Psychiatric disorders – Anxiety, personality disorders, depression, and paranoid disorders
Stressful life events inthe 6 months before onset
Alopecia areata canbe classified according to its pattern, as follows:
Reticular – Hair loss ismore extensive andthe patches coalesce
Ophiasis – Hair loss is localized tothe sides and lower backofthe scalp
Sisaipho (ophiasis spelled backwards) – Hair loss spares the sides andbackofthe head
Alopecia totalis – 100% hair loss onthe scalp
Alopecia universalis – Complete loss of hair onall hair-bearing areas
Nail involvement, predominantly ofthe fingernails, isfoundin 6.8-49.4% of patients, most commonly in severe cases. Pitting isthemost common; other reported abnormalities have included trachyonychia, Beau lines, onychorrhexis, onychomadesis, koilonychias, leukonychia, and red lunulae
See Clinical Presentation formore detail.
Diagnosis usually canbemadeon clinical grounds. A scalp biopsy seldom is needed, butitcanbe helpful whenthe clinical diagnosis is less certain.
See Workup formore detail.
Treatment isnot mandatory, becausethe condition is benign, and spontaneous remissions and recurrences are common. Treatment canbe topical or systemic. [ 1 ]
Intralesional corticosteroid therapy is usually recommended for alopecia areata with less than 50% involvement. Administration isas follows:
Injections are administered intradermally usinga 3-mL syringe anda 30-gauge needle
Triamcinolone acetonide (Kenalog) isusedmost commonly; concentrations vary from 2.5-10 mg/mL
The lowest concentration isusedonthe face
A concentration of 5 mg/mL is usually sufficient onthe scalp
Less than 0.1 mL is injected per site, and injections are spread outto cover the affected areas (approximately 1 cm between injection sites)
Injections are administered every 4-6 weeks
Topical corticosteroid therapy canbe useful, especially in children who cannot tolerate injections. It is administered as follows:
Fluocinolone acetonide cream 0.2% (Synalar HP) twice daily or betamethasone dipropionate cream 0.05% (Diprosone) hasbeen used
For refractory alopecia totalis or alopecia universalis, 2.5 g of clobetasol propionate under occlusion witha plastic film 6 days/wk for 6 months helped a minority of patients
Treatment must be continued fora minimum of 3 months before regrowth canbe expected, and maintenance therapy often is necessary
Systemic corticosteroids (ie, prednisone) arenotan agent of choice for alopecia areata becauseofthe adverse effects associated withboth short- and long-term treatment. Some patients may experience initial benefit, butthe dose needed to maintain cosmetic growth is usually so high that adverse effects are inevitable, andmost patients relapse after discontinuation of therapy.
Topical immunotherapy [ 2 ] is defined asthe induction and periodic elicitation ofan allergic contact dermatitis by topical application of potent contact allergens
Commonly used agents include squaric acid dibutylester (SADBE) and diphencyprone (DPCP) [ 3 ]
Both short-contact and overnight treatments havebeen used
Anthralin concentrations varied from 0.2-1%
Minoxidil appears tobe effective inthe treatment of extensive disease (50-99% hair loss) butisoflittle benefit in alopecia totalis or alopecia universalis
The 5% solution appears tobemore effective
No morethan 25 drops are applied twice per day regardless ofthe extent ofthe affected area
Initial regrowth canbe seen within 12 weeks, but continued application is needed to achieve cosmetically acceptable regrowth
Psoralen plus UV-A
Both systemic and topical PUVA therapies havebeen used
20-40 treatments usually are sufficient inmost cases
Most patients relapse within afew months (mean, 4-8 months) after treatment is stopped
Topical cyclosporine has shown limited efficacy
Methotrexate, withor without systemic corticosteroids, has shown mixed results [ 4 , 5 ]
Dermatography hasbeenusedto camouflage the eyebrows of patients with alopecia areata; on average, 2-3 sessions lasting 1 hour eachwere required foreach patient
Hairpieces are useful for patients with extensive disease
See Treatment and Medication formore detail.
Alopecia areata isa recurrent nonscarring type of hair loss thatcan affect any hair-bearing area. Clinically, alopecia areata can manifest manydifferent patterns. Although medically benign, alopecia areata can cause tremendous emotional and psychosocial distress in affected patients andtheir families.
The exact pathophysiology of alopecia areata remains unknown. The most widely accepted hypothesis isthat alopecia areata isa T-cell–mediated autoimmune condition thatismost likely to occur in genetically predisposed individuals. [ 6 ]
Much evidence supports the hypothesis that alopecia areata isan autoimmune condition. The process appears tobe T-cell mediated, but antibodies directed to hair follicle structures alsohavebeenfoundwith increased frequency in alopecia areata patients compared withcontrol subjects. Using immunofluorescence, antibodies to anagen-phase hair follicles werefoundinasmanyas 90% of patients with alopecia areata compared with less than 37% ofcontrol subjects. The autoantibody response is heterogeneous and targets multiple structures ofthe anagen-phase hair follicle. The outer root sheath isthe structure targeted most frequently, followed bythe inner root sheath, the matrix, andthe hair shaft. Whether these antibodies play a direct role inthe pathogenesis or whether theyarean epiphenomenon isnot known.
Histologically, lesional biopsy findings of alopecia areata show a perifollicular lymphocytic infiltrate around anagen-phase hair follicles. The infiltrate consists mostly of T-helper cells and, toa lesser extent, T-suppressor cells. CD4 + and CD8 + lymphocytes likely play a prominent role becausethe depletion ofthese T-cell subtypes resultsin complete or partial regrowth of hair inthe Dundee experimental bald rat (DEBR) model of alopecia areata. The animals subsequently lose hair again once the T-cell population is replete. The fact thatnotall animals experience complete regrowth suggests thatother mechanisms likely are involved. Total numbers of circulating T lymphocytes havebeen reported atboth decreased and normal levels.
Studies in humans also reinforce the hypothesis of autoimmunity. Studies have shown that hair regrows when affected scalp is transplanted onto SCID (severe combined immunodeficiency) mice thatare devoid of immune cells. Autologous T lymphocytes isolated froman affected scalp were cultured with hair follicle homogenates and autologous antigen-presenting cells. Following initial regrowth, injection ofthe T lymphocytes intothe grafts resulted in loss of regrown hairs. Injections of autologous T lymphocytes thatwerenot cultured with follicle homogenates didnot trigger hair loss.
A similar experiment on nude (congenitally athymic) mice failed to trigger hair loss in regrown patches of alopecia areata after serum from affected patients was injected intravenously intothe mice. However, thesame study showed that mice injected with alopecia areata serum showed an increased deposition of immunoglobulin and complement in hair follicles ofboth grafted and nongrafted skin compared with mice injected withcontrol serum, which showed no deposition.
In addition, research has shown that alopecia areata canbe induced using transfer of grafts from alopecia areata–affected mice onto normal mice. Transfer of grafts from normal mice to alopecia areata–affected mice similarly resulted in hair loss inthe grafts.
Clinical evidence favoring autoimmunity suggests that alopecia areata is associated withother autoimmune conditions, themost significant ofwhichare thyroid diseases and vitiligo (see History). For instance, ina retrospective cross-sectional review of 2115 patients with alopecia areata who presented to academic medical centers in Boston overan 11-year period, comorbid autoimmune diagnoses included thyroid disease (14.6%), diabetes mellitus (11.1%), inflammatory bowel disease (6.3%), systemic lupus erythematosus (4.3%), rheumatoid arthritis(3.9%), and psoriasis and psoriatic arthritis (2.0%). Other comorbid conditions found included atopy (allergic rhinitis, asthma, and/or eczema; 38.2%), contact dermatitis andother eczema (35.9%), mental health problems (depression or anxiety; 25.5%), hyperlipidemia (24.5%), hypertension (21.9%), and GERD (17.3%). [ 7 , 8 ]
In conclusion, the beneficial effect of T-cell subtype depletion on hair growth, the detection of autoantibodies, the ability to transfer alopecia areata from affected animals to nonaffected animals, andthe induction of remission by grafting affected areas onto immunosuppressed animals are evidence in favor ofan autoimmune phenomenon. Certain factors within the hair follicles, and possibly inthe surrounding milieu, trigger an autoimmune reaction. Some evidence suggests a melanocytic target within the hair follicle. Adding or subtracting immunologic factors profoundly modifies the outcome of hair growth.
Many factors favor a genetic predisposition for alopecia areata. The frequency of positive family history for alopecia areata in affected patients hasbeen estimated tobe 10-20% compared with 1.7% incontrol subjects. [ 6 ] The incidence is higher in patients withmore severe disease (16-18%) compared with patients with localized alopecia areata (7-13%). Reports of alopecia areata occurring in twins alsoareof interest. No correlation hasbeenfound between the degree of involvement of alopecia areata andthe type of alopecia areata seen in relatives.
Several genes havebeen studied anda large amount of research has focused on human leukocyte antigen. Two studies demonstrated that human leukocyte antigen DQ3 (DQB1*03) wasfoundinmorethan 80% of patients with alopecia areata, which suggests thatitcanbea marker for general susceptibility to alopecia areata. The studies alsofoundthat human leukocyte antigen DQ7 (DQB1*0301) and human leukocyte antigen DR4 (DRB1*0401) were present significantly morein patients with alopecia totalis and alopecia universalis. [ 9 , 10 , 11 ]
Another gene of interest isthe interleukin 1 receptor antagonist gene, which may correlate with disease severity. Finally, the high association of Down syndrome with alopecia areata suggests involvement ofa gene located on chromosome 21.
In summary, genetic factors likely play an important role in determining susceptibility and disease severity. Alopecia areata is likely tobethe result of polygenic defects rather thana single gene defect. The role of environmental factors in initiating or triggering the condition is yet tobe determined.
Interleukin 1 and tumor necrosis factor were shown tobe potent inhibitors of hair growth in vitro. Subsequent microscopic examination ofthese cultured hair follicles showed morphologic changes similar tothose seen in alopecia areata.
Another areaof interest concerns the modification of perifollicular nerves. The fact that patients with alopecia areata occasionally report itching or pain on affected areas raises the possibility of alterations inthe peripheral nervous system. Circulating levels ofthe neuropeptide calcitonin gene-related peptide (CGRP) were decreased in 3 patients with alopecia areata compared withcontrol subjects. CGRP has multiple effects onthe immune system, including chemotaxis and inhibition of Langerhans cell antigen presentation and inhibition of mitogen-stimulated T-lymphocyte proliferation.
CGRP also increases vasodilatation and endothelial proliferation. Similar findings were reported inanother study, inwhich decreased cutaneous levels of substance P andof CGRP butnotof vasoactive intestinal polypeptide werefoundin scalp biopsy specimens. The study also noted a lower basal blood flow and greater vasodilatation following intradermal CGRP injection in patients with alopecia areata compared withcontrol subjects. More studies are needed to shed light onthe significance ofthese findings.
Other hypotheses havebeen proposed to explain the pathophysiology of alopecia areata, butmore evidence is needed to support them. Alopecia areata was believed to possibly havean infectious origin, butno microbial agent hasbeen isolated consistently in patients. Many efforts havebeenmadeto isolate cytomegalovirus, butmost studies havebeen negative. [ 12 ]
Prevalence inthe general population is 0.1-0.2%. The lifetime risk of developing alopecia areata is estimated tobe 1.7%. Alopecia areata is responsible for 0.7-3% of patients seen by dermatologists. [ 13 , 14 ]
All races are affected equally by alopecia areata; no increase in prevalence hasbeenfoundina particular ethnic group.
Data concerning the sex ratio for alopecia areata vary slightly inthe literature. In one study including 736 patients, a male-to-female ratio of 1:1 was reported. [ 15 ] In another study ona smaller numberof patients, a slight female preponderance was seen.
Alopecia areata can occur atany age from birth tothe late decades of life. Congenital cases havebeen reported. Peak incidence appears to occur from age 15-29 years. As manyas 44% of people with alopecia areata have onset at younger than 20 years. Onset in patients older than 40 years is seen in less than 30% of patients with alopecia areata.[#IntroductionMortalityMorbidity]
Alopecia areata isa benign condition andmost patients are asymptomatic; however, itcan cause emotional and psychosocial distress in affected individuals. Self-consciousness concerning personal appearance can become important. Openly addressing these issues with patients is important in helping them cope withthe condition.
The natural history of alopecia areata is unpredictable. Most patients haveonlyafew focal areas of alopecia, and spontaneous regrowth usually occurs within 1 year. Estimates indicate less than 10% of patients experience extensive alopecia and less than 1% have alopecia universalis. Patients with extensive long-standing conditions are less likely to experience significant long-lasting regrowth.
Adverse prognostic factors include nail abnormalities, atopy, onset ata young age, and severe forms of alopecia areata.
Patient education isa key factor in alopecia areata. Inform patients ofthe chronic relapsing nature of alopecia areata. Reassure patients thatthe condition is benign and does not threaten their general health.
Most patients try tofindan explanation about why thisis happening to them. Reassure these patients thattheyhave done nothing wrong andthatitisnottheir fault.
Inform patients that expectations regarding therapy shouldbe realistic.
Support groups areavailableinmany cities; itis strongly recommended that patients be urged to contact the National Alopecia Areata Foundation at 710 C St, Suite 11, San Rafael, CA 94901 or view the Web site.
Many patients are reluctant touse hairpieces ortakepartin support groups because, at first, these often are perceived as last-resort options. Take thetimeto discuss the options with patients becausetheyareof great benefit.
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Chantal Bolduc, MD, FRCPC Assistant Professor, Department of Dermatology, University of Montreal Faculty of Medicine; Physician, Innovaderm Research, Inc
Chantal Bolduc, MD, FRCPC isa member ofthe following medical societies: Canadian Dermatology Foundation
Disclosure: Nothing to disclose.
Harvey Lui, MD, FRCPC Professor and Head, Department of Dermatology and Skin Science, Vancouver General Hospital, University of British Columbia; Medical Director, The Skin Centre, Lions Laser Skin Centre and Psoriasis and Phototherapy Clinic, Vancouver General Hospital
Harvey Lui, MD, FRCPC isa member ofthe following medical societies: Canadian Medical Association , American Society for Photobiology , Photomedicine Society , European Academy of Dermatology and Venereology , National Psoriasis Foundation , Canadian Dermatology Association , College of Physicians and Surgeons of British Columbia , North American Hair Research Society , Canadian Dermatology Foundation , American Academy of Dermatology , American Society for Laser Medicine and Surgery
Disclosure: Received consulting fee from Astellas for review panel membership; Received consulting fee from Amgen/Wyeth for speaking and teaching; Received honoraria from LEO Pharma for speaking and teaching; Received grant/research funds from LEO Pharma for investigator; Received grant/research funds from Galderma for other.
Jerry Shapiro, MD, FRCPC Clinical Associate Professor, Department of Medicine, Division of Dermatology, University of British Columbia Faculty of Medicine, Canada
Disclosure: Nothing to disclose.
Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD isa member ofthe following medical societies: American Academy of Dermatology , Texas Medical Association , Association of Military Dermatologists , Texas Dermatological Society
Disclosure: Nothing to disclose.
Lester F Libow, MD Dermatopathologist, South Texas Dermatopathology Laboratory
Lester F Libow, MD isa member ofthe following medical societies: American Academy of Dermatology , American Society of Dermatopathology , Texas Medical Association
Disclosure: Nothing to disclose.
Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine
Dirk M Elston, MD isa member ofthe following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
Leonard Sperling, MD Chair, Professor, Department of Dermatology, Uniformed Services University ofthe Health Sciences
Leonard Sperling, MD isa member ofthe following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.