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.
Alopecia areata is a disease that happens when the immune system attacks hair follicles and causes hair loss. Hair follicles are the structures in skin that form hair. While hair can be lost from any part of the body, alopecia areata usually affects the head and face.
Pathophysiology of Alopecia
Growth cycle
Hair grows in cycles. Each cycle consists of phases:
- Anagen: A long (2- to 6-year) growing phase
- Catagen: A brief (3-week) transitional apoptotic phase
- Telogen: A short (2- to 3-month) resting phase
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
- Anagen effluvium—a disruption of the growing phase causing abnormal loss of anagen hairs
- Telogen effluvium—significantly more than 100 hairs/day going into resting phase
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.
Causes
The alopecias comprise a large group of disorders with multiple and varying etiologies
The most common cause of alopecia is
- Androgenetic alopecia (male-pattern or female-pattern hair loss)
Androgenetic alopecia is an androgen-dependent hereditary disorder in which dihydrotestosterone plays a major role. The prevalence of this form of alopecia increases with age, and it affects over 70% of men (male-pattern hair loss) and 57% of all women (female-pattern hair loss) over the age of 80 (1). The prevalence is lower in Asian and Black people than in White people.
Some Causes of Alopecia
| Alopecia Disorder | Causes or Descriptions |
|---|---|
| Nonscarring diffuse hair loss | |
| Anagen effluvium (caused by agents that impair or disrupt the anagen cycle) | Chemotherapeutic agentsPoisoning (eg, thallium, arsenic, other metals)Radiation (also causes scarring focal hair loss) |
| Androgenetic alopecia (male-pattern or female-pattern hair loss) | Androgens (eg, dihydrotestosterone)FamilialPathologic hyperandrogenism (virilization in females—see Hirsutism)Polycystic ovary syndrome |
| Congenital disorders | Congenital atrichia with papulesEctodermal dysplasia |
| Primary hair shaft abnormalities | Easy hair breakage (trichorrhexis nodosa)Genetic disordersLoose anagen hair syndromeOveruse of hair dryers (bubble hair) |
| 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) |
| Alopecia areata | 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) |
| Systemic lupus erythematosus | Commonly causes diffuse hair loss |
| Nonscarring focal hair loss | |
| Alopecia areata | 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) |
| Other | Hair loss due to compulsive hair pulling, twisting, or teasing (trichotillomania)Postoperative (pressure-induced) alopeciaPrimary hair shaft abnormalities (can also cause nonscarring diffuse alopecia)Secondary syphilisTemporal triangular alopecia |
| Tinea capitis* | Microsporum audouiniiMicrosporum canisTrichophyton schoenleiniiTrichophyton tonsurans |
| Traction alopecia* | Traction due to braids, rollers, or ponytails (occurs primarily at frontal and temporal hairlines) |
| Scarring hair loss (focal or diffuse) | |
| Acne keloidalis nuchae | Folliculitis on the occipital scalp that results in scarring alopecia |
| Central centrifugal cicatricial alopecia | Progressive scarring alopecia on the crown or vertex of the scalpMost common cause of alopecia in Black patients, typically occurring in women of African descent |
| Chronic cutaneous (discoid) lupus | Discoid lupus lesions of the scalp |
| Dissecting cellulitis of the scalp | Boggy inflammatory nodules that coalesce with sinus tract formationPart of the follicular occlusion tetrad† |
| Lichen planopilaris and frontal fibrosing alopecia | Typically perifollicular erythema and follicular hyperkeratosisFrontal fibrosing alopecia, a variant of lichen planopilaris, characterized by hair loss and scarring in the frontal region of the scalp |
| Secondary scarring alopecias | BurnsMorphea (localized scleroderma)Progressive systemic sclerosis (scleroderma)Radiation therapy (also causes nonscarring diffuse hair loss)SarcoidosisSkin cancerSuperinfected kerion (due to severe primary syphilis or severe tinea capitis)Trauma |
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
The following findings are of particular concern:
- Virilization in women
- Signs of systemic illness or constellations of nonspecific findings possibly indicating poisoning
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 |
|---|---|
| Asymmetric, bizarre, irregular hair loss pattern | Trichotillomania |
| Circular, discrete patches of loss; short, broken hairs; exclamation point hairs at periphery of patches | Alopecia areata |
| Patchy hair loss that appears moth-eaten | Secondary syphilis |
| Pruritus, erythema, and scaling | Chronic cutaneous lupus, lichen planopilarisTinea capitis (particularly if adenopathy is present) |
| Pustules | Scarring dermatologic or infectious process (eg, dissecting cellulitis of the scalp, acne keloidalis nuchae) |
| Scalp and body hair loss | Alopecia universalis |
| Unruly or unusually wooly hair | Primary hair shaft abnormality |
| Virilization (see Hirsutism) | Adrenal disorder or tumorPituitary adenomaOvarian tumorsAnabolic steroid use (sometimes surreptitious) |
Treatment
- Drugs (including hormonal modulators)
- Laser light therapy
- Surgery
Androgenetic alopecia
Minoxidil works by mechanisms that are not completely understood to shorten the telogen phase, lengthen the anagen phase, and promote growth in hair follicle diameter and length. Topical minoxidil (2% for women, 2% or 5% for men) 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. Low-dose oral minoxidil in doses ranging from 0.25 to 5 mg once/day is sometimes used off-label, but concerns about cardiovascular adverse effects limit its use (1, 2).
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 Male Sexual Dysfunction); hypersensitivity reactions; gynecomastia; myopathy; and rarely symptoms of depression. 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 sometimes used off-label in women of nonchildbearing potential; it 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. Physician-dispensed and 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 (3).
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 (4).
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; its variant, frontal fibrosing alopecia; and chronic cutaneous lupus lesions may be treated with drugs such as oral antimalarials, topical or intralesional 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.
