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Alopecia Areata Treatment & Management

  • Author: Chantal Bolduc, MD, FRCPC; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Apr 08, 2016
 

Approach Considerations

See the treatment algorithm below.

Treatment algorithm for alopecia areata. Treatment algorithm for alopecia areata.

Treatment is not mandatory because the condition is benign, and spontaneous remissions and recurrences are common. Treatments used are believed to stimulate hair growth, but no evidence indicates they can influence the ultimate natural course of alopecia areata. Treatment modalities usually are considered first according to the extent of hair loss and the patient's age.

Assessment of the efficacy of a treatment must be considered with care because the condition is highly unpredictable in presentation, evolution, and response to treatment. Little data exist regarding the natural evolution of the condition. For example, in patients with less than 40% scalp involvement, a study showed no benefit with treatment (minoxidil 1% and topical immunotherapy) over placebo.[19] The high spontaneous remission rate makes clearly assessing the true efficacy of a therapy difficult unless appropriate controls with placebo treatment are studied.

For patients with extensive alopecia areata (>40% hair loss), little data exist on the natural evolution. The rate of spontaneous remission appears to be less than in patients with less than 40% involvement. Vestey and Savin[20] reviewed 50 patients with extensive alopecia areata. Of the 50 patients, 24% experienced spontaneous complete or nearly complete regrowth at some stage during the observation period of 3-3.5 years. The relapse rate is high in patients with severe forms of alopecia areata.

Patients with alopecia totalis or alopecia universalis usually have a poorer prognosis, and treatment failure is seen in most patients with any therapy.

Because alopecia areata is believed to be an autoimmune condition, different immunomodulators have been used to treat this condition. Additional treatment options for alopecia areata include minoxidil and other treatment modalities.

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Topical Treatments

Corticosteroids

Corticosteroid therapies can include intralesional injections or topical application.

Intralesional steroids

For intralesional steroids, few studies are available regarding efficacy; however, they are used widely in the treatment of alopecia areata. Intralesional steroids are the first-line treatment in localized conditions and are usually superior to topical corticosteroids.[21]

In a study including 84 patients, regrowth on treated areas was present in 92% of patients with patchy alopecia areata and 61% of patients with alopecia totalis. Regrowth persisted 3 months after treatment in 71% of patients with patchy alopecia areata and 28% of patients with alopecia totalis. Regrowth usually is seen within 4-6 weeks in responsive patients. Patients with rapidly progressive, extensive, or long-standing alopecia areata tend to respond poorly.

Another study showed regrowth in most patients (480) treated with intralesional steroids, except in 2 patients with alopecia universalis.

Hair growth may persist for 6-9 months after a single injection. Injections are administered intradermally using a 3-mL syringe and a 30-gauge needle.

Triamcinolone acetonide (Kenalog) is used most commonly; concentrations vary from 2.5-10 mg/mL. The lowest concentration is used on the face. A 2015 study showed no difference in regrowth when using 2.5 mg/mL, 5 mg/mL, or 10 mg/mL and all were superior to placebo. Although all concentrations were well tolerated, more cases of reversible skin atrophy were seen in the 10-mg/ml group.[22] The lowest concentration should always be used on the face to avoid skin atrophy. Caution should be used in patients with glaucoma when treating the eyebrows. It may be best to consult with their ophthalmologists.

Less than 0.1 mL is injected per site, and injections are spread out to cover the affected areas (approximately 1 cm between injection sites; see image below).

Corticosteroid injection. Corticosteroid injection.

Adverse effects mostly include pain during injection and minimal transient atrophy (10%). The presence of atrophy should prompt a reduction in the triamcinolone acetonide concentration and avoidance of the atrophic site.

Injections are administered every 4-6 weeks.

Although intralesional injections of triamcinolone acetonide are usually recommended for alopecia areata with less than 50% involvement, a report showed that 6 of 10 patients had regrowth.[23] Although injections may work in extensive alopecia areata, results are unlikely if no response is observed at 6 months (personal observation).

Topical steroids

For topical steroids, again, few studies have been performed regarding efficacy in the treatment of alopecia areata; they can however be useful, especially in children who cannot tolerate injections.

Fluocinolone acetonide cream 0.2% (Synalar HP) twice per day induced a satisfactory-to-excellent response in 61% of patients, which was maintained in 71% of patients. Children younger than 10 years responded better, as did patients with a duration of hair loss of less than 1 year.

Betamethasone dipropionate cream 0.05% (Diprosone) showed similar efficacy.

A 2005 study by Tosti et al[24] in patients with alopecia totalis or alopecia universalis showed that the use of 2.5 g of clobetasol propionate under occlusion with a plastic film 6 d/wk for 6 months induced regrowth in 8 (28.5%) of 28 patients. Regrowth was seen 6-14 weeks after the onset of therapy. Regrowth was maintained for at least 6 months after cessation of therapy in 5 (62.5%) of 8 patients. Even though only 17.8% of patients showed long-term benefits from that treatment, it should be kept in mind that the study was performed in a subgroup of patients that is usually refractory to treatment.

Treatment must be continued for a minimum of 3 months before regrowth can be expected, and maintenance therapy often is necessary.

Despite these data, the authors do not believe that monotherapy with a topical steroid has been of great benefit in the authors' practice.

The most common adverse effect is local folliculitis, which appears after a few weeks of treatment. Telangiectases and local atrophy also have been reported. No systemic adverse effects have been reported.

Immunotherapy

Topical immunotherapy[1] is defined as the induction and periodic elicitation of an allergic contact dermatitis by topical application of potent contact allergens.

Commonly used agents for immunotherapy include squaric acid dibutylester (SADBE) and diphencyprone (DPCP).[2] These 2 sensitizers are not present in the natural or industrial environment. These are compounded investigational agents not approved by the US Food and Drug Administration for use in alopecia. Dinitrochlorobenzene (DNCB) has become less popular as a result of reports that it is mutagenic in the Ames assay (a bacterial assay).

No rigorous toxicologic and pharmacologic studies have been performed on the use of these agents in humans.

Although DPCP and SADBE have not been found mutagenic in the Ames assay, neither is approved by the US Food and Drug Administration, and unknowns still exist concerning their safety profiles.

No contaminants have been found in SADBE. Acetone solutions and alcohol solutions of SADBE are equally stable for 2 months under storage conditions.

DPCP occasionally can contain mutagenic contaminants; therefore, it should be screened periodically to ensure purity. No formal data are available on DPCP regarding its longevity in solution.

Cosmetically acceptable regrowth with topical immunotherapy rates in patients with severe alopecia areata (>50% involvement) varies from 22-68%. Most studies have a success rate of 30-50%. Wiseman et al[25] retrospectively reported the results of a large cohort of 148 consecutive patients treated with DPCP.

Their analysis showed that the cumulative patient response at 32 months was 77.9%. The response rate varied with the extent of the alopecia. Cosmetically acceptable regrowth was seen in 17.4% of patients with alopecia totalis or alopecia universalis, 60.3% in patients with 75-99% hair loss, 88.1% in patients with 50-74% hair loss, and 100% regrowth in those with 25-49% hair loss.

Age at onset was also a significant variable, with older age at onset leading to a better prognosis. A lag period of 3 months was usually present between the onset of therapy and the presence of regrowth.

The median time to achieve significant regrowth was 12.2 months. Some patients showed regrowth on the treated side after 18 months of therapy. No benefit is achieved with continuing therapy after 24 months in the absence of regrowth. The relapse rate after reaching significant regrowth was 62.6%.

In a report of a 5-year experience with the use of DPCP, 97 subjects received continued therapy with DPCP. A response rate of greater than 75% was seen in 15% at 6 months, 49% at 12 months, 53% at 18 months, and 56% at 24 months. The only variable that seemed to affect response to treatment was the baseline extent of the alopecia areata. A greater than 75% response rate was seen in 100% of patients with 25-49% hair loss at baseline, 77% of those with 50-74% loss at baseline, 54% of those with 75-99% loss at baseline, 50% of alopecia totalis patients, and 41% of alopecia universalis patients demonstrated a response. Maintenance treatment (once every 1-4 wk) appeared to reduce the risk of relapse (>25% hair loss). Only 18% of patients experienced relapse on maintenance therapy, compared with 57% in those who discontinued treatment.[26]

The type of alopecia areata before treatment, duration of the disease, and the presence of nail changes were found to predict a lower response to treatment. Age at onset and sex of the patient do not appear to influence the prognosis. Controversy exists concerning whether atopy is an adverse prognosis factor.

Topical immunotherapy has been used for almost 20 years; no serious adverse effects have been reported.

The most common side effect, which is desired, is a mild contact dermatitis (redness, scaling, itching).

Adverse effects include cervical lymphadenopathy and pigment changes. Vitiligo developed on the application site in 6.7-7.5% of patients. Transient leukoderma on a distant untreated area has been reported. Of patients who develop vitiligo, 31% (4 of 13) had a history of vitiligo. Only 0.75% of patients developed hyperpigmentation. Confetti-type dyschromia (ie, hyperpigmentation, hypopigmentation) has been described as an adverse effect of DPCP treatment and occurred in 1.6% of 243 patients treated. Less common adverse effects include erythema multiforme–like eruptions and urticaria, which were reported in 3 patients treated with DPCP.

The mechanism of action of topical immunotherapy is unknown. Antigenic competition has been hypothesized. That is, the introduction of a second antigen can initiate a new infiltrate containing T-suppressor cells and suppressor macrophages that may modify the preexisting infiltrate and allow regrowth.

Because topical immunotherapy involves the production of contact sensitivity in a previously naive patient, it is best to seek approval for the treatment by the ethics review board and to have the patient sign an informed consent.

Both SADBE and DPCP appear to be equally effective. Acetone-based solutions usually are preferred because they evaporate quickly, allowing patients to wear a hat or wig immediately after treatment. Quick drying also decreases the chances of dissemination to other body parts by contact.

Treatment is provided weekly.

The patient first is sensitized directly on the scalp with a 2% concentration on a small area (2 cm).

The following week, a low concentration (0.0001%) is applied.

The concentration is increased slowly every week as needed until a mild tolerable allergic contact dermatitis is elicited. Many concentrations are available that achieve this goal.

Treating only half of the head allows the physician to use the untreated half as a control. Once regrowth occurs on the treated half, treatment can be applied to the entire scalp. If regrowth initially occurs on both sides, spontaneous remission is likely, although treatment cannot be excluded as the cause.

Avoid severe contact dermatitis. Patients are advised to avoid light exposure on the scalp for 48 hours because light degrades the chemical. Patients also are advised not to wash the scalp for 48 hours.

Initial regrowth may be seen at weeks 12-24. Once cosmetically acceptable regrowth is achieved, the treatment can be tapered gradually. Almost all patients relapse if the treatment is discontinued, and maintenance treatment is needed.

Anthralin

The efficacy of anthralin was assessed in 3 studies, which unfortunately were uncontrolled.

Both short-contact and overnight treatments have been used. Anthralin concentrations varied from 0.2-1%.

A 2004 study by Tang et al[27] showed no benefit in using anthralin. Other studies showed a response rate of 20-75%, respectively, for patchy alopecia areata and a 25% response rate for alopecia totalis. The mean time to response was 11 weeks, and the mean time to cosmetic response was 23 weeks. Anthralin was used by Tang et al in balding C3H/HeJ mice, which is one animal model for alopecia areata. Half the body was treated with anthralin 0.2%, while the other side was treated with the vehicle ointment. Regrowth was seen on the treated side in 64% of mice after 10 weeks. Four mice had almost complete regrowth. The untreated side showed either no regrowth or continued hair loss. Cytokine studies performed with an RNase protection assay showed that tumor necrosis factor-alpha and -beta were inhibited in mice that responded to treatment.

Most patients experienced irritant contact dermatitis. Whether the dermatitis is necessary for efficacy remains under debate.

Cosmetically acceptable regrowth was maintained during therapy in 71% of responders. No correlation exists between duration of the current episode and response to treatment.

Adverse effects include pruritus, erythema, scaling folliculitis, local pyoderma, and regional lymphadenopathy. Withholding treatment for a few days results in rapid disappearance of adverse effects. Treatment then can be reinstituted, but anthralin should be left on for shorter periods. Staining of clothes and skin can be a concern.

The mechanism of action of anthralin is unknown. Most likely, it creates inflammation by generating free radicals, which have antiproliferative and immunosuppressive actions.

Combination of DPCP and anthralin

A small retrospective study showed better results using both DPCP and anthralin compared with DPCP alone.[28]

Minoxidil

Minoxidil appears to be effective in the treatment of alopecia areata in patients with extensive disease (50-99% hair loss). Response rates in that group vary from 8-45%. Minoxidil was of little benefit in patients with alopecia totalis or alopecia universalis.

The 5% solution appears to be more effective.

No more than 25 drops are applied twice per day regardless of the extent of the affected area.

Initial regrowth can be seen within 12 weeks, but continued application is needed to achieve cosmetically acceptable regrowth.

Minoxidil usually is well tolerated. Adverse effects include distant hypertrichosis (5%) and irritation (7%).

The exact mechanism of action of minoxidil remains unclear. Minoxidil does not appear to have either a hormonal or an immunosuppressant effect. Minoxidil most likely has a direct mitogenic effect on epidermal cells, both in vitro and in vivo. Anagen-phase hair bulbs plucked from men applying minoxidil showed a significant increase in proliferation index as measured by DNA flow cytometry. Minoxidil also has been shown to prolong the survival time of keratinocytes in vitro. Finally, minoxidil may oppose intracellular calcium entry. Calcium influx normally enhances epidermal growth factors to inhibit hair growth. Minoxidil is converted to minoxidil sulfate, which is a potassium channel agonist and enhances potassium ion permeability, thus opposing the entry of calcium into cells. Local vasodilatation does not appear to play a primary role in hair growth associated with minoxidil.

Prostaglandin analogs

Retrospective studies using either latanoprost or bimatoprost showed some regrowth of the eyelids while using intralesional triamcinolone concomitantly on the scalp and eyebrows,[29, 30] but all prospective studies using either drugs did not show statistically significant changes when used to treat either the eyelids or eyebrows.[31, 32, 33, 34]

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Systemic Treatments

Psoralen plus UV-A

Many studies have been performed regarding the efficacy of psoralen plus UV-A (PUVA) in the treatment of alopecia areata, and the initial response rate varies from 20-73%. The relapse rate, unfortunately, is high (50-88%). Most patients relapse within a few months (mean 4-8 mo) after treatment is stopped.

Both systemic and topical PUVA therapies have been used.

The number of treatments required for regrowth varies, but 20-40 treatments usually are sufficient in most cases.

A younger age at onset, a longer duration of disease, and the presence of alopecia totalis or alopecia universalis appear to indicate a poorer outcome. Taylor and Hawk[35] published 10 years of experience with PUVA. The initial response rate (>90% regrowth) was comparable to other studies and was 43.8% for partial alopecia areata and 50% for alopecia totalis and alopecia universalis. However, after excluding patients with vellus hair regrowth and patients who relapsed rapidly in the follow-up period (approximately 4 mo), they found the success rate to be, at best, 6.3% for partial alopecia areata and 12.5% for alopecia totalis and alopecia universalis. They concluded that PUVA generally is not an effective long-term treatment for alopecia areata. PUVA is a relatively safe treatment modality; adverse effects include burning and, possibly, an increased risk of skin cancer.

Prednisone

The use of systemic steroids for the treatment of alopecia areata is sometimes justifiable, but hair loss frequently follows discontinuation of the medication and benefits must be carefully weighed against long-term risks. Some authors support a beneficial role of systemic steroids in halting the progression of alopecia areata,[36] but many others have had poor results with this form of therapy.

The rate of regrowth varies greatly (27-89%), and many dose regimens have been used in these studies.

Although the initial regrowth appears promising, the prednisone dose necessary to maintain cosmetic growth usually must be high enough that adverse effects are inevitable, and most patients relapse after therapy is discontinued.

Some benefit was shown using minoxidil 2% solution applied twice per day following a 6-week taper of prednisone, but the relapse rate remained at a minimum of 50% at 4 months in the treated group.

Adverse effects from systemic therapy were common in these reports and included diabetes, weight gain, hypertension, psychological changes, osteoporosis, suppression of the adrenocorticotropic axes, striae, acne, hypertrichosis, and purpura.

Systemic steroids most likely are effective via their immunosuppressive effects.

An initial benefit may occur by using systemic prednisone in some patients, but the relapse rate is high, and it does not appear to alter the course of the condition.

Systemic prednisone is not an agent of choice for alopecia areata because of the adverse effects associated with both short- and long-term treatment.

Methylprednisolone administered at a dose of 500 mg/day for 3 days or 5 mg/kg twice a day over 3 days has been used in patients with widespread disease causing severe emotional distress.[37, 38] Risks and benefits of systemic steroid therapy must be weighed carefully. Predictors of response include disease duration of 6 months or less, age younger than 10 years at disease onset, and multifocal disease.

Cyclosporine

Cyclosporine has been used both topically and systemically in the treatment of alopecia areata.

Topical cyclosporine has not proven to be effective in severe alopecia areata because no patient (0 of 10) showed benefit with application of a 10% cyclosporin A (CsA) solution twice per day for 12 months.

Another study of 14 patients using a 5% solution of cyclosporine twice per day for 4-6 months reported vellus growth in 3 of 14 patients and normal hair growth in 3 patients with patchy alopecia areata. No regrowth was seen in 8 of the patients.

Neither study showed systemic absorption of CsA, and routine blood examination showed only a transient increase of hepatic enzymes in 1 patient.

Oral cyclosporine was effective in the DEBR model for alopecia areata. All rats had a full pelage by 5 weeks of treatment with 10 mg/kg/d, 5 d/wk for 7 weeks. Studies in humans also have proven efficacy with doses of 6 mg/kg/d for 3 months in 6 patients. All patients experienced regrowth, and cosmetically acceptable regrowth was seen in 3 of 6 patients. Unfortunately, all patients relapsed within 3 months of discontinuation of cyclosporine. No evidence indicates that CsA can prevent hair loss during an active episode because reports have described patients taking CsA who developed alopecia areata while they were under treatment for unrelated conditions.

The mechanism of action of cyclosporine remains unclear. It may act through its immunosuppressive effect, because, in patients who regrew hair, clearance of immune cells from the hair follicles and alteration in the balance of regulatory lymphocytes occurred (ie, decrease of the CD4/CD8 ratio). Cyclosporine causes hypertrichosis in patients treated for conditions unrelated to hair loss. The mechanism by which cyclosporine stimulates hair growth remains unknown.

In conclusion, topical cyclosporine has shown limited efficacy. Although systemic CsA appears to be effective in alopecia areata, the adverse effect profile, the recurrence rate after treatment discontinuation, and thus, the inability to produce long-term remissions, make CsA unattractive for the treatment of alopecia areata.

Tacrolimus

Regrowth was shown on the application site of topical tacrolimus in 2 studies using the DEBR model. Oral tacrolimus was ineffective. No benefit was shown in the use of topical tacrolimus for alopecia areata in a small 2005 study by Price et al that included 11 patients.[39]

Interferon

A study of 11 patients with alopecia areata ranging from patchy alopecia areata to alopecia universalis showed no benefit using intralesional interferon alfa-2 (1.5 million IU, 3 times per wk for 3 wk).

Dapsone

Dapsone at 50 mg twice per day was used in a 6-month, double-blind, placebo-controlled study. Of patients in the study, 54% (7 of 13) withdrew from the dapsone group because of adverse effects such as malaise. Of the remaining 6 patients, 3 experienced generalized growth of terminal hair, compared with 4 (4 of 13) patients in the placebo group, who experienced only sparse patchy regrowth of vellus hair. The authors concluded that although dapsone showed some efficacy, the high incidence of adverse effects rendered it unacceptable. Another study showed a rate of success comparable to the occurrence of spontaneous regrowth reported in the literature.

Methotrexate

Joly[40] reported 22 patients with long-standing, severe alopecia areata who responded well to methotrexate, with or without systemic corticosteroids. Although the results from that study are surprisingly good, a more standardized study involving more patients is needed because other dermatologists have not had such good efficacy with methotrexate. A 2016 study suggests that long-term maintenance treatment is usually required to maintain hair growth.[41] Risks versus benefits must be carefully weighed.

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Other Treatment Modalities

Many other modalities have been reported to have variable response rates in small studies. These include latanoprost,[42] nitrogen mustard, massage and relaxation, isoprinosine, acupuncture, and aromatherapy, among others. The efficacy of these treatments needs to be demonstrated in larger, placebo-controlled trials before they can be recommended.

Biological agents

Data are mixed, with many prospective, randomized placebo controlled studies[43, 44] and case reports published in the last few years regarding the use of biologic agents (including adalimumab, alefacept, etanercept and infliximab) in the treatment of alopecia areata, failing to show efficacy, and some patients developed alopecia areata while under treatment with biologic agents for other conditions.

There are only case reports regarding the use of tofacitinib and baricitinib in the treatment of alopecia areata.[45, 46] Clinical trials are ongoing to assess the true efficacy of tofacitinib.

Simvastatin/ezetimibe

A prospective, open-label pilot study using simvastatin/ezetimibe showed some response that seemed to be maintained while taking the drug, but most relapsed once it was discontinued.[47] Only 19 of 29 patients completed the study. One patient was noncompliant, but reasons for lost to follow-up or withdrawal are not specified for the other patients.

Platelet-rich plasma (PRP)

PRP has both proliferation-inducing as well as anti-inflammatory effects. A small randomized, double-blind, placebo- and active-controlled, half-head study has shown PRP to be superior to both intra-lesional triamcinolone acetonide and placebo.[48]

Zinc

One study showed a correlation between low serum zinc levels and disease severity, as well as duration and resistance to therapies,{ref} 26147750 anda few reports show some benefit to using zinc gluconate (30-50 mg/day) in the treatment of alopecia areata.[49, 50] However, another study did not find a statistically significant difference in zinc concentration in serum and hair between alopecia areata patients and controls.[51]

Nonpharmacologic methods

A systematic MEDLINE search could not find any study with sufficient validity to provide scientific evidence of benefit with complementary and alternative medicine therapies for alopecia areata.[52]

A study on hypnosis for refractory alopecia areata did not show efficacy of regrowth, but it did show that hypnosis can improve depression, anxiety, and quality of life in affected patients.[53]

Cosmetic treatments for patients with alopecia areata include dermatography and hairpieces. Dermatography has been used to camouflage the eyebrows of patients with alopecia areata. Follow-up visits at 4 years showed that 30 of 39 of patients demonstrated excellent cosmetic results and 3 had good results. On average, 2-3 sessions lasting 1 hour each were required for each patient. No adverse effects were reported. Hairpieces are useful for patients with extensive disease and allow them to carry on their usual social life. Reassure patients about the natural look provided by hairpieces.

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Surgical Care

Surgical intervention has no role in the treatment of alopecia areata.

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Prevention

Alopecia areata is highly unpredictable. No treatment is effective in preventing or halting progression of the condition. No trigger can be found to explain disease exacerbation in most patients.

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Contributor Information and Disclosures
Author

Chantal Bolduc, MD, FRCPC Assistant Professor, Department of Dermatology, University of Montreal Faculty of Medicine; Physician, Innovaderm Research, Inc

Chantal Bolduc, MD, FRCPC is a member of the following medical societies: Canadian Dermatology Foundation

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Abbott, Galderma, Lilly, Novartis, Léo Pharma, Amgen, Celgene, Janssen<br/>Serve(d) as a speaker or a member of a speakers bureau for: Abbott, Galderma, Lilly, Novartis, Léo Pharma, Amgen, Celgene, Janssen.

Coauthor(s)

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 is a member of the 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.

Specialty Editor Board

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 is a member of the 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 is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, Texas Medical Association

Disclosure: Nothing to disclose.

Chief Editor

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 is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Leonard Sperling, MD Chair, Professor, Department of Dermatology, Uniformed Services University of the Health Sciences

Leonard Sperling, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

References
  1. Hoffmann R, Happle R. Topical immunotherapy in alopecia areata. What, how, and why?. Dermatol Clin. 1996 Oct. 14(4):739-44. [Medline].

  2. Rokhsar CK, Shupack JL, Vafai JJ, Washenik K. Efficacy of topical sensitizers in the treatment of alopecia areata. J Am Acad Dermatol. 1998 Nov. 39(5 Pt 1):751-61. [Medline].

  3. van der Steen P, Traupe H, Happle R, Boezeman J, Sträter R, Hamm H. The genetic risk for alopecia areata in first degree relatives of severely affected patients. An estimate. Acta Derm Venereol. 1992 Sep. 72(5):373-5. [Medline].

  4. Pullen LC. Alopecia Areata Associated With Autoimmune Comorbidity. Available at http://www.medscape.com/viewarticle/804646. Accessed: May 27, 2013.

  5. Huang KP, Mullangi S, Guo Y, Qureshi AA. Autoimmune, Atopic, and Mental Health Comorbid Conditions Associated With Alopecia Areata in the United States. JAMA Dermatol. 2013 May 22. 1-5. [Medline].

  6. Colombe BW, Lou CD, Price VH. The genetic basis of alopecia areata: HLA associations with patchy alopecia areata versus alopecia totalis and alopecia universalis. J Investig Dermatol Symp Proc. 1999 Dec. 4(3):216-9. [Medline].

  7. Colombe BW, Price VH, Khoury EL, Garovoy MR, Lou CD. HLA class II antigen associations help to define two types of alopecia areata. J Am Acad Dermatol. 1995 Nov. 33(5 Pt 1):757-64. [Medline].

  8. Price VH, Colombe BW. Heritable factors distinguish two types of alopecia areata. Dermatol Clin. 1996 Oct. 14(4):679-89. [Medline].

  9. Jackow C, Puffer N, Hordinsky M, Nelson J, Tarrand J, Duvic M. Alopecia areata and cytomegalovirus infection in twins: genes versus environment?. J Am Acad Dermatol. 1998 Mar. 38(3):418-25. [Medline].

  10. Safavi K. Prevalence of alopecia areata in the First National Health and Nutrition Examination Survey. Arch Dermatol. 1992 May. 128(5):702. [Medline].

  11. Safavi KH, Muller SA, Suman VJ, Moshell AN, Melton LJ 3rd. Incidence of alopecia areata in Olmsted County, Minnesota, 1975 through 1989. Mayo Clin Proc. 1995 Jul. 70(7):628-33. [Medline].

  12. Muller SA, Winkelmann RK. Alopecia areata. An evaluation of 736 patients. Arch Dermatol. 1963 Sep. 88:290-7. [Medline].

  13. Sharma VK, Dawn G, Kumar B. Profile of alopecia areata in Northern India. Int J Dermatol. 1996 Jan. 35(1):22-7. [Medline].

  14. Puavilai S, Puavilai G, Charuwichitratana S, Sakuntabhai A, Sriprachya-Anunt S. Prevalence of thyroid diseases in patients with alopecia areata. Int J Dermatol. 1994 Sep. 33(9):632-3. [Medline].

  15. Werth VP, White WL, Sanchez MR, Franks AG. Incidence of alopecia areata in lupus erythematosus. Arch Dermatol. 1992 Mar. 128(3):368-71. [Medline].

  16. Wang SJ, Shohat T, Vadheim C, Shellow W, Edwards J, Rotter JI. Increased risk for type I (insulin-dependent) diabetes in relatives of patients with alopecia areata (AA). Am J Med Genet. 1994 Jul 1. 51(3):234-9. [Medline].

  17. Perini GI, Veller Fornasa C, Cipriani R, Bettin A, Zecchino F, Peserico A. Life events and alopecia areata. Psychother Psychosom. 1984. 41(1):48-52. [Medline].

  18. Karadag Köse O, Güleç AT. Clinical evaluation of alopecias using a handheld dermatoscope. J Am Acad Dermatol. 2012 Aug. 67(2):206-14. [Medline].

  19. Tosti A, De Padova MP, Minghetti G, Veronesi S. Therapies versus placebo in the treatment of patchy alopecia areata. J Am Acad Dermatol. 1986 Aug. 15(2 Pt 1):209-10. [Medline].

  20. Vestey JP, Savin JA. Natural history of severe alopecia areata. Br J Dermatol. 1987 Oct. 117(4):531. [Medline].

  21. Devi M, Rashid A, Ghafoor R. Intralesional Triamcinolone Acetonide Versus Topical Betamethasone Valearate in the Management of Localized Alopecia Areata. J Coll Physicians Surg Pak. 2015 Dec. 25 (12):860-2. [Medline].

  22. Chu TW, AlJasser M, Alharbi A, Abahussein O, McElwee K, Shapiro J. Benefit of different concentrations of intralesional triamcinolone acetonide in alopecia areata: An intrasubject pilot study. J Am Acad Dermatol. 2015 Aug. 73 (2):338-40. [Medline].

  23. Chang KH, Rojhirunsakool S, Goldberg LJ. Treatment of severe alopecia areata with intralesional steroid injections. J Drugs Dermatol. 2009 Oct. 8(10):909-12. [Medline].

  24. Tosti A, Piraccini BM, Pazzaglia M, Vincenzi C. Clobetasol propionate 0.05% under occlusion in the treatment of alopecia totalis/universalis. J Am Acad Dermatol. 2003 Jul. 49(1):96-8. [Medline].

  25. Wiseman MC, Shapiro J, MacDonald N, Lui H. Predictive model for immunotherapy of alopecia areata with diphencyprone. Arch Dermatol. 2001 Aug. 137(8):1063-8. [Medline].

  26. El-Zawahry BM, Bassiouny DA, Khella A, Zaki NS. Five-year experience in the treatment of alopecia areata with DPC. J Eur Acad Dermatol Venereol. 2010 Mar. 24(3):264-9. [Medline].

  27. Tang L, Cao L, Sundberg JP, Lui H, Shapiro J. Restoration of hair growth in mice with an alopecia areata-like disease using topical anthralin. Exp Dermatol. 2004 Jan. 13(1):5-10. [Medline].

  28. Durdu M, Özcan D, Baba M, Seçkin D. Efficacy and safety of diphenylcyclopropenone alone or in combination with anthralin in the treatment of chronic extensive alopecia areata: a retrospective case series. J Am Acad Dermatol. 2015 Apr. 72 (4):640-50. [Medline].

  29. Vila TO, Camacho Martinez FM. Bimatoprost in the treatment of eyelash universalis alopecia areata. Int J Trichology. 2010 Jul. 2 (2):86-8. [Medline].

  30. Coronel-Pérez IM, Rodríguez-Rey EM, Camacho-Martínez FM. Latanoprost in the treatment of eyelash alopecia in alopecia areata universalis. J Eur Acad Dermatol Venereol. 2010 Apr. 24 (4):481-5. [Medline].

  31. Ross EK, Bolduc C, Lui H, Shapiro J. Lack of efficacy of topical latanoprost in the treatment of eyebrow alopecia areata. J Am Acad Dermatol. 2005 Dec. 53 (6):1095-6. [Medline].

  32. Faghihi G, Andalib F, Asilian A. The efficacy of latanoprost in the treatment of alopecia areata of eyelashes and eyebrows. Eur J Dermatol. 2009 Nov-Dec. 19 (6):586-7. [Medline].

  33. Roseborough I, Lee H, Chwalek J, Stamper RL, Price VH. Lack of efficacy of topical latanoprost and bimatoprost ophthalmic solutions in promoting eyelash growth in patients with alopecia areata. J Am Acad Dermatol. 2009 Apr. 60 (4):705-6. [Medline].

  34. Ochoa BE, Sah D, Wang G, Stamper R, Price VH. Instilled bimatoprost ophthalmic solution in patients with eyelash alopecia areata. J Am Acad Dermatol. 2009 Sep. 61 (3):530-2. [Medline].

  35. Taylor CR, Hawk JL. PUVA treatment of alopecia areata partialis, totalis and universalis: audit of 10 years' experience at St John's Institute of Dermatology. Br J Dermatol. 1995 Dec. 133(6):914-8. [Medline].

  36. Sharma VK. Pulsed administration of corticosteroids in the treatment of alopecia areata. Int J Dermatol. 1996 Feb. 35(2):133-6. [Medline].

  37. Acikgoz G, Ozmen I, Cayirli M, Yeniay Y, Kose O. Pulse methylprednisolone therapy for the treatment of extensive alopecia areata. J Dermatolog Treat. 2014 Apr. 25(2):164-6. [Medline].

  38. Friedland R, Tal R, Lapidoth M, Zvulunov A, Ben Amitai D. Pulse corticosteroid therapy for alopecia areata in children: a retrospective study. Dermatology. 2013. 227(1):37-44. [Medline].

  39. Price VH, Willey A, Chen BK. Topical tacrolimus in alopecia areata. J Am Acad Dermatol. 2005 Jan. 52(1):138-9. [Medline].

  40. Joly P. The use of methotrexate alone or in combination with low doses of oral corticosteroids in the treatment of alopecia totalis or universalis. J Am Acad Dermatol. 2006 Oct. 55(4):632-6. [Medline].

  41. Anuset D, Perceau G, Bernard P, Reguiai Z. Efficacy and Safety of Methotrexate Combined with Low- to Moderate-Dose Corticosteroids for Severe Alopecia Areata. Dermatology. 2016. 232 (2):242-8. [Medline].

  42. Ross EK, Bolduc C, Lui H, Shapiro J. Lack of efficacy of topical latanoprost in the treatment of eyebrow alopecia areata. J Am Acad Dermatol. 2005 Dec. 53(6):1095-6. [Medline].

  43. Price VH. Treatment of hair loss. N Engl J Med. 1999 Sep 23. 341(13):964-73. [Medline].

  44. Strober BE, Siu K, Alexis AF, Kim G, Washenik K, Sinha A, et al. Etanercept does not effectively treat moderate to severe alopecia areata: an open-label study. J Am Acad Dermatol. 2005 Jun. 52(6):1082-4. [Medline].

  45. Craiglow BG, King BA. Killing two birds with one stone: oral tofacitinib reverses alopecia universalis in a patient with plaque psoriasis. J Invest Dermatol. 2014 Dec. 134 (12):2988-90. [Medline].

  46. Jabbari A, Dai Z, Xing L, Cerise JE, Ramot Y, Berkun Y, et al. Reversal of Alopecia Areata Following Treatment With the JAK1/2 Inhibitor Baricitinib. EBioMedicine. 2015 Apr. 2 (4):351-5. [Medline].

  47. Lattouf C, Jimenez JJ, Tosti A, Miteva M, Wikramanayake TC, Kittles C, et al. Treatment of alopecia areata with simvastatin/ezetimibe. J Am Acad Dermatol. 2015 Feb. 72 (2):359-61. [Medline].

  48. Trink A, Sorbellini E, Bezzola P, Rodella L, Rezzani R, Ramot Y, et al. A randomized, double-blind, placebo- and active-controlled, half-head study to evaluate the effects of platelet-rich plasma on alopecia areata. Br J Dermatol. 2013 Sep. 169 (3):690-4. [Medline].

  49. Park H, Kim CW, Kim SS, Park CW. The therapeutic effect and the changed serum zinc level after zinc supplementation in alopecia areata patients who had a low serum zinc level. Ann Dermatol. 2009 May. 21 (2):142-6. [Medline].

  50. Lux-Battistelli C. Combination therapy with zinc gluconate and PUVA for alopecia areata totalis: an adjunctive but crucial role of zinc supplementation. Dermatol Ther. 2015 Jul-Aug. 28 (4):235-8. [Medline].

  51. Dastgheib L, Mostafavi-Pour Z, Abdorazagh AA, Khoshdel Z, Sadati MS, Ahrari I, et al. Comparison of zn, cu, and fe content in hair and serum in alopecia areata patients with normal group. Dermatol Res Pract. 2014. 2014:784863. [Medline].

  52. van den Biggelaar FJ, Smolders J, Jansen JF. Complementary and alternative medicine in alopecia areata. Am J Clin Dermatol. 2010. 11(1):11-20. [Medline].

  53. Willemsen R, Haentjens P, Roseeuw D, Vanderlinden J. Hypnosis in refractory alopecia areata significantly improves depression, anxiety, and life quality but not hair regrowth. J Am Acad Dermatol. 2010 Mar. 62(3):517-8. [Medline].

 
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Alopecia areata affecting the beard.
Alopecia areata affecting the arms.
Patchy alopecia areata.
Ophiasis pattern of alopecia areata.
Sisaipho pattern of alopecia areata.
Alopecia totalis.
Diffuse alopecia areata.
Corticosteroid injection.
Treatment algorithm for alopecia areata.
 
 
 
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