecia
Finding |
Possible Causes |
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Asymmetric, bizarre, irregular hair loss pattern |
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Circular, discrete patches of loss; short, broken hairs; exclamation point hairs at periphery of patches |
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Patchy hair loss that appears moth-eaten |
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Pruritus, erythema, and scaling |
Chronic cutaneous lupus, lichen planopilaris Tinea capitis (particularly if adenopathy present) |
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Pustules |
Scarring dermatologic or infectious process (eg, dissecting cellulitis of the scalp, acne keloidalis nuchae) |
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Scalp and body hair loss |
Alopecia universalis |
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Unruly or unusually wooly hair |
Primary hair shaft abnormality |
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Virilization (see Hirsutism and Hypertrichosis) |
Adrenal disorder or tumor Anabolic steroid use (sometimes surreptitious) |
Anagen effluvium is a physiologic disruption of the anagen (growing) phase. It typically occurs several weeks after chemotherapy or radiation therapy. An abrupt loss of hairs in the anagen phase along with sparse broken anagen hairs is depicted.
This photo shows typical acneiform lesions and deep keloidal scarring alopecia in a young male with acne keloidalis nuchae.
Trichotillomania is characterized by patches of decreased hair density and variable hair length with uninvolved areas of the scalp appearing completely normal. Totally hairless areas are rare because patients tend to pull only the longer hairs that they can grasp.
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 levels of appropriate hormones (eg, testosterone and dehydroepiandrosterone sulfate [DHEAS]) measured (see Hirsutism and Hypertrichosis : 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 sequentially pulling out about 50 individual hairs abruptly (“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.
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 2 times a day 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 months. 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 5-alpha-reductase enzyme, blocking conversion of testosterone to dihydrotestosterone, and is useful for male-pattern hair loss. Finasteride 1 mg orally once/day can stop hair loss and can stimulate hair growth. Efficacy is usually evident within 6 to 8 months of treatment. Adverse effects include decreased libido; erectile and ejaculatory dysfunction, which may persist even after cessation of treatment (see Erectile 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.
Dutasteride, a drug used to treat benign prostatic hyperplasia, is a stronger inhibitor of 5-alpha-reductase than finasteride and is sometimes used to treat androgenetic alopecia.
Hormonal modulators such as oral contraceptives or spironolactone may be useful for female-pattern hair loss.
Low-level laser light therapy is an alternate or additional treatment for androgenetic alopecia that has been shown to promote hair growth. Over-the-counter devices are available.
Autologous platelet-rich plasma injected into the scalp is thought to contain growth factors that promote hair follicle growth and maintenance (1).
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 (2).
Hair loss due to other causes
Underlying disorders are treated.
Treatment for alopecia areata includes topical, intralesional, or, in severe cases, systemic corticosteroids, topical minoxidil, topical anthralin, topical immunotherapy (diphenylcyclopropenone or squaric acid dibutylester), or methotrexate.
Treatment for traction alopecia is elimination of physical traction or stress to the scalp.
Treatment for tinea capitis is oral antifungals.
Trichotillomania is difficult to treat, but behavior modification, clomipramine, or a selective serotonin reuptake inhibitor (SSRI—eg, fluoxetine, fluvoxamine, paroxetine, sertraline, citalopram) may be of benefit.
Scarring alopecia as in central centrifugal cicatricial alopecia or dissecting cellulitis of the scalp is best treated with an oral tetracycline plus a potent topical corticosteroid. Severe or chronic acne keloidalis nuchae can be treated similarly or with intralesional triamcinolone; if mild, topical retinoids, topical antibiotics, and/or topical benzoyl peroxide may suffice.
Lichen planopilaris and chronic cutaneous lupus lesions may be treated with drugs such as oral antimalarials, topical or oral corticosteroids, topical or oral retinoids, topical tacrolimus, or oral immunosuppressants.
Hair loss due to chemotherapy (anagen effluvium) 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 is usually temporary as well and abates after the precipitating agent is eliminated.
Treatment references
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1. Hesseler MJ, Shyam N: Platelet-rich plasma and its utilities in alopecia: A systematic review. Dermatol Surg Epub ahead of print, June 2019. doi: 10.1097/DSS.0000000000001965.
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2. Adil A, Godwin M: The effectiveness of treatments for androgenetic alopecia: A systematic review and meta-analysis. J Am Acad Dermatol 77(1):136–141.e5, 2017. doi: 10.1016/j.jaad.2017.02.054.
Key Points
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Androgenetic alopecia (male-pattern and female-pattern hair loss) is the most common type of hair loss.
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Concomitant virilization in women or scarring hair loss should prompt a thorough evaluation for an underlying disorder.
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Microscopic hair examination or scalp biopsy may be required for definitive diagnosis.
Drugs Mentioned In This Article
| Drug Name | Select Trade |
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benzoyl peroxide |
No US brand names |
spironolactone |
ALDACTONE |
triamcinolone |
KENALOG |
clomipramine |
ANAFRANIL |
methotrexate |
OTREXUP |
tetracycline |
ACHROMYCIN V |
Dutasteride |
AVODART |
fluvoxamine |
LUVOX |
Finasteride |
PROPECIA, PROSCAR |
paroxetine |
PAXIL |
sertraline |
ZOLOFT |
tacrolimus |
PROGRAF |
citalopram |
CELEXA |
fluoxetine |
PROZAC, SARAFEM |
anthralin |
No US brand name |
Minoxidil |
ROGAINE |
lithium |
LITHOBID |
