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 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 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: Classification and Causes of Alopecia). Table 1 Classification and Causes of Alopecia Classification Causes Nonscarring diffuse hair loss Anagen effluvium (caused by agents that impair or disrupt the anagen cycle) Chemotherapeutic agents Poisoning (eg, boric acid, mercury, thallium) Radiation (also causes scarring focal hair loss) Androgenetic alopecia (male- or female-pattern hair loss) Androgens (dihydrotestosterone) Familial Pathologic hyperandrogenism (in females—see Hair Disorders: Hirsutism) Congenital disorders Congenital atrichia with papules Ectodermal dysplasia
Primary hair shaft abnormalities (trichodystrophies) Easy hair breakage (trichorrhexis nodosa) Genetic disorders Loose anagen hair syndrome Overuse of hair dryers (bubble hair) Telogen effluvium (increased number of hairs entering resting phase) Drugs (eg, antimitotic chemotherapeutic agents, anticoagulants, retinoids, oral contraceptives, ACE inhibitors, β-blockers, lithium
, antithyroid drugs, anticonvulsants, heavy metals, vitamin A excess) Endocrine problems (eg, hyperthyroidism, hypothyroidism, menopause, postpartum) Nutritional deficiencies Physiologic or psychologic stress (eg, surgery, systemic illness/postfebrile illness) Nonscarring focal hair loss Alopecia areata T-cell–mediated autoimmune disorder
Hair loss is most commonly focal but may be diffuse (alopecia totalis or alopecia universalis) Other 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 Tinea capitis Microsporum audouinii Microsporum canis Trichophyton schoenleinii Trichophyton tonsurans Traction alopecia Traction from braids, rollers, or ponytails (occurs primarily at frontal and temporal hairlines) Scarring focal hair loss Acne keloidalis nuchae*
Folliculitis on the occipital scalp that results in scarring alopecia Central centrifugal scarring alopecia† Scarring on the crown that enlarges over time Chronic cutaneous lupus Discoid lupus lesions of the scalp Dissecting cellulitis of the scalp* Boggy inflammatory nodules that coalesce with sinus tract formation Part of the follicular occlusion tetrad Lichen planopilaris Lichen planus of the scalp Secondary scarring alopecias Burns Morphea Radiation therapy (also causes nonscarring diffuse hair loss) Sarcoidosis Skin cancer Superinfected kerion (severe primary syphilis or severe tinea capitis) Trauma
*Usually affects black men. † Most often affects black women
Nonscarring alopecia results from processes that reduce or slow hair growth without irreparably damaging the hair follicle. Disorders that primarily affect the hair shaft also are considered nonscarring alopecia. Etiology The alopecias comprise a large group of disorders with multiple and varying etiologies (see Table 1: Hair Disorders: Classification and Causes of Alopecia). The most common cause of alopecia is Androgenetic alopecia (male-pattern or femalepattern hair loss) Androgenetic alopecia is an androgen-dependent hereditary disorder in which dihydrotestosterone plays a major role. Other common causes of hair loss are Drugs (including chemotherapeutic agents) Infection
Systemic illnesses (particularly those that cause high fever, systemic lupus, endocrine disorders, and nutritional deficiencies) Less common causes are primary hair shaft abnormalities, autoimmune disease, 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 (virilizing syndrome). 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: Classification and 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, lichen planus, atopy, psoriasis, discoid lupus lesions, hidradenitis, 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 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.). Fig. 1 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). Table 2 Interpreting 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 Hair loss with a patchy, moth-eaten appearance Secondary syphilis Pruritus, erythema, and scaling Chronic cutaneous lupus Tinea capitis (particularly if adenopathy 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 Adrenal disorder or tumor Polycystic ovary syndrome Surreptitious anabolic steroid use
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 and female-pattern hair loss generally requires no testing. When it occurs in young men with no family history, the physician should question the patient about anabolic steroid use and other drugs. In addition to questions regarding 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: Hirsutism). The pull test helps evaluate diffuse scalp hair loss. Gentle traction is exerted on a bunch of hairs (40 to 60) on at least 3 different areas of the scalp, and the number of extracted hairs is counted and examined microscopically. Normally, < 3 telogen-phase hairs should come out with each pull. If at least 3 hairs are obtained with each pull or if > 10 hairs total are obtained, the pull test is positive and suggestive of telogen effluvium.
The pluck test pulls individual hairs out 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, 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 lupus erythematosus, 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 in 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. One mL of topical drug applied bid 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 levels in older men, which should be taken into account when that 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 (diphencyprone 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 topical or 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 central centrifugal scarring alopecia, dissecting cellulitis of the scalp, and acne keloidalis nuchae is best treated by a longacting oral tetracycline
in combination with a potent topical corticosteroid. Lichen planopilaris and chronic cutaneous lupus lesions may be treated with oral antimalarial drugs, 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 Androgenetic alopecia (male-pattern and femalepattern baldness) is the most common type of hair loss. Concomitant virilization in women or scarring hair loss should prompt a thorough evaluation as to the underlying disorder.
Microscopic hair examination or scalp biopsy may be required for definitive diagnosis. 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 Examination 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 thyroid-stimulating hormone (TSH), vitamin B12, and autoantibodies are indicated only when coexisting disease is suspected.
Treatment Corticosteroids Sometimes topical anthralin , minoxidil
or both 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 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).
Hirsutism is the excessive growth of thick or dark hair in women in locations that are more typical of male hair 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, and clitoral hypertrophy. Etiology There are a number of causes of hirsutism (see Table 3: Hair Disorders: Some Causes of Hirsutism). Overall, the most common causes are the following: Polycystic ovary syndrome Familial hirsutism Table 3 Some Causes of Hirsutism
Causes Examples Adrenal disorders Adrenal tumor Congenital or delayed-onset adrenal hyperplasia Cushing's syndrome Androgenic drugs Anabolic steroids Danazol
Oral contraceptives (high-progesterone type) Ectopic hormone production Lung cancer and carcinoid tumors (ectopic ACTH secretion) Choriocarcinomas (β-human chorionic gonadotropin) Endocrine disorders that indirectly influence androgen balance Hyperinsulinemia Hypothyroidism Familial hirsutism May be secondary to a familial increased end-organ response to normal plasma androgen levels
Ovarian disorders Ovarian hyperthecosis Ovarian tumors Polycystic ovary syndrome Pituitary disorder Cushing's disease Prolactin-secreting pituitary adenoma Acromegaly Drugs (phenothiazines)
Androgen excess: Hirsutism typically results from abnormally high androgen activity as a result of increased central production of androgens (eg, from 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 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 as part of a rare familial disorder. Table 4 Causes of Hypertrichosis Causes Examples Disorders Acrodynia Anorexia CNS disorders Dermatomyositis Familial HIV infection if advanced Malnutrition
Paraneoplastic syndromes Porphyria Pretibial myxedema Repeated skin trauma, friction, inflammation Systemic illness Traumatic brain injury Nonandrogenic drugs Acetazolamide
Corticosteroids (systemic or topical) Cyclosporine
Fenoterol Hexachlorobenzene Interferon-α Minoxidil
Prostaglandin E1 Psoralen Streptomycin
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 cold intolerance, fatigue, and weight gain (hypothyroidism); 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: Virilization Abrupt appearance of hirsutism Pelvic or abdominal mass Interpretation of findings: Excess hair growth beginning after use of an anabolic steroid or other causative drug (seeTable 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: Some Symptoms and Signs for Diagnosis of Hirsutism). Table 5
Some Symptoms and Signs for Diagnosis of Hirsutism Symptoms and Signs Possible Diagnosis Abrupt-onset hirsutism, pelvic mass on examination Adrenal or ovarian cancer Acanthosis nigricans Polycystic ovary syndrome or other hyperinsulinemic state Central obesity, moon facies, striae, hypertension, proximal muscle weakness Cushing's syndrome Galactorrhea, amenorrhea (with or without visual field deficits) Pituitary disorder causing hyperprolactinemia Irregular menses or amenorrhea, acne, obesity, hirsutism beginning after puberty Polycystic ovary syndrome Signs of malnutrition, poor dentition (particularly in adolescent females) Eating disorder Weight loss, fevers Paraneoplastic syndromes caused by occult cancer
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: Free and total testosterone DHEAS Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) Androstenedione Thyroid-stimulating hormone (TSH) Prolactin 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). Imaging: Pelvic ultrasonography, CT, or both should be done to rule out pelvic or adrenal cancer, particularly when a pelvic mass is appreciated, 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's syndrome or an adrenal mass on imaging studies should have 24-h urine cortisol levels measured. Treatment The underlying disorder should be treated, including stopping or changing causative drugs. Treatment for hirsutism itself is unnecessary if the patient does not find 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 and the roots and can be achieved via mechanical means (eg, tweezing, plucking, or 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/day, decreases hair growth and, with long-term use, may decrease the need to manually remove hair. 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 Antiandrogenic drugs Sometimes other agents 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 as 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 less effective than other antiandrogenic agents. Corticosteroids are used for adrenal suppression. Gonadotropin-releasing hormone agonists (eg, leuprolide acetate, nafarelin , or triptorelin) can be used for severe forms of ovarian hyperandrogenism under the direction of a gynecologist or endocrinologist. Key Points
Hirsutism may be familial, and the degree of hair growth may vary with ethnicity. Polycystic ovary syndrome is the most frequent cause of hirsutism. Virilization suggests an androgenic disorder that requires further evaluation. Abrupt onset of hirsutism may indicate cancer. Skip main navigation and go to sub navigation menu. Skip main navigation and go to main content of page. Skip main navigation and go to related information. Enter Search Text Home Health Information Research Funding News & Events About Us Portal en español You are here: Home > Health_Info > Alopecia_Areata > Questions and Answers About Alopecia Areata Health Information Change text size View Print-Friendly Page Subscribe to NIAMS Update Download Adobe Reader Related Information Alopecia Areata (fast facts, easy-to-read)
¿Qué es la alopecia areata? (Esenciales: hojas informativas de fácil lectura) Hair Loss in Women (information package) Order a NIAMS Publication to be mailed Alopecia Areata Find a Clinical Trial Journal Articles Alopecia Areata Publication Date: April 2009 Questions and Answers about Alopecia Areata This booklet contains general information about alopecia areata (al-oh-PEE-shah ar-ee-AH-tah). It describes what alopecia is, its causes, and treatment options. Information is also provided on current research. If you have further questions after reading this booklet, you may wish to discuss them with your doctor. What Is Alopecia Areata? Alopecia areata is considered an autoimmune disease, in which the immune system, which is designed to protect the body from foreign invaders such as viruses and bacteria, mistakenly attacks the hair follicles, the tiny cup-shaped structures from which hairs grow. This can lead to hair loss on the scalp and elsewhere. In most cases, hair falls out in small, round patches about the size of a quarter. In many cases, the disease does not extend beyond a few bare patches. In some people, hair loss is more extensive. Although uncommon, the disease can progress to cause total
loss of hair on the head (referred to as alopecia areata totalis) or complete loss of hair on the head, face, and body (alopecia areata universalis). Alopecia areata is just one cause of alopecia, or hair loss. Others include: Traction alopecia – a condition that occurs when ponytails or tight braids put so much stress on the hair that it falls out. If this happens repeatedly it can cause scarring and root damage that will prevent hair from growing back. Cicatricial alopecia – a group of related disorders in which inflammation destroys the hair follicles and replaces them with scar tissue. Also referred to as scarring alopecia, this cause of permanent hair loss is often seen in skin conditions such as discoid lupus erythematosus and lichen planus. Androgenic alopecia – also called male-pattern or female-pattern baldness, a condition in which the growth phase of the normal hair cycle shortens, making hair more fragile. Over time hairs falls out easily leaving a characteristic pattern of thinning or baldness. Trichotillomania – a mental condition in which people have an uncontrollable urge to pull out their hair. This can lead to patchy bald spots on the head. Telogen effluvium – hair loss related to a change in the normal hair cycle. This may be caused by an emotional shock – such as the death of a loved one – or physical shock, such as high fever, illness or surgery.
Hair loss can also have other causes including fungal infections and certain medications; however, this publication focuses only on alopecia areata. What Causes It? Who Is Most Likely to Get It? Is My Hair Loss a Symptom of a Serious Disease? Can I Pass It On to My Children? Will My Hair Ever Grow Back? What Can I Expect Next? How Is It Treated? How Will Alopecia Areata Affect My Life? How Can I Cope With the Effects of This Disease? Is Research Close to Finding Better Treatments or a Cure? How Can I Take Part in Research? Where Can People Find More Information About Alopecia Areata? Key Words What Causes It? In alopecia areata, immune system cells called white blood cells attack the rapidly growing cells in the hair follicles that make the hair. The affected hair follicles become small and drastically slow down hair production. Fortunately, the stem cells that continuously supply the follicle with new cells do not seem to be targeted. So the follicle always has the potential to regrow hair. Scientists do not know exactly why the hair follicles undergo these changes, but they suspect that a combination of genes may predispose some people to the disease. In those who are genetically predisposed, some type of trigger – perhaps a virus
or something in the person’s environment – brings on the attack against the hair follicles. Who Is Most Likely to Get It? Alopecia areata affects nearly 2 percent of Americans of both sexes and of all ages and ethnic backgrounds. It often begins in childhood. If you have a close family member with the disease, your risk of developing it is slightly increased. If your family member lost his or her first patch of hair before age 30, the risk to other family members is greater. Overall, one in five people with the disease has a family member who has it as well. Is My Hair Loss a Symptom of a Serious Disease? Alopecia areata is not a life-threatening disease. It does not cause any physical pain, and people with the condition are generally healthy otherwise. But for most people, a disease that unpredictably affects their appearance the way alopecia areata does is a serious matter. The effects of alopecia areata are primarily socially and emotionally disturbing. In alopecia universalis, however, loss of eyelashes and eyebrows and hair in the nose and ears can make the person more vulnerable to dust, germs, and foreign particles entering the eyes, nose, and ears. Alopecia areata often occurs in people whose family members have other autoimmune diseases, such as diabetes, rheumatoid arthritis, thyroid disease, systemic lupus erythematosus, pernicious anemia, or
Addison’s disease. People who have alopecia areata do not usually have other autoimmune diseases, but they do have a higher occurrence of thyroid disease, atopic eczema, nasal allergies, and asthma. Can I Pass It On to My Children? It is possible, but not likely, for alopecia areata to be inherited. Most children with alopecia areata do not have a parent with the disease, and the vast majority of parents with alopecia areata do not pass it along to their children. Alopecia areata is not like some genetic diseases in which a child has a 50–50 chance of developing the disease if one parent has it. Scientists believe that there may be a number of genes that predispose certain people to the disease. It is highly unlikely that a child would inherit all of the genes needed to predispose him or her to the disease. Even with the right (or wrong) combination of genes, alopecia areata is not a certainty. In identical twins, who share all of the same genes, the concordance rate is only 55 percent. In other words, if one twin has the disease, there is only a 55-percent chance that the other twin will have it as well. This shows that other factors besides genetics are required to trigger the disease. To learn more about the genes and other factors involved in alopecia areata risk, the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) is funding an alopecia areata registry. The registry is an organized network of five centers
throughout the United States that will identify and register patients with the disease and collect data and blood samples (which contain genes). Data, including genetic information, will be made available to researchers studying the genetic basis and other aspects of disease and disease risk. (For more information about the registry, see “How Can I Take Part in Research?”) Will My Hair Ever Grow Back? There is every chance that your hair will regrow, but it may also fall out again. No one can predict when it might regrow or fall out. The course of the disease varies from person to person. Some people lose just a few patches of hair, then the hair regrows, and the condition never recurs. Other people continue to lose and regrow hair for many years. A few lose all the hair on their head; some lose all the hair on their head, face, and body. Even in those who lose all their hair, the possibility for full regrowth remains. In some, the initial hair regrowth is white, with a gradual return of the original hair color. In most, the regrown hair is ultimately the same color and texture as the original hair. What Can I Expect Next? The course of alopecia areata is highly unpredictable, and the uncertainty of what will happen next is probably the most difficult and frustrating aspect of the disease. You may continue to lose hair, or your hair loss may stop. The hair you have lost may or may not grow back, and you may or may not continue to develop new bare patches.
How Is It Treated? Although there is neither a cure for alopecia areata nor drugs approved for its treatment, some people find that medications approved for other purposes can help hair grow back, at least temporarily. The following are some treatments for alopecia areata. Keep in mind that although these treatments may promote hair growth, none of them prevent new patches or actually cure the underlying disease. Consult your health care professional about the best option for you. Corticosteroids – Corticosteroids are powerful antiinflammatory drugs similar to a hormone called cortisol, which is produced in the body. Because these drugs suppress the immune system if given orally, they are often used in the treatment of various autoimmune diseases, including alopecia areata. Corticosteroids may be administered in three ways for alopecia areata: Local injections – Injections of steroids directly into hairless patches on the scalp and sometimes the brow and beard areas are effective in increasing hair growth in most people. It usually takes about 4 weeks for new hair growth to become visible. Injections deliver small amounts of cortisone to affected areas, avoiding the more serious side effects encountered with long-term oral use. The main side effects of injections are transient pain, mild swelling, and sometimes changes in pigmentation, as well as small indentations in the skin that go away when injections are stopped. Because injections can be painful, they may not be the preferred treatment for children. After 1 or 2
months, new hair growth usually becomes visible, and the injections usually have to be repeated monthly. The cortisone removes the confused immune cells and allows the hair to grow. Large areas cannot be treated, however, because the discomfort and the amount of medicine become too great and can result in side effects similar to those of the oral regimen. Oral corticosteroids – Corticosteroids taken by mouth are a mainstay of treatment for many autoimmune diseases and may be used in more extensive alopecia areata. But because of the risk of side effects of oral corticosteroids, such as hypertension and cataracts, they are used only occasionally for alopecia areata and for shorter periods of time. Topical ointments – Ointments or creams containing steroids rubbed directly onto the affected area are less traumatic than injections and, therefore, are sometimes preferred for children. However, corticosteroid ointments and creams alone are less effective than injections; they work best when combined with other topical treatments, such as minoxidil or anthralin. Minoxidil (5 percent) (Rogaine1) – Topical minoxidil solution promotes hair growth in several conditions in which the hair follicle is small and not growing to its full potential. Minoxidil is FDA-approved for treating male and female pattern hair loss. It may also be useful in promoting hair growth in alopecia areata. The solution, applied twice daily, has been shown to promote hair growth in both adults and children, and may be used on the scalp, brow, and beard areas. With regular and proper use of the solution, new hair growth appears in about 12 weeks.
1Brand names included in this booklet are provided as examples only, and their inclusion does not mean that these products are endorsed by the National Institutes of Health or any other Government agency. Also, if a particular brand name is not mentioned, this does not mean or imply that the product is unsatisfactory. Anthralin – Anthralin, a synthetic tar-like substance that alters immune function in the affected skin, is an approved treatment for psoriasis. Anthralin is also commonly used to treat alopecia areata. Anthralin is applied for 20 to 60 minutes (“short contact therapy”) to avoid skin irritation, which is not needed for the drug to work. When it works, new hair growth is usually evident in 8 to 12 weeks. Anthralin is often used in combination with other treatments, such as corticosteroid injections or minoxidil, for improved results. Sulfasalazine – A sulfa drug, sulfasalazine has been used as a treatment for different autoimmune disorders, including psoriasis. It acts on the immune system and has been used to some effect in patients with severe alopecia areata. Topical sensitizers – Topical sensitizers are medications that, when applied to the scalp, provoke an allergic reaction that leads to itching, scaling, and eventually hair growth. If the medication works, new hair growth is usually established in 3 to 12 months. Two topical sensitizers are used in alopecia areata: squaric acid dibutyl ester (SADBE) and diphenylcyclopropenone (DPCP). Their safety and consistency of formula are currently under review.
Oral cyclosporine – Originally developed to keep people’s immune systems from rejecting transplanted organs, oral cyclosporine is sometimes used to suppress the immune system response in psoriasis and other immune-mediated skin conditions. But suppressing the immune system can also cause problems, including an increased risk of serious infection and possibly skin cancer. Although oral cyclosporine may regrow hair in alopecia areata, it does not turn the disease off. Most doctors feel the dangers of the drug outweigh its benefits for alopecia areata. Photochemotherapy – In photochemotherapy, a treatment used most commonly for psoriasis, a person is given a light-sensitive drug called a psoralen either orally or topically and then exposed to an ultraviolet light source. This combined treatment is called PUVA. In clinical trials, approximately 55 percent of people achieve cosmetically acceptable hair growth using photochemotherapy. However, the relapse rate is high, and patients must go to a treatment center where the equipment is available at least two to three times per week. Furthermore, the treatment carries the risk of developing skin cancer. Alternative therapies – When drug treatments fail to bring sufficient hair regrowth, some people turn to alternative therapies. Alternatives purported to help alopecia areata include acupuncture, aroma therapy, evening primrose oil, zinc and vitamin supplements, and Chinese herbs. Because many alternative therapies are not backed by clinical trials, they may or may not be effective for regrowing hair. In fact, some may actually make hair loss worse.
Furthermore, just because these therapies are natural does not mean that they are safe. As with any therapy, it is best to discuss these treatments with your doctor before you try them. In addition to treatments to help hair grow, there are measures that can be taken to minimize the physical dangers or discomforts of lost hair. Sunscreens are important for the scalp, face, and all exposed areas. Eyeglasses (or sunglasses) protect the eyes from excessive sun, and from dust and debris when eyebrows or eyelashes are missing. Wigs, caps, or scarves protect the scalp from the sun and keep the head warm. Antibiotic ointment applied inside the nostrils helps to protect against organisms invading the nose when nostril hair is missing. How Will Alopecia Areata Affect My Life? This is a common question, particularly for children, teens, and young adults who are beginning to form lifelong goals and who may live with the effects of alopecia areata for many years. The comforting news is that alopecia areata is not a painful disease and does not make people feel sick physically. It is not contagious, and people who have the disease are generally healthy otherwise. It does not reduce life expectancy and it should not interfere with the ability to achieve such life goals as going to school, working, marrying, raising a family, playing sports, and exercising.
The emotional aspects of living with hair loss, however, can be challenging. Many people cope by learning as much as they can about the disease; speaking with others who are facing the same problem; and, if necessary, seeking counseling to help build a positive self-image. How Can I Cope With the Effects of This Disease? Living with hair loss can be hard, especially in a culture that views hair as a sign of youth and good health. Even so, most people with alopecia areata are well-adjusted, contented people living full lives. The key to coping is valuing yourself for who you are, not for how much hair you have or don’t have. Many people learning to cope with alopecia areata find it helpful to talk with other people who are dealing with the same problems. Nearly 2 percent of Americans have this disease at some point in their lives, so you are not alone. If you would like to be in touch with others with the disease, the National Alopecia Areata Foundation (NAAF) can help through its pen pal program, message boards, annual conference, and support groups that meet in various locations nationwide. To find contact information for NAAF and other organizations that can help people with alopecia areata, see “Where Can People Find More Information About Alopecia Areata?” Another way to cope with the disease is to minimize its effects on your appearance. If you have total hair loss, a wig or hairpiece can look natural and stylish. For small patches of hair loss, a hair-colored powder, cream, or crayon applied to the scalp can make hair
loss less obvious by eliminating the contrast between the hair and the scalp. Skillfully applied eyebrow pencil can mask missing eyebrows. Children with alopecia areata may prefer to wear bandanas or caps. There are many styles available to suit a child’s interest and mood – some even have ponytails attached. For women, attractive scarves can hide patchy hair loss; jewelry and clothing can distract attention from patchy hair; and proper makeup can camouflage the effects of lost facial hair. If you would like to learn more about camouflaging the cosmetic aspects of alopecia areata, ask your doctor or members of your local support group to recommend a cosmetologist who specializes in working with people whose appearance is affected by medical conditions. Is Research Close to Finding Better Treatments or a Cure? Although a cure is not imminent, researchers are making headway toward a better understanding of the disease. This increased understanding will likely lead the way to better treatments for alopecia areata and eventually a way to prevent or even cure it. Alopecia research ranges from the most basic studies of the mechanisms of hair growth and hair loss in mice to testing medications and ways to apply medications to help regrow hair in people. Both the National Institutes of Health and the National Alopecia Areata Foundation support research into the
disease and its treatment. Here are some areas of research that hold promise. Developing an animal model – This is a critical first step toward understanding the disease, and much progress has been made. Researchers have identified an inbred strain of mice that spontaneously develops a condition similar to the adult-onset form of alopecia areata. This mouse model has already allowed researchers to identify some genetic factors that are involved in development of the disease. By studying mice with a disease similar to human alopecia areata, researchers hope to learn more about the mechanism of the disease and eventually develop immune system treatments for the disease in people. Mapping genes – Scientists are studying the possible genetic causes and mechanism of the disease both in families that have one or more people with the disease and in the general population. An understanding of the genetics of the disorder will aid in disease prevention, early intervention, and development of specific therapies. Studying hair follicle development – By studying how hair follicles form in mouse embryos, researchers hope to gain a better understanding of hair cycle biology that may lead to treatments for the underlying disease process. Understanding stem cell biology – Epithelial stem cells are immature cells that are responsible for
regenerating and maintaining a variety of tissues, including the skin and the hair follicles. Stem cells in the follicle appear to be spared from injury in alopecia areata, which may explain why the potential for regrowth is always there in people with the disease. By studying the biology of these cells, scientists hope to gain a better understanding of factors that trigger the disease. How Can I Take Part in Research? A good place to start is the National Alopecia Areata Registry sponsored by NIAMS. The registry, a network of five centers, will identify and register patients with the disease and collect information and blood samples (containing genes). Data, including genetic information, will be made available to researchers studying the genetic basis and other aspects of the disease and disease risk. The registry is seeking U.S. residents with alopecia areata, alopecia totalis, or alopecia universalis diagnosed by a dermatologist. Although the registry itself will not be involved in any kind of treatment for alopecia areata, people who register will be made aware of studies for which they may qualify. To take part in the registry, people don’t have to live near or travel to one of the five centers; however, they do have to meet some requirements to participate. For more information, log onto the registry Web site at www.AlopeciaAreataRegistry.org or have your doctor get in touch with the contacts involved with the registry:
Phone: 713–792–5999 Toll free: 866–837–1050 E-mail: [email protected]
Where Can People Find More Information About Alopecia Areata? You can get additional information through the following organizations: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse National Institutes of Health 1 AMS Circle Bethesda, MD 20892-3675 Phone: 301-495-4484 Toll Free: 877-22-NIAMS (226-4267) TTY: 301-565-2966 Fax: 301-718-6366 Email: [email protected]
Website: http://www.niams.nih.gov National Center for Complementary and Alternative Medicine National Institutes of Health P.O. Box 7923 Gaithersburg, MD 20898 Phone: 301-519-3153 Toll Free: 888-644-6226 TTY: 866-464-3615 Fax: 866-464-3616 Email: [email protected]
Website: http://nccam.nih.gov American Academy of Dermatology (AAD)
P.O. Box 4014 Schaumberg, IL 60618-4014 Phone: 847-330-0230 Toll Free: 866-503-SKIN (7546) Fax: 847-240-1859 Website: http://www.aad.org National Alopecia Areata Foundation (NAAF) 14 Mitchell Blvd. San Rafael, CA 94903 Phone: 415-472-3780 Fax: 415-472-5343 Email: [email protected]
Website: http://www.naaf.org American Hair Loss Council 30 South Main Shenandoah, PA 17976 Email: [email protected]
Website: http://www.ahlc.org Key Words Acupuncture – a traditional Chinese system of healing in which symptoms are relieved by inserting needles beneath the skin at selected points and then stimulating the points by rotating the needles or exposing them to heat or electrical current. Addison’s disease – a condition that occurs when the adrenal glands (a pair of glands situated on top of the kidneys) fail to secrete enough corticosteroid hormones. Without treatment, the disease can be fatal.
Alopecia areata – an autoimmune, often reversible disease in which loss of hair occurs in sharply defined areas usually involving the scalp or beard, but at times every hair on the body. Alopecia areata totalis – a form of alopecia areata characterized by the total loss of hair from the scalp and face. Alopecia areata universalis – a form of alopecia areata in which all hair on the scalp, face, and body is lost. Aroma therapy – the therapeutic use of essential oils (highly concentrated aromatic extracts distilled from a variety of aromatic plant materials including grasses, leaves, flowers, needles and twigs, fruit peels, wood, and roots) to promote the health of body, mind, and spirit. Autoimmune disease – a disease that results when the immune system mistakenly attacks the body’s own tissues. Rheumatoid arthritis and systemic lupus erythematosus are autoimmune diseases (“auto” means self). Chemotherapy – the use of strong drugs to suppress the immune system. Though originally associated with cancer treatment, chemotherapy is used for many different diseases involving the immune system.
Corticosteroids – potent anti-inflammatory hormones that are made naturally in the body or synthetically (man-made) for use as drugs. They are also called glucocorticoids. The most commonly prescribed drug of this type is prednisone. Cyclosporine – a strong drug that suppresses the immune system. Originally developed to keep the body’s immune system from rejecting transplanted organs, cyclosporine is being used increasingly in autoimmune diseases, including (in rare cases) alopecia areata. Diabetes – a disease in which the body does not produce or properly use insulin, a hormone that is necessary to convert sugar, starches, and other food into energy. Evening primrose oil – the oil of a weedy plant containing the essential fatty acid gamma linolenic acid (GLA), which is converted into anti-inflammatory agents by the body. Evening primrose oil is available as a nutritional supplement and touted as a pain and inflammation reliever. Hair bulb – a bulbous collection of actively growing cells at the base of the follicle that constantly produces a strand of hair. Hair follicle – a small cup-shaped structure in the skin from which hair grows. The cup is lined with cells and connective tissue.
Immune system – a complex network of specialized cells and organs that work together to defend the body against attacks by “foreign” invaders such as bacteria and viruses. In some rheumatic conditions, it appears that the immune system does not function properly and may even work against the body. Pernicious anemia – a potentially dangerous form of anemia, usually caused by an autoimmune process, which results in a deficiency of vitamin B-12. Rheumatoid arthritis – an autoimmune disease that targets primarily the membrane lining the joints, leading to pain, stiffness, swelling, and joint deformity. Systemic lupus erythematosus – a chronic autoimmune disease of the connective tissue that can attack and damage the skin, joints, blood vessels, and internal organs. Topical sensitizers – medications that, when applied to the scalp, provoke an allergic reaction that leads to itching, scaling, and often hair growth. They include squaric acid dibutyl ester and diphenylcyclopropenone. Acknowledgments NIAMS gratefully acknowledges the assistance of George Cotsarelis, M.D., University of Pennsylvania Medical Center, Philadelphia; Vicki Kalabokes, National Alopecia Areata Foundation, San Rafael, CA; Alan Moshell, M.D., NIAMS, NIH; David Norris, M.D., University of Colorado Health Sciences Center,
Denver; and Vera Price, M.D., University of California, San Francisco, in the preparation of this booklet. Mary Anne Dunkin was the author of this booklet. The mission of the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), a part of the Department of Health and Human Services’ National Institutes of Health (NIH), is to support research into the causes, treatment, and prevention of arthritis and musculoskeletal and skin diseases, the training of basic and clinical scientists to carry out this research, and the dissemination of information on research progress in these diseases. The National Institute of Arthritis and Musculoskeletal and Skin Diseases Information Clearinghouse is a public service sponsored by the NIAMS that provides health information and information sources. Additional information can be found on the NIAMS Web site at http://www.niams.nih.gov/. For Your Information This publication contains information about medications used to treat the health condition discussed in this booklet. When this booklet was printed, we included the most up-to-date (accurate) information available. Occasionally, new information on medication is released. For updates and for any questions about any medications you are taking, please contact the U.S. Food and Drug Administration at U.S. Food and Drug Administration
Toll Free: 888-INFO-FDA (888-463-6332) Website: http://www.fda.gov/ For updates and questions about statistics, please contact Centers for Disease Control and Prevention’s National Center for Health Statistics Toll Free: 800–232–4636 Website: http://www.cdc.gov/nchs This booklet is not copyrighted. Readers are encouraged to duplicate and distribute as many copies as needed. Additional copies of this booklet are available from National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Clearinghouse National Institutes of Health 1 AMS Circle Bethesda, MD 20892-3675 Phone: 301-495-4484 Toll Free: 877-22-NIAMS (226-4267) TTY: 301-565-2966 Fax: 301-718-6366 Email: [email protected]
Website: http://www.niams.nih.gov NIH Publication No. 09-5143
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Causes of specific types of hair loss Pattern baldness (androgenetic alopecia). In maleand female-pattern baldness, the time of growth shortens, and the hairs are not as thick or sturdy. With each growth cycle, the hairs become rooted more superficially and more easily fall out. Heredity likely plays a key role. A history of androgenetic alopecia on either side of your family increases your risk of balding. Heredity also affects the age at which you begin to lose hair and the developmental speed, pattern and extent of your baldness. Cicatricial (scarring) alopecia. This type of permanent hair loss occurs when inflammation damages and scars the hair follicle. This prevents new hair from growing. This condition can be seen in several skin conditions, including lupus erythematosus or lichen planus. It's not known what triggers or causes this inflammation.
Alopecia areata. This is classified as an autoimmune disease, but the cause is unknown. People who develop alopecia areata are generally in good health. A few people may have other autoimmune disorders, including thyroid disease. Some scientists believe that some people are genetically predisposed to develop alopecia areata and that a trigger, such as a virus or something else in the environment, sets off the condition. A family history of alopecia areata makes you more likely to develop it. With alopecia areata, your hair generally grows back, but you may lose and regrow your hair a number of times. Telogen effluvium. This type of hair loss is usually due to a change in your normal hair cycle. It may occur when some type of shock to your system — emotional or physical — causes hair roots to be pushed prematurely into the resting state. The affected growing hairs from these hair roots fall out. In a month or two, the hair follicles become active again and new hair starts to grow. Telogen effluvium may follow emotional distress, such as a death in the family or a physiological stress, such as a high fever, sudden or excessive weight loss, extreme diets, nutritional deficiencies, surgery, or metabolic disturbances. Hair typically grows back once the condition that caused it corrects itself, but it usually take months. Traction alopecia. Excessive hairstyling or hairstyles that pull your hair too tightly cause traction alopecia. If the pulling is stopped before there's scarring of your scalp and permanent damage to the root, hair usually grows back normally. Other causes of hair loss
Poor nutrition. Having inadequate protein or iron in your diet or poor nourishment in other ways can cause you to experience hair loss. Fad diets, crash diets and certain illnesses, such as eating disorders, can cause poor nutrition. Medications. Certain drugs used to treat gout, arthritis, depression, heart problems and high blood pressure may cause hair loss in some people. Taking birth control pills also may result in hair loss for some women. Disease. Diabetes and lupus can cause hair loss. Medical treatments. Undergoing chemotherapy or radiation therapy may cause you to develop alopecia. Under these conditions, healthy, growing (anagen) hairs can be affected. After your treatment ends, your hair typically begins to regrow. Hormonal changes. Hormonal changes and imbalances can cause temporary hair loss. This could be due to pregnancy, childbirth, discontinuation of birth control pills, the onset of menopause, or an overactive or underactive thyroid gland. The hair loss may be delayed by three months following a hormonal change, and it'll take another three months for new hair to grow back. During pregnancy, it's normal to have thicker, more luxuriant hair. It's also common to lose more hair than normal about three months after delivery. If a hormonal imbalance is associated with an overproduction of testosterone, there may be a thinning of hair over the crown of the scalp. Correcting hormonal imbalances may stop hair loss. Hair treatments. Chemicals used for dying, tinting, bleaching, straightening or permanent waves can cause hair to become damaged and break off if they
are overused or used incorrectly. Overstyling and excessive brushing also can cause hair to fall out if the hair shaft becomes damaged. Scalp infection. Infections, such as ringworm, can invade the hair and skin of your scalp, leading to hair loss. Once infections are treated, hair generally grows back. Ringworm, a fungal infection, can usually be treated with a topical or oral antifungal medication. Trichotillomania (hair-pulling disorder). Trichotillomania is a type of mental illness in which people have an irresistible urge to pull out their hair, whether it's from the scalp, their eyebrows or other areas of the body. Hair pulling from the scalp often leaves them with patchy bald spots on the head, which they may go to great lengths to disguise. Causes of trichotillomania are still being researched, and no specific cause has yet been found.