Version July 2025
INTRODUCTION —
Alopecia areata is a chronic immune-mediated disorder that targets anagen hair follicles and causes nonscarring hair loss. The condition most commonly presents with discrete, smooth patches of alopecia on the scalp but may also affect other hair-bearing areas, such as the eyebrows, eyelashes, beard, torso, and extremities (picture 1A-I). In severe alopecia areata, patients may experience complete loss of all scalp hair (historically referred to as "alopecia totalis") or complete loss of all hair on the body (historically called "alopecia universalis") (picture 2A-B).
The clinical manifestations and diagnosis of alopecia areata will be discussed here. The treatment of alopecia areata and the general approach to the evaluation and diagnosis of hair loss are reviewed separately.
●(See "Alopecia areata: Management".)
●(See "Evaluation and diagnosis of hair loss".)
EPIDEMIOLOGY —
Alopecia areata occurs worldwide, but the incidence and prevalence vary geographically and across subpopulations. Epidemiologic studies from the United States and the United Kingdom have estimated the overall incidence between 0.21 and 0.26 per 1000 patient-years (approximately 1 new case per 4000 population per year) [1-4] and the point prevalence at 0.16 to 0.21 percent (approximately 1 in 500 have active alopecia areata) [5-7]. The cumulative lifetime incidence (the lifetime risk) is around 2 percent (ie, 1 in 50 will develop alopecia areata at some time in their lives) [2,8].
The incidence and prevalence of alopecia areata are greater in non-White populations than in White populations [3,4,6]. The reason for this has not yet been established. Other social and environmental factors may also impact the frequency of alopecia areata [3,9-11].
Alopecia areata can occur for the first time at any age, with onset peaking during the third decade. The sex incidence is probably equal.
PATHOGENESIS —
Alopecia areata is an autoimmune disease in which hair follicles in the growth phase (anagen) prematurely transition to the nonproliferative involution (catagen) and resting (telogen) phases, leading to sudden hair shedding and inhibition of hair regrowth (figure 1). Unlike cicatricial alopecias, the inflammatory process in alopecia areata does not lead to permanent destruction of the hair follicle. (See "Evaluation and diagnosis of hair loss", section on 'Hair cycle' and "Evaluation and diagnosis of hair loss", section on 'Cicatricial alopecia'.)
The mechanisms leading to alopecia areata are not fully understood. Key events may include the loss of follicular immune privilege and the development of an associated T cell-mediated immune attack on cells within the hair bulb. Genetic susceptibility to alopecia areata also plays a role.
●Loss of immune privilege and immune dysregulation – The combination of loss of immune privilege at the hair follicle and other immunologic events is likely necessary for the development of alopecia areata [12].
The loss of immune privilege is postulated to involve unknown local stressors or events that inhibit the expression of hair follicle immune privilege "guardians" (eg, transforming growth factor [TGF]-beta and alpha-melanocyte-stimulating hormone [MSH]) and stimulate the expression of major histocompatibility complex class I polypeptide-related sequence A (MICA) on hair follicle cells.
These events can lead to activation of natural killer (NK) cells and local secretion of interferon (IFN)-gamma and interleukin (IL) 15. IFN-gamma stimulates the expression of major histocompatibility complex (MHC)-I protein on hair follicle cells, which may allow the presentation of previously hidden antigens to T cells. IL-15 inhibits the suppressive function of regulatory T cells and promotes proliferation of NK cells and T cells.
IFN-gamma and IL-15 activate target immune cells via the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway. The importance of this pathway is illustrated by the efficacy of JAK inhibitors for alopecia areata [13-15]. (See "Alopecia areata: Management", section on 'Other Janus kinase inhibitors'.)
A mouse study suggests that a defect in hair follicle immune privilege may not always be necessary, supporting a role for broader immune system dysfunction in the pathogenesis [16].
●Genetic predisposition – Familial and twin studies support a genetic predisposition to alopecia areata [17-19]. In one study of 206 patients with alopecia areata, 20 percent had a first-degree relative with the disease [17]. In a twin study, among 19 pairs of monozygotic twins, both twins had alopecia areata in 42 percent of twin pairs [19]. In contrast, among 31 pairs of dizygotic twins, both twins had alopecia areata in only 10 percent of twin pairs.
Genome-wide association studies have confirmed associations of alopecia areata with human leukocyte antigen (HLA) genes [20-26]. The HLA-DQB1*03 allele, among others, may be an important marker for susceptibility to alopecia areata [25,27].
A strong association of alopecia areata with genes within the ULBP gene cluster on chromosome 6q25.1 has also been detected. The ULBP cluster codes for activating ligands of the NKG2D receptor, supporting a role for NK cells and certain CD8+ T cells in the pathogenesis of this disease [20].
Several susceptibility loci that have been associated with other autoimmune diseases (eg, cytotoxic T lymphocyte-associated antigen 4 [CTLA-4], IL-2/IL-21, IL-2 receptor-alpha [IL-2RA]) have also been identified, indicating that alopecia areata may share a common pathway with other autoimmune diseases, such as type 1 diabetes mellitus and rheumatoid arthritis. (See "Pathogenesis of type 1 diabetes mellitus", section on 'Genetic susceptibility' and "HLA and other susceptibility genes in rheumatoid arthritis", section on 'Rheumatoid arthritis susceptibility genes outside the HLA region'.)
Other factors, such as infections, drugs, and vaccinations, have been proposed as contributors to episodes of alopecia areata. Some patients report severe stress, especially emotional stress, as a precipitating event, although many patients have no such history. Remote events, such as childhood trauma, have also been associated with the development of alopecia areata in adults [28]. Although associations between alopecia areata and low serum vitamin D levels have been reported, the clinical significance of this finding is uncertain [29-31].
CLINICAL FEATURES —
Key clinical features of alopecia areata include the pattern and speed of hair loss, exclamation point hairs, and associated nail dystrophy.
Hair loss — Alopecia areata most commonly occurs on the scalp but may occur on any hair-bearing area, such as the eyelashes, eyebrows, beard, extremities, or other areas (picture 1A-D, 1G-I). Hair loss is typically asymptomatic. Occasionally, pruritus, tingling, or a burning sensation precedes the loss of hair.
●Patchy alopecia – Patchy alopecia, which manifests as smooth, circular, discrete areas of complete hair loss that develop over a period of a few weeks, is the most common clinical presentation (picture 1B and picture 1A). The patches may remain discrete or enlarge and coalesce.
Initial sparing of white hairs is a proposed contributor to the perception of rapid graying of the hair in some adults with alopecia areata.
In males, involvement of the beard may be the initial or only manifestation (picture 1G). In a retrospective study of 55 adult males with new-onset alopecia areata limited to the beard and a mean follow-up period of 29 months (range 12 to 144 months), 46 percent developed scalp involvement, usually within 12 months [32].
●Extensive alopecia – In a subset of patients, patchy alopecia progresses to total loss of scalp hair (traditionally referred to as "alopecia totalis") or loss of all hair over the entire skin surface (traditionally referred to as "alopecia universalis") [6]. In a United States cross-sectional study of electronic records that identified 1812 patients with a diagnosis of alopecia areata, approximately 9 percent had a loss of all scalp hair and/or all body hair [6]. In some patients, extensive loss may develop rapidly. (See 'Course and prognosis' below.)
●Other patterns – Less common patterns of hair loss include the ophiasis pattern, the rare sisaipho pattern, and the diffuse alopecia areata variant.
•Ophiasis pattern – A band-like area of alopecia extending across the occipital scalp (picture 1F) [33].
•Sisaipho (ophiasis inversus) pattern – Alopecia involving the frontal, temporal, and parietal scalp but sparing hair along the scalp periphery (picture 3), resembling male pattern hair loss [34].
•Diffuse alopecia areata – Generalized thinning of scalp hair has been reported as a rare variant. In some patients, diffuse alopecia areata may present as acute, extensive hair loss that is followed by regrowth of hair within several months (acute diffuse and total alopecia) (picture 4) [35,36]
Exclamation point hairs — Exclamation point hairs, short broken hairs for which the proximal end of the hair is narrower than the distal end, are a common and pathognomonic finding in alopecia areata (picture 5A-B) [37]. Exclamation point hairs are typically found at the edges of expanding patches and can be extracted with minimal traction. (See 'Diagnosis' below.)
Nail abnormalities — Nail involvement is estimated to occur in 10 to 20 percent of patients with alopecia areata, with the potential for more frequent nail involvement in patients with severe disease [37]. Nail disease may precede, follow, or coexist with active hair loss. Nail involvement has been associated with greater severity of disease [38]. (See "Overview of nail disorders".)
Nail findings may include [38]:
●Pitting of the nail plate (most common) (picture 6)
●Trachyonychia (roughening of the nail plate) (picture 7)
●Onychorrhexis (longitudinal fissuring of the nail plate)
●Red spotting on the lunulae
●Onycholysis (separation of the distal nail plate from the nail bed)
●Onychomadesis (detachment of the proximal nail plate from the nail bed)
COURSE AND PROGNOSIS
●Overview – Alopecia areata may resolve spontaneously, improve, persist, recur, or progress to complete loss of all scalp and/or body hair. The initial clinical presentation appears to play an important role in prognosis. Limited patchy alopecia with onset in adulthood appears to have the most favorable prognosis. It has been estimated that around 50 percent of patients with limited patchy alopecia will recover within one year, although most experience more than one episode of the disease [39-42].
Data on risk of progression to complete loss of all scalp hair and/or body hair are limited. In a retrospective population-based study in Olmsted County, Minnesota, that included 292 patients diagnosed with alopecia areata during a 15-year period (1975 to 1989), 7 percent had documentation of progression to complete scalp and/or body hair loss during the study period [1]. Higher rates of progression have also been reported, particularly among patients presenting with greater disease severity and children [43].
●Prognostic factors – The following factors have been associated with increased risk for a poor prognosis or high likelihood of relapse [39]:
•Onset in childhood [43,44]
•Severe disease, especially complete loss of scalp hair with or without loss of body hair [43]
•Duration of more than one year [45]
•Band-like involvement of the peripheral temporal and occipital scalp (ophiasis pattern) [44]
•Nail disease [44,45]
•Atopy [46,47]
•Family history of alopecia areata [47,48]
Disease severity appeared to be a relevant factor in a study of 191 patients with alopecia areata who presented to a university dermatology clinic in Italy between 1983 and 1990 and who were contacted by phone in 2005 to give self-reports of their clinical status [43]. Patients with less severe disease at presentation were more likely to report being free of disease at follow-up (68 percent with less than 25 percent hair loss initially, 32 percent with 25 to 50 percent hair loss initially, 8 percent with more than 50 percent hair loss initially). Patients with more severe disease at the time of presentation were also more likely to report worsening patterns of alopecia.
●Hair regrowth – Patients may exhibit persistent areas of alopecia and patches with regrowth of hair simultaneously. Regrowth sometimes begins with the appearance of fine, white vellus hairs (picture 8).
ASSOCIATED DISORDERS —
Alopecia areata has been associated with other dermatologic and nondermatologic disorders.
●Dermatologic and systemic disorders – Disease association studies support links between alopecia areata and atopic and certain autoimmune conditions. For example:
•A population-based cohort study that analyzed data from 8051 adults with a new diagnosis of alopecia areata and over 32,000 matched controls in a primary care database in the United Kingdom found a higher prevalence of both atopic and autoimmune disease in the alopecia areata group compared with the control group (37 versus 27 percent for atopic disease and 12 versus 8 percent for autoimmune disease) [49]. In particular, the alopecia areata group demonstrated increased risk for new-onset atopic dermatitis (adjusted hazard ratio [aHR] 1.91, 95% CI 1.67-2.19), allergic rhinitis (aHR 1.32, 95% CI 1.14-1.54), autoimmune hypothyroidism (aHR 1.65, 95% CI 1.35-2.02), systemic lupus erythematosus (aHR 4.51, 95% CI 1.88-10.82), and vitiligo (aHR 2.39, 95% CI 1.49-3.82).
•A nationwide study from Taiwan that included 4334 patients with alopecia areata found associations with vitiligo (odds ratio [OR] 5.23, 95% CI 3.06-9.00), lupus erythematosus (OR 3.95, 95% CI 3.05-5.11), psoriasis (OR 2.80, 95% CI 2.24-3.50), atopic dermatitis (OR 2.24, 95% CI 1.95-2.58), thyroid disease (OR 1.89, 95% CI 1.68-2.13), and allergic rhinitis (OR 1.29, 95% CI 1.18-1.41) among all patients compared with control subjects and differences in disease associations based upon the age of onset of alopecia areata [50].
An increased risk for type 1 diabetes mellitus has been reported in relatives of individuals with alopecia areata [51]. However, there does not appear to be an increased risk for diabetes among those with the disease.
●Genetic disorders – Genetic disorders associated with an increased risk for alopecia areata include Down syndrome (trisomy 21, MIM #190685) and polyglandular autoimmune syndrome type 1 (MIM #240300) [52-55]. The latter is a rare autosomal recessive disorder that results from a mutation in the autoimmune regulator (AIRE) gene on chromosome 21. In a study of 1000 institutionalized patients with Down syndrome, the prevalence of alopecia areata was approximately 6 percent [52]. Approximately one-third of patients with polyglandular autoimmune syndrome type 1 have alopecia areata [55,56]. (See "Down syndrome: Clinical features and diagnosis" and "Causes of primary adrenal insufficiency (Addison disease)", section on 'Type 1 (monogenic)'.)
●Psychosocial disorders – Hair loss can be distressing for many patients with alopecia areata. The disease is often associated with impaired health-related quality of life, which can be profound and which does not necessarily correlate well with the severity of hair loss [57,58]. Loss of self-esteem, altered self-image, emotional and psychosocial difficulties, and psychiatric comorbidities are common features, and assessment of their impact on the individual patient (and their family) is an important facet of management.
Overall, data also support an association of alopecia areata with psychiatric disorders, such as depression and anxiety, although not all studies have reached this conclusion [8,59-61]. The findings of a systematic review and meta-analysis that included eight studies with a total of over 6000 patients with alopecia areata and over 20,0000 control individuals support associations with anxiety and depression (pooled OR 2.50, 95% CI 1.54-4.06 and pooled OR 2.71, 95% CI 1.52-4.82, respectively) [60]. Of note, the four studies that did not report an association with anxiety or depression were performed in children or in patients with less severe hair loss.
Further study is necessary to clarify the nature of the relationship between alopecia areata and psychiatric disorders. A population-based retrospective study in the United Kingdom that assessed records from approximately 12 million patients who were followed for up to 26 years found a bidirectional association between alopecia areata and major depressive disorder [62]. In the analysis, major depressive disorder was associated with an increased risk for subsequent development of alopecia areata (hazard ratio [HR] 1.90, 95% CI 1.67-2.15). Similarly, alopecia areata was associated with an increased risk for subsequent development of major depressive disorder (HR 1.34, 95% CI 1.23-1.46).
HISTOPATHOLOGY —
The pathologic findings in alopecia areata vary with the acuity of hair loss in the biopsied area [63].
●Acute – In sites of acute disease with active hair shedding, the presence of intense peribulbar lymphocytic inflammatory infiltrates surrounding anagen follicles is characteristic. These infiltrates are often described as resembling swarms of bees. In addition, signs of follicular insult may be seen, such as follicular edema, cellular necrosis, microvesiculation, and pigment incontinence.
●Chronic – Follicular miniaturization characterizes the findings in sites of chronic alopecia. The inflammatory infiltrate is variable and usually less pronounced than in early lesions. In addition, because of the transition of anagen follicles to the catagen and telogen stages in alopecia areata, biopsy specimens from areas of chronic involvement reveal high proportions of follicles in catagen or telogen stages. (See 'Pathogenesis' above.)
DIAGNOSIS —
The patient history and physical examination are usually sufficient for diagnosis. Clinical features that should raise suspicion for alopecia areata include smooth, discrete areas of rapid hair loss with absent or minimal erythema. (See 'Clinical features' above.)
History — The patient history should include assessment of the onset and duration of hair loss as well as associated symptoms. In most patients, alopecia areata presents as sudden, asymptomatic hair loss. Given the potential for spontaneous resolution and relapse, patients may report a history of previous hair loss.
The general approach to the patient interview for hair loss is discussed in detail separately. (See "Evaluation and diagnosis of hair loss", section on 'Patient interview'.)
Physical examination — The physical examination should include careful examination of the hair, scalp, and other hair-bearing areas to assess the distribution and extent of hair loss and to detect findings suggestive of other hair or scalp diseases.
●Supportive findings – Smooth, round, or irregular areas of nonscarring hair loss are typical of alopecia areata. (See "Evaluation and diagnosis of hair loss", section on 'Physical examination'.)
Close visual inspection may reveal exclamation point hairs, a pathognomonic finding of alopecia areata (picture 5A). However, exclamation point hairs are sometimes difficult to detect, and their absence does not exclude the diagnosis. The examination of the scalp should also include assessment for follicular orifices within patches of alopecia, as the absence of these suggests cicatricial (scarring) alopecia. (See "Evaluation and diagnosis of hair loss", section on 'Visual inspection'.)
Performance of a hair pull test can be useful for confirming active hair loss. (See "Evaluation and diagnosis of hair loss", section on 'Hair pull test'.)
Examination of the nails may yield nail abnormalities that support the diagnosis. (See 'Nail abnormalities' above.)
●Dermoscopy – Dermoscopic examination of the hair and scalp (also known as trichoscopy) can be helpful for visualizing findings consistent with alopecia areata [64-67]. Dermoscopic findings include yellow dots, short vellus hairs, black dots, tapering hairs, and broken hairs (table 1 and picture 9A-C). Dystrophic hair fibers with monilethrix-like constrictions also may be seen [68]. (See "Overview of dermoscopy of the hair and scalp".)
Scalp biopsy — Scalp biopsies are typically reserved for patients in whom the diagnosis is uncertain despite a careful history and physical examination.
●Site – Ideally, biopsies are to be taken from the edge of a patch of active hair loss and positioned to include at least a few remaining hairs.
●Number and type of specimens – Obtaining specimens that allow for both horizontal and vertical sectioning is preferred for histopathologic examination [69]. This is typically done by obtaining two adjacent 4 mm punch biopsy specimens that extend into the subcutaneous fat. Horizontal sections will provide information on the hair cycle, numbers of hair follicles, and inflammation. Vertical sections are particularly helpful when the differential includes a scarring alopecia. (See "Skin biopsy techniques", section on 'Punch biopsy' and 'Histopathology' above.)
ADDITIONAL EVALUATION —
Patients with alopecia areata may benefit from an assessment for signs or symptoms of thyroid disease and other associated disorders. (See 'Associated disorders' above.)
Thyroid studies — Because of the association between alopecia areata and autoimmune thyroid disease and the relatively high frequency of thyroid disease in the general population, an assessment for thyroid disease is an important component of patient management [70,71]. Approaches to thyroid assessment vary. Whereas some clinicians limit testing to patients with signs or symptoms concerning for thyroid disease, others advise laboratory testing for all patients. (See 'Associated disorders' above.)
We assess all adults and children with alopecia areata for signs and symptoms of thyroid disease. The risk of thyroid disease is probably greater in those with severe forms of alopecia areata and, compared with that in the age-matched population, in children [72,73]. (See 'Associated disorders' above and "Diagnosis of and screening for hypothyroidism in nonpregnant adults", section on 'Signs and/or symptoms of hypothyroidism present' and "Diagnosis of hyperthyroidism", section on 'Symptoms'.)
In the presence of clinical features of thyroid disease, patients should have their thyroid-stimulating hormone (TSH) level checked and addressed if abnormal. The assessment of thyroid function tests in patients at risk for thyroid disease who are not known to have thyroid disease and do not have symptoms of thyroid disease is controversial [74]. (See "Diagnosis of and screening for hypothyroidism in nonpregnant adults", section on 'Screening in the absence of signs and/or symptoms of hypothyroidism'.)
Thyroid disorders may develop later in the course of alopecia areata. If TSH testing is performed in patients with alopecia areata, it should be recognized that a normal result does not exclude disease in the future, and the subsequent development of symptoms of thyroid disease should prompt re-evaluation [69,75]. Testing for thyroid antibodies may have some predictive value in identifying those at increased risk. (See "Laboratory assessment of thyroid function".)
A retrospective study suggests that laboratory testing for thyroid dysfunction in children with alopecia areata may be more likely to be abnormal in certain populations [76]. Among 298 children (ages 10 months to 19 years) with alopecia areata who had thyroid function studies performed, 59 (20 percent) had abnormal results. Factors associated with increased risk for abnormalities included a personal history of Down syndrome or atopy and a family history of thyroid disease. Age, disease duration, pattern of alopecia, and a diagnosis of autoimmune disease were not associated with abnormal thyroid studies.
Other — Adults and children with clinical signs or symptoms suggestive of other autoimmune diseases should be evaluated for those disorders. In the absence of such features, routine testing for other autoimmune diseases (eg, celiac disease) is not advised [77]. (See 'Associated disorders' above.)
DIFFERENTIAL DIAGNOSIS —
The differential diagnosis of alopecia areata primarily includes other causes of nondiffuse hair loss, such as androgenetic alopecia, cicatricial alopecias, secondary syphilis, tinea capitis, triangular alopecia, and trichotillomania. (See "Evaluation and diagnosis of hair loss".)
●Androgenetic alopecia – Androgenetic alopecia occurs in characteristic male and female patterns and characteristically manifests with slow, progressive hair thinning, rather than the rapid development of areas of complete hair loss that is typical of alopecia areata (picture 10A-B). The rare sisaipho pattern of alopecia areata can resemble male pattern androgenetic alopecia (picture 3). A biopsy can distinguish androgenetic alopecia from alopecia areata in challenging cases. (See "Male pattern hair loss (androgenetic alopecia in males): Pathogenesis, clinical features, and diagnosis" and "Female pattern hair loss (androgenetic alopecia in females): Pathogenesis, clinical features, and diagnosis".)
●Cicatricial (scarring) alopecia – Cicatricial alopecia may be the result of diverse pathologies, such as lichen planopilaris (picture 11), frontal fibrosing alopecia (picture 12), central centrifugal cicatricial alopecia (picture 13), and discoid lupus erythematosus (picture 14). All are characterized by permanent destruction of hair follicles.
Hair loss is usually patchy, and there is loss of follicular orifices in sites of alopecia, a finding indicative of scarring. Additional features vary depending on the primary pathology and may include erythema, scaling, follicular plugging, and pustulation. Skin biopsies are often indicated to confirm a diagnosis of cicatricial alopecia. (See "Evaluation and diagnosis of hair loss", section on 'Cicatricial alopecia'.)
●Secondary syphilis – Areas of patchy hair loss may appear in secondary syphilis. The patches are often described to have a "moth-eaten" appearance rather than the smooth and discrete areas characteristic of alopecia areata (picture 15). Serologic testing for syphilis can confirm the diagnosis. (See "Syphilis: Screening and diagnostic testing".)
●Tinea capitis – Tinea capitis typically presents with scaly patches of hair loss on the scalp and is most common in children (picture 16A-B). Inflammation and cervical lymphadenopathy may also be present. Tinea capitis should always be considered in children presenting with patchy hair loss.
In contrast, alopecia areata produces smooth areas of hair loss that lack scale. A potassium hydroxide (KOH) preparation or fungal culture can confirm a diagnosis of tinea capitis. (See "Tinea capitis: Clinical features and diagnosis".)
●Trichotillomania – Trichotillomania is a disorder in which individuals compulsively pull hair from the scalp or other body areas. The disorder produces unusual patterns of broken hairs of varying length, which leads to a characteristic "wire brush" feel as compared with the smooth hair loss of alopecia areata (picture 17A-B).
The history and physical examination are usually sufficient for diagnosis. However, a biopsy in the area of alopecia can help to differentiate alopecia areata from trichotillomania disorders when necessary. (See "Skin picking (excoriation) disorder and related disorders", section on 'Trichotillomania'.)
●Triangular alopecia – Triangular alopecia is a developmental abnormality of hair follicles that presents in infancy or childhood as a triangular or round patch of hair loss near the frontotemporal hair line (picture 18). The disorder may be unilateral or bilateral and persists throughout life. Close examination and biopsy specimens reveal vellus hairs.
The diffuse variant of alopecia areata may be difficult to distinguish clinically from telogen effluvium when hair loss is not severe. A biopsy can be used to differentiate between the two disorders. In addition, more pronounced hair thinning in the bitemporal region is more consistent with telogen effluvium than alopecia areata, and a positive hair pull test in alopecia areata may reveal both dystrophic anagen and telogen hairs, in contrast to the isolated telogen hairs in telogen effluvium [35]. (See "Telogen effluvium".)
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Alopecia".)
INFORMATION FOR PATIENTS —
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Hair loss (The Basics)")
●Beyond the Basics topics (see "Patient education: Alopecia areata (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Epidemiology – Alopecia areata is a chronic, often relapsing disorder characterized by nonscarring hair loss (picture 1A-D, 1F-I). The disorder can affect individuals of any age. (See 'Epidemiology' above.)
●Pathogenesis – The pathogenesis of alopecia areata is thought to involve autoimmune-mediated disruption of the normal hair cycle, leading to the inhibition of normal hair growth. A loss of the immune-privileged status of the hair follicle is considered a key pathogenic event. Genetic predisposition also contributes to the development of the disorder. (See 'Pathogenesis' above.)
●Clinical features – Patients with alopecia areata most often present with smooth, circular, discrete areas of complete hair loss that develop over a period of a few weeks. Exclamation point hairs, short broken hairs for which the proximal end of the hair is narrower than the distal end, are common findings (picture 5A). Patients may also have associated nail abnormalities. (See 'Clinical features' above.)
●Disease course – The course of alopecia areata is unpredictable. Many patients with limited patchy hair loss experience regrowth, but recurrence is common. A minority of patients progress to total loss of scalp hair or loss of all hair (picture 2A-B). Poor prognostic factors for alopecia areata include young age of onset, severe disease, long duration of disease, ophiasis pattern, nail disease, and an atopic history. (See 'Course and prognosis' above.)
●Associated disorders – Alopecia areata has been associated with autoimmune diseases and other disorders. Patients with clinical signs or symptoms suggestive of other autoimmune diseases (eg, thyroid disease) should be evaluated for those disorders. (See 'Associated disorders' above and 'Additional evaluation' above.)
●Diagnosis – The diagnosis of alopecia areata is often made based on the patient history and physical examination. Biopsies can be performed when the diagnosis is uncertain. (See 'Diagnosis' above.)
