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Alopecia areata: Management

Alopecia areata: Management
Literature review current through: Jan 2024.
This topic last updated: Nov 02, 2023.

INTRODUCTION — Alopecia areata is a chronic, relapsing, immune-mediated, inflammatory disorder that affects hair follicles and results in nonscarring hair loss. The severity of the disorder ranges from small patches of alopecia on any hair-bearing area to the complete loss of scalp, eyebrow, eyelash, and body hair (picture 1A-J). (See "Alopecia areata: Clinical manifestations and diagnosis", section on 'Clinical features'.)

The management of alopecia areata involves both offering treatment to patients who desire intervention and addressing the psychologic needs of the patient (algorithm 1). A variety of topical, intralesional, and systemic agents, as well as devices, have been used for alopecia areata, but the response to treatment varies widely, and well-designed clinical trials are limited. (See 'Approach to treatment' below and 'Preferred initial therapies' below and 'Refractory disease' below and 'Other therapies' below.)

The management of alopecia areata will be discussed here. The clinical manifestations and diagnosis of the disorder are reviewed separately. (See "Alopecia areata: Clinical manifestations and diagnosis".)

APPROACH TO TREATMENT — The management of patients with alopecia areata consists of several important components, including (algorithm 1):

Education about the course and prognosis of alopecia areata (see "Alopecia areata: Clinical manifestations and diagnosis", section on 'Disease course' and 'Information for patients' below)

The decision to proceed (or not to proceed) with medical treatment (see 'Decision to treat' below)

Treatment selection (see 'Preferred initial therapies' below)

Provision of resources for psychosocial support (see 'Psychosocial support' below)

Discussion of cosmetic options (see 'Cosmetic options' below)

Decision to treat — The decision to treat is a shared decision with the patient that involves careful consideration of the patient's preferences and the risks and benefits of treatment. Responses to treatment vary, recurrence is common, and alopecia areata may spontaneously improve, with limited, patchy alopecia areata generally exhibiting the most favorable prognosis. It is estimated that up to 50 percent of patients who present with patchy alopecia areata experience spontaneous hair regrowth within one year. (See "Alopecia areata: Clinical manifestations and diagnosis", section on 'Disease course'.)

In our experience, the unpredictable course and psychologic and cosmetic effects of alopecia areata prompt many patients to attempt treatment. Some patients may elect to defer treatment because of factors such as a desire to avoid the potential adverse effects of treatment; the uncertainty of achieving sustained, cosmetically satisfactory hair regrowth; the absence of a curative treatment; or the achievement of psychologic acceptance of hair loss.

Psychosocial support — Psychosocial support plays an important role in the management of alopecia areata.

Psychologic impact – Alopecia areata can negatively impact quality of life and has been associated with increased risk for psychiatric disorders, such as depression and anxiety [1-4]. In a population-based, retrospective, cohort study that included patients from the ages of 10 to 90 years registered in a medical records database in the United Kingdom, having alopecia areata was associated with an increased risk for a subsequent diagnosis of major depressive disorder, and having a major depressive disorder also appeared to increase the risk for alopecia areata [1]. Studies of children and adolescents with alopecia areata have also found increased rates of psychiatric symptoms, such as anxiety and depression [5,6].

Role of the clinician – In view of the variable efficacy of current forms of treatment, the clinician has a role in helping patients adapt to hair loss. Supportive communication that reflects the clinician's sensitivity to the psychologic impact of hair loss may be helpful [3]. Input from other health professionals, such as a clinical or behavioral health psychologist or psychiatrist, may be needed.

Resources for support – In our experience, many patients are helped by involvement in patient support groups. With children, psychosocial support for caregivers may also be helpful [7]. Caregivers can experience distress over the child's hair loss and may also influence the child's perception and response to hair loss.

The National Alopecia Areata Foundation (NAAF) is a useful resource for support for children and adults with alopecia areata and their family members and caregivers. NAAF maintains an informative website, publishes a newsletter, and provides names of local support groups. (See 'Information for patients' below.)

Cosmetic options — Some patients who elect to forgo treatment or who have incomplete responses desire products or techniques to address persistent scalp, eyebrow, or eyelash hair loss. Wigs; hairpieces; shaving of the scalp; and protein powders, sprays, or lotions designed to make hair appear more full may be helpful for scalp hair loss [8].

Eyebrow tattooing can be helpful for loss of eyebrows. Patients with alopecia of the eyelashes may choose to apply false eyelashes. False eyelashes are widely available in pharmacies and beauty supply stores.

PREFERRED INITIAL THERAPIES — The initial treatment approach for patients who desire medical intervention is influenced by the severity of alopecia (algorithm 1). Disease severity categories are not strictly defined, but accepted categories include:

Limited, patchy hair loss – Loss of less than 50 percent of scalp hair (see 'Limited, patchy hair loss' below)

Extensive hair loss – Loss of more than 50 percent of scalp hair (see 'Extensive hair loss' below)

Limited, patchy hair loss — Intralesional corticosteroid injection is our preferred initial treatment for adults with limited, patchy alopecia areata (algorithm 1). Children and other patients who cannot tolerate injections can be treated with topical corticosteroids. Topical corticosteroids are the preferred initial therapy for children [9]. (See 'Intralesional corticosteroids' below.)

Topical immunotherapy, topical anthralin, and the systemic therapies used for more extensive alopecia areata are options for patients who fail to respond to local corticosteroid therapy. The risks of systemic therapy should be considered carefully. (See 'Extensive hair loss' below and 'Refractory disease' below.)

Intralesional corticosteroids — The preference for intralesional corticosteroid therapy for the initial treatment of limited, patchy hair loss in adults is primarily based upon the relative safety of this intervention and extensive clinical experience that suggests benefit (algorithm 1). Efficacy data from clinical studies are limited [10]. (See 'Potent topical corticosteroids' below.)

Administration – Intralesional injections should be performed on both existing and newly forming patches of alopecia. The goals of treatment are to promote regrowth and limit hair loss. Often, patients with <25 percent scalp hair loss are the best candidates because of difficulty tolerating the high number of injections required to treat larger areas. (See "Intralesional corticosteroid injection".)

Regimens – Typical regimens for injection include:

-ScalpTriamcinolone acetonide (2.5 to 10 mg/mL) injected into the upper subcutis; concentrations greater than 5 mg/mL are primarily reserved for experienced clinicians due to risk for local adverse effects.

-Eyebrow or beardTriamcinolone acetonide (2.5 to 5 mg/mL) injected into the upper subcutis.

Small volumes (0.1 mL or less) are injected into multiple sites 1 cm apart (picture 2). The dose per visit is largely determined by the extent of disease and patient tolerance but is usually around 20 mg or less on the scalp. The dose of triamcinolone acetonide administered should not exceed 40 mg per treatment session due to the potential for systemic adverse effects. (See "Intralesional corticosteroid injection", section on 'Adverse effects and pitfalls'.)

Facial injection should be approached cautiously, particularly in patients with highly pigmented skin, in whom treatment-induced hypopigmentation can be prominent. Clinicians should consider referring patients who need facial injections to a dermatologist. (See "Intralesional corticosteroid injection", section on 'Adverse effects and pitfalls'.)

New growth is usually visible within six to eight weeks. The treatment may be repeated as necessary every four to six weeks and is stopped once regrowth is complete. If there is no response after six months, treatment should be discontinued [11], and alternative treatments may be attempted.

Pain reduction – Intralesional corticosteroid therapy is often performed without anesthesia. However, if desired, the affected areas may be pretreated with a topical anesthetic cream (eg, lidocaine 2.5% and prilocaine 2.5% cream). The cream is applied generously and is placed under occlusion with a tightly fitting shower cap or plastic wrap before treatment. When using lidocaine and prilocaine cream, we typically apply the cream 30 to 60 minutes prior to treatment. (See "Clinical use of topical anesthetics in children", section on 'Lidocaine-prilocaine' and "Intralesional corticosteroid injection", section on 'Reducing injection pain'.)

Efficacy – Data on intralesional corticosteroids for alopecia areata are limited [12-15]. One nonrandomized, comparative study found regrowth of tufts of hair at 33 of 34 sites injected with triamcinolone hexacetonide in 11 patients and at 16 of 25 sites injected with triamcinolone acetonide in 17 patients [12]. In a separate series, complete regrowth of hair occurred after four months in 40 of 62 patients (63 percent) treated with monthly injections of triamcinolone acetonide [13].

A 12-week, randomized trial in which 105 patients with localized alopecia areata were randomized to treatment with betamethasone valerate 0.1% foam applied twice daily, intralesional triamcinolone acetonide (10 mg/mL) administered every three weeks, or topical tacrolimus 0.1% ointment applied twice daily found >75 percent hair regrowth in 54, 60, and 0 percent of patients, respectively [15]. Of note, 27 patients dropped out of the study prior to completion and were not included in the analysis of data. (See 'Potent topical corticosteroids' below.)

Triamcinolone acetonide concentrations on both the lower and higher ends of the suggested treatment ranges (eg, 2.5 to 10 mg/mL for scalp alopecia areata) appear effective for inducing hair regrowth [16-18]. Some data suggest that higher concentrations may be more effective, albeit with greater risk for adverse effects:

In one trial, 83 patients with 231 patches of alopecia were randomly assigned to receive one of three concentrations of triamcinolone acetonide, one of three concentrations of betamethasone dipropionate, or saline (each administered every four weeks for a maximum of six treatments) [17]. At six months, at least 75 percent hair regrowth occurred in 97 percent of lesions treated with triamcinolone acetonide 10 mg/mL compared with 88, 56, and 0 percent of patients treated with triamcinolone acetonide 5 mg/mL, triamcinolone acetonide 3.3 mg/mL, or saline, respectively. However, local adverse effects occurred in 86 percent of patients in the triamcinolone acetonide 10 mg/mL group compared with only 16 percent in the triamcinolone acetonide 5 mg/mL group and 6 percent in the triamcinolone acetonide 3.3 mg/mL group.

Adverse effects – Local skin atrophy is a potential side effect that usually resolves within a few months. Other cutaneous side effects include telangiectasias and hypopigmentation. Systemic adverse effects of intralesional corticosteroid injections, such as adrenal suppression and Cushing syndrome, occur infrequently. (See "Intralesional corticosteroid injection", section on 'Adverse effects and pitfalls'.)

Potent topical corticosteroids — We usually reserve first-line therapy with topical corticosteroids for children and adults who cannot tolerate intralesional injections (algorithm 1) [19-21]. While potent topical corticosteroids are frequently used to treat alopecia areata, evidence for their effectiveness is limited.

Administration – We typically treat scalp involvement with a high-potency topical corticosteroid, such as betamethasone dipropionate 0.05% cream, lotion, or ointment.

Scalp involvement – The topical corticosteroid is applied to affected areas and 1 cm beyond once daily (table 1). The entire scalp is treated if a large area is involved.

We do not apply topical corticosteroids under occlusion. Although occlusion increases topical corticosteroid potency, the potential for increased adverse effects and insufficient evidence to confirm greater efficacy in alopecia areata lead us to avoid occlusion.

The response to treatment of the scalp should be evaluated after three months. We discontinue the topical corticosteroid and consider alternative therapies at this point if patients do not have hair regrowth. For patients who have hair regrowth, we continue the topical corticosteroid and gradually taper the frequency of application.

The best regimen for tapering and discontinuing topical corticosteroids in patients who respond is unclear. We tend to individualize our approach and taper more quickly for patients with robust hair regrowth than for patients with slower, less dramatic improvement. In general, we are able to taper and discontinue topical corticosteroid therapy over the course of three to six months.

Eyebrow or beard involvement – Long-term treatment with high-potency topical corticosteroids is usually avoided for beard and eyebrow involvement because of the potential for corticosteroid-induced skin atrophy in this area [22].

When utilizing topical corticosteroid therapy in these areas, we typically opt for a medium-potency topical corticosteroid initially and assess for a response after approximately six weeks, rather than three months, to minimize risk of corticosteroid-induced skin atrophy (table 1). If there is no response, a high-potency topical corticosteroid can be tried, with reassessment for signs of response after six weeks. Topical corticosteroid therapy is subsequently discontinued if hair regrowth is absent. (See "Topical corticosteroids: Use and adverse effects", section on 'Adverse effects'.)

Efficacy – Examples of studies investigating the efficacy of topical corticosteroids for alopecia areata include the following:

A trial in 70 patients with patchy alopecia areata randomly assigned patients to apply either 0.25% desoximetasone cream or placebo twice daily [23]. After 12 weeks of therapy, a larger number of patients treated with desoximetasone experienced complete regrowth of hair (58 versus 39 percent, relative risk 1.5, 95% CI 0.83-2.59). However, the difference was not statistically significant. More patients treated with the corticosteroid experienced at least mild improvement, and this result did achieve statistical significance.

A 12-week, randomized trial in which 105 patients with localized alopecia areata were randomized to treatment with betamethasone valerate 0.1% foam applied twice daily, intralesional triamcinolone acetonide (10 mg/mL) administered every three weeks, or topical tacrolimus 0.1% ointment applied twice daily found >75 percent hair regrowth in 54, 60, and 0 percent of patients, respectively [15]. Of note, 27 patients dropped out of the study prior to completion and were not included in the analysis of data. (See 'Intralesional corticosteroids' above.)

Preferential use of a potent topical corticosteroid over lower-potency corticosteroids is supported by the findings of a 24-week, randomized trial performed in 41 children with alopecia areata involving at least 10 percent of the scalp surface area. The trial found that twice-daily treatment with clobetasol propionate 0.05% cream (a high-potency topical corticosteroid) for two six-week cycles separated by six weeks was more effective for decreasing the area of scalp hair loss than hydrocortisone 1% cream (a low-potency topical corticosteroid) administered via the same regimen [19]. After 24 weeks, 85 percent of children treated with clobetasol propionate had at least a 50 percent reduction in the surface area with hair loss compared with only 33 percent of children treated with hydrocortisone.

Adverse effects – Similar to intralesional corticosteroids, side effects of topical therapy include local skin atrophy, telangiectasias, hypopigmentation, and adrenal suppression [24-26]. (See "Topical corticosteroids: Use and adverse effects", section on 'Adverse effects'.)

Extensive hair loss — Oral baricitinib, oral ritlecitinib, and topical immunotherapy are our preferred initial therapies for adults with extensive alopecia areata (generally more than 50 percent hair loss) (algorithm 1). Although other Janus kinase (JAK) inhibitors have been used for the treatment of alopecia areata, oral baricitinib and oral ritlecitinib are our preferred JAK inhibitors based upon large, randomized trials that support efficacy. Oral baricitinib and ritlecitinib are also the only US Food and Drug Administration (FDA)- and European Medicines Agency (EMA)-approved medications for alopecia areata. (See 'Treatment selection' below and 'Oral baricitinib' below and 'Other Janus kinase inhibitors' below.)

Adjunctive local or systemic corticosteroid therapy can also be appropriate in the initial treatment of extensive hair loss. (See 'Treatment selection' below.)

Treatment selection — The efficacy of topical immunotherapy and oral baricitinib has not been directly compared. Selection between topical immunotherapy and oral baricitinib or oral ritlecitinib for the initial treatment of adults with extensive alopecia areata is based upon consideration of safety, patient preference, and treatment availability (algorithm 1). Topical immunotherapy requires careful, repeated application of the contact allergen in a clinical or home setting and may induce discomfort related to cutaneous adverse effects. Oral JAK inhibitors are easier to administer but have the potential for systemic adverse effects, and there is uncertainty about long-term efficacy and safety. (See 'Topical immunotherapy' below and 'Oral baricitinib' below.)

We typically reserve intralesional and topical corticosteroid therapy for treatment of strategic sites (eg, frontal hairline, eyebrows) in patients with extensive hair loss. Systemic glucocorticoids are occasionally used for temporarily slowing rapid, extensive hair loss, but adverse effects limit long-term use of this therapy. (See 'Adjunctive local corticosteroids' below and 'Rapidly progressing hair loss' below.)

Oral baricitinib — Oral baricitinib, a selective, reversible Janus kinase 1 (JAK1) and Janus kinase 2 (JAK2) inhibitor, has demonstrated efficacy for severe alopecia areata in adults (algorithm 1) [27]. In 2022, the FDA and the EMA approved baricitinib for the treatment of adults with severe alopecia areata. Continuation of treatment is likely necessary to maintain improvement.

Administration – Standard adult dosing for baricitinib is 2 mg once daily with an increase to 4 mg once daily if the response is not adequate [28]. Patients with nearly complete or complete scalp hair loss may be treated initially with 4 mg once daily. The dose is decreased to 2 mg once daily upon achievement of an adequate response.

The best timing for increasing the dose from 2 to 4 mg per day is not clear. We increase the dose to 4 mg per day if the response is inadequate or absent after three months of treatment with the 2 mg dose. If there is no evidence of a response after a total of six months of baricitinib therapy, we discontinue the drug.

Patients should be assessed for viral hepatitis, latent tuberculosis, renal insufficiency, and pregnancy prior to starting therapy. Baseline and periodic monitoring of a complete blood count with differential and platelets, liver function tests, and lipid levels are indicated. Additional periodic assessments include evaluation for signs or symptoms of infection, skin examinations (in patients at increased risk for skin cancer,) and abdominal symptoms (for patients at risk for gastrointestinal perforation). (See "Overview of the Janus kinase inhibitors for rheumatologic and other inflammatory disorders", section on 'Pretreatment screening and precautions'.)

Efficacy – Phase 3 trials support superiority of oral baricitinib over placebo [27]. In the BRAVE-AA1 (n = 654) and BRAVE-AA2 (n = 546) trials, adults with severe alopecia areata (Severity of Alopecia Tool [SALT] score ≥50) were randomly assigned to baricitinib 4 mg per day, baricitinib 2 mg per day, or placebo in a 3:2:2 ratio. At week 36, the proportion of patients in the baricitinib 4 mg, baricitinib 2 mg, and placebo groups who achieved a SALT score of ≤20 in BRAVE-AA1 was 39, 23, and 6 percent, respectively (difference between baricitinib 4 mg and placebo of 32.6 percentage points, 95% CI 25.6-39.5 and difference between baricitinib 2 mg and placebo of 16.6 percentage points, 95% CI 9.5-23.8). In BRAVE-AA2, 36, 19, and 3 percent of patients in the 4 mg, 2 mg, and placebo groups achieved this endpoint, respectively (difference between baricitinib 4 mg and placebo of 32.6 percentage points, 95% CI 25.6-39.6 and difference between baricitinib 2 mg and placebo of 16.1 percentage points, 95% CI 9.1-23.2).

Data from a retrospective study suggest benefit of oral baricitinib for beard alopecia areata in adults [29]. Complete beard regrowth occurred in 24 of 60 adults (40 percent) given combination therapy with oral baricitinib (1.7 to 6.8 mg per day, mean dose 3.9±1.5 mg per day) and oral minoxidil (0.25 to 10 mg per day, mean dose 2.4±2.5 mg per day).

Data on use of oral baricitinib in children are more limited, and additional study is necessary to confirm efficacy and safety in this population. In a retrospective study, 23 of 29 adolescents aged 12 to 17 years (79 percent) treated with a combination of oral baricitinib (mean final dose 3.9 mg per day) and low-dose oral minoxidil (mean dose 0.7 mg per day) experienced at least a 60 percent reduction in the SALT score [29].

Adverse effects – In the BRAVE-AA1 and BRAVE-AA2 trials, acne, elevated levels of creatinine kinase, and elevated levels of low-density lipoprotein (LDL) cholesterol and high-density lipoprotein (HDL) cholesterol occurred more frequently in the baricitinib groups than in the placebo group [27]. In BRAVE-AA2, urinary tract infections were more common in the baricitinib groups than in the placebo group.

Oral JAK inhibitor therapy may also be associated with risk for serious adverse effects. The FDA has issued boxed warnings for oral JAK inhibitors due to concern for increased risk for serious infections, mortality, malignancy, major adverse cardiovascular events, and thrombosis [30]. An analysis of safety data from 1303 patients in the BRAVE-AA1 and BRAVE-AA2 trials that also included data from long-term extension phases (total of 1868 patient-years of exposure to baricitinib, median exposure of 532 days) identified 34 cases of herpes zoster, 16 serious infections, 3 malignancies other than nonmelanoma skin cancer, 1 pulmonary embolism, 1 gastrointestinal perforation, 1 opportunistic infection, and 0 deaths among patients with any exposure to baricitinib [31]. Patients with a history of recent (within three months) cardiovascular events or with history or elevated risk for venous thromboembolism were excluded from the trials. (See "Overview of the Janus kinase inhibitors for rheumatologic and other inflammatory disorders", section on 'Adverse effects'.)

Oral ritlecitinib — Oral ritlecitinib, an inhibitor of Janus kinase 3 (JAK3) and the tyrosine kinase expressed in hepatocellular carcinoma (TEC) kinase family, has demonstrated efficacy for alopecia areata. In 2023, the FDA and EMA approved oral ritlecitinib for the treatment of severe alopecia areata in adults and adolescents 12 years and older. Continuation of treatment is likely necessary to maintain improvement.

Administration – The suggested dose of ritlecitinib for adults and adolescents is 50 mg once daily.

Efficacy – Data from a 48-week, phase 2b-3 trial (ALLEGRO trial) support efficacy of ritlecitinib [32,33]. In the trial, adults (n = 613) and adolescents (n = 105) with at least 50 percent scalp hair loss (including some patients with alopecia totalis and alopecia universalis) were randomly assigned to one of seven once-daily treatment groups (ritlecitinib 200 mg per day for four weeks, then 50 mg per day; ritlecitinib 200 mg per day for four weeks, then 30 mg per day; ritlecitinib 50 mg per day; ritlecitinib 30 mg per day; ritlecitinib 10 mg per day; placebo for 24 weeks followed by ritlecitinib 200 mg per day for four weeks, then 50 mg per day; or placebo for 24 weeks followed by ritlecitinib 50 mg per day).

At week 24, patients in all analyzed ritlecitinib groups (efficacy in the ritlecitinib 10 mg per day group was not analyzed in comparison with placebo) were more likely to have a SALT score ≤20 than patients in the placebo groups. This outcome occurred in 31 percent of patients in the ritlecitinib 200 mg per day, then 50 mg per day group; 22 percent of patients in the 200 mg per day, then 30 mg per day group; 23 percent of patients in the 50 mg per day group; 14 percent of patients in the 30 mg per day group; and 2 percent of patients in the placebo group. The differences in response rates for the ritlecitinib groups compared with placebo were 29.1 percent (95% CI 21.2-37.9) for the 200 mg per day, then 50 mg per day group; 20.8 percent (95% CI 13.7-29.2) for the 200 mg per day, then 30 mg per day group; 21.9 percent (95% CI 14.7-30.2) for the 50 mg per day group; and 12.8 percent (95% CI 6.7-20.4) for the 30 mg per day group.

Adverse effects – Potential adverse effects of ritlecitinib or other JAK inhibitors may include increased risk for serious infection; death; malignancy; lymphoproliferative disorders; major adverse cardiovascular events; thromboembolic events; and hematologic, hepatic, and creatine phosphokinase laboratory abnormalities.

In the ALLEGRO trial, the most frequently reported adverse effects at week 24 across all groups were upper respiratory infection, nasopharyngitis, and headache [32]. During the placebo-controlled phase, rates of nasopharyngitis were higher in the ritlecitinib groups (10 to 14 percent) than the placebo groups (6 percent). Over 48 weeks, 16 serious adverse effects occurred in 14 patients, including five serious infections, one pulmonary embolism, two malignancies (breast cancer), and eight cases of herpes zoster. No deaths, major cardiovascular events, or opportunistic infections occurred. Elevations in creatinine kinase more than twice the upper limit of normal occurred in 50 patients, but none required cessation of treatment, and no cases of rhabdomyolysis occurred.

Topical immunotherapy — Topical immunotherapy involves the application of a potent contact allergen to the affected area to precipitate hair regrowth (algorithm 1) [34,35]. The procedure is usually performed by dermatologists.

The mechanism of efficacy of topical immunotherapy is unknown, but an immunomodulatory effect on the inflammatory infiltrate surrounding affected hair follicles is thought to play a role. Theories for the mechanism of action have focused on the inhibition of the pathologic immune response via antigenic competition [36], the induction of lymphocyte apoptosis [37], or an effect on the type or function of lymphocytes in the inflammatory infiltrate [38-40].

Administration – Topical immunotherapy can be performed with diphenylcyclopropenone (DPCP) or squaric acid dibutyl ester (SADBE). The agents for topical immunotherapy are obtained from compounding pharmacies. Careful handling during preparation and treatment is essential to avoid inadvertent contact with the skin, which results in sensitization of pharmacists or clinicians.

When both agents are available, DPCP is often favored over SADBE because it is less expensive and more stable in solution. SADBE must be refrigerated. DPCP is degraded by light and should be stored in an amber glass bottle or another protective container.

Diphenylcyclopropenone – Treatment with DPCP involves a regimen of repeated application:

-Topical immunotherapy with DPCP begins with the application of a 2% solution to a small area (eg, 4x4 cm2), usually on the scalp, to sensitize the patient [10]. One to two weeks later, treatment is initiated with the application of a 0.001% concentration of the allergen to the affected areas.

-Patients should be instructed to wash off DPCP after 24 to 48 hours. While the product is on the skin, the treated areas should be protected from sun exposure with an opaque scarf or hat.

-For patients who exhibit a severe, eczematous response to sensitization, an additional week should pass before starting treatment, and an even lower initial concentration of DPCP should be used.

-Treatments are usually repeated once weekly with slowly increasing concentrations of DPCP to a maximum concentration of 2%. Typically, the concentration that induces a mild dermatitis is utilized for all subsequent treatments. A retrospective study suggests that the development of clinically evident dermatitis may not be necessary for efficacy of DPCP. However, additional study is necessary to confirm this finding [41].

-Signs of hair growth are expected by approximately three months, and the frequency of treatment is reduced once maximal hair growth is attained [12,42]. Treatment is often discontinued if there is no response after 6 to 12 months [43,44]. However, improvement requiring longer courses of DPCP therapy has been reported [42].

Squaric acid dibutyl ester – The procedure for sensitization and treatment with SADBE is similar. Sensitization is performed with a 2% solution and is followed by weekly 24-hour applications of the agent. Treatment begins with a low concentration solution (such as 0.0001%) that is increased until mild dermatitis is elicited. Further study is necessary to confirm the findings of a small, retrospective study that suggest an initial, eczematous reaction to sensitization is not always necessary for successful treatment [45].

Opinions vary on whether patients should be allowed to apply SADBE or DPCP at home [10]. Limited data suggest that treatment can be safe and effective; however, additional study is necessary to clarify which patients are the best candidates for home treatment [46].

Efficacy – Randomized trials evaluating topical immunotherapy are lacking, and uncontrolled studies have found variable rates of response [9,34,35,47].

A systematic review and meta-analysis of studies evaluating contact immunotherapy with DPCP or SADBE for patchy alopecia areata, alopecia totalis, and/or alopecia universalis found an overall rate of complete (90 to 100 percent) hair regrowth of 32.3 percent (95% CI 25.3-40.2) [47]. Patients with patchy alopecia areata had better complete response rates (43 percent) than patients with either alopecia totalis or universalis (25 percent).

Factors associated with poorer hair regrowth outcomes included a SALT score ≥50 (odds ratio [OR] 3.05, 95% CI 2.26-4.11), atopic disease (OR 1.61, 95% CI 1.03-2.50), and nail involvement (OR 2.06, 95% CI 1.26-3.36). Although longer disease duration is often considered a negative prognostic factor, disease duration ≥1 year was not a statistically significant prognostic factor in this study (OR 1.56, 95% CI 0.95-2.55). Relapse after treatment was common. Analysis of studies reporting treatment status at the time of relapse revealed recurrence rates among patients not receiving and receiving maintenance treatment of 38 and 49 percent, respectively.

Adverse effects – Severe dermatitis is a potential side effect of topical immunotherapy. If a vesicular or bullous reaction occurs, the contact allergen should be washed from the skin, and treatment with a topical corticosteroid should be initiated. Other potential side effects include lymphadenopathy, urticaria, vitiligo, and dyschromia [11]. Use in pregnant women is not recommended [11].

Adjunctive local corticosteroids — We typically reserve intralesional and topical corticosteroid therapy for treatment of strategic sites (eg, frontal hairline, eyebrows) in patients with extensive disease. (See 'Intralesional corticosteroids' above and 'Potent topical corticosteroids' above.)

Although a minority of patients with extensive alopecia areata may have significant regrowth with local corticosteroid therapy, these interventions are less frequently used alone due to concern for lower efficacy in this subgroup [48-50]. One retrospective study reported better responses to topical immunotherapy compared with intralesional corticosteroids for patients with patches of hair loss exceeding 50 cm2 in size [51].

An additional concern for intralesional corticosteroid therapy is the large number of injections required.

Rapidly progressing hair loss — Although most patients with extensive hair loss are most appropriately treated with other interventions as initial treatment, systemic glucocorticoids are occasionally prescribed as a temporary measure to slow hair loss in patients with rapidly progressing, extensive hair loss (algorithm 1). After completion of the systemic glucocorticoid course, these patients are transferred to a JAK inhibitor, topical immunotherapy, or an alternative therapy.

Although systemic glucocorticoids appear to stimulate hair growth, the adverse effects associated with these agents limit the duration of therapy, and recurrence of hair loss frequently occurs after the discontinuation of treatment [52,53]. Various glucocorticoids and dosing schedules have been used, such as 40 to 60 mg per day in adults or 1 mg/kg per day in children tapered over four to six weeks. Evidence of hair regrowth is expected within this period. Pulsed oral glucocorticoids may also induce hair regrowth; however, data on pulsed therapy are limited, and superiority over daily glucocorticoid therapy has not been proven [54-57].

The efficacy of a prednisone taper (from 40 to 0 mg over the course of six weeks in patients weighing at least 40 kg) was investigated in a prospective study of 32 children and adults with alopecia areata, including 16 patients with alopecia totalis or universalis [58]. After six weeks, 13 patients achieved at least 50 percent hair regrowth, including four patients with 75 to 99 percent hair loss at baseline and four patients with alopecia universalis. Two patients worsened during prednisone therapy. Relapse was common after the discontinuation of prednisone.

Eyelash loss — Eyelash involvement may improve during systemic therapy for alopecia areata. In the BRAVE-AA1 and BRAVE-AA2 randomized trials, patients treated with 4 mg of baricitinib per day were more likely to achieve an Eyelash Hair Loss score of 0 or 1 (full eyelash coverage or minimal gaps) after 36 weeks than patients in the placebo groups [27]. (See 'Oral baricitinib' above.)

There are no established topical treatments for eyelash disease. False eyelashes are a cosmetic option for patients. (See 'Cosmetic options' above.)

Topical prostaglandin analogues have been studied for eyelash involvement, but their efficacy remains uncertain and use cannot be recommended. The majority of studies of topical prostaglandin analogues, including a 16-week, randomized trial of 11 patients, have shown no benefit [59-61]. However, a nonrandomized, prospective study reported benefit with a longer course of therapy. Of 44 patients with eyelash alopecia treated with latanoprost ophthalmic solution for two years, complete or moderate regrowth occurred in 17.5 and 27.5 percent, respectively [62]. None of the 10 patients in the control group attained similar levels of response.

REFRACTORY DISEASE — Other therapies, such as other oral Janus kinase (JAK) inhibitors, dupilumab, oral immunosuppressants, or topical anthralin, may be of benefit for patients who fail or cannot receive initial therapies (algorithm 1). The best approach to disease refractory to initial therapies is not established, and different approaches may be reasonable. Treatment selection involves consideration of efficacy and safety data, patient preference, and treatment availability.

Other Janus kinase inhibitors — Janus kinase (JAK) inhibitors induce hair growth in alopecia areata. A beneficial effect of JAK inhibitors on alopecia areata may result from inhibition of T lymphocyte activation [63].

However, further study is necessary prior to conclusions about long-term efficacy and safety [64]. The US Food and Drug Administration (FDA) has issued boxed warnings for oral JAK inhibitors related to risk for serious infections, mortality, malignancy, major adverse cardiovascular events, and thrombosis [30].

Oral tofacitinib – Regrowth of hair during treatment with oral tofacitinib (a selective JAK inhibitor that primarily inhibits Janus kinase 1 [JAK1] and Janus kinase 3 [JAK3]) has been documented in patients with alopecia areata [65-72]. Patients are typically treated with 5 mg twice daily.

A retrospective study of 90 adults with severe alopecia areata (at least 40 percent scalp hair loss, alopecia totalis, or alopecia universalis) who had stable or worsening disease for at least six months and received oral tofacitinib (5 to 10 mg twice daily) for at least four months (with or without adjuvant prednisone) supports benefit [65]. Of the 65 patients with a duration of the current disease episode of 10 years or less, 77 percent had a clinical response (at least 6 percent improvement in the Severity of Alopecia Tool [SALT] score), and 58 percent achieved greater than 50 percent improvement in the SALT score over 4 to 18 months of treatment. Patients with a disease episode longer than 10 years appeared less likely to respond to treatment; the clinical response rate in this population was 32 percent (8 of 25 patients). No serious adverse effects occurred during treatment.

Data on oral tofacitinib use in children are limited [68,73,74]. In a series of four children (ages 8 to 10 years) with refractory alopecia totalis or alopecia universalis treated with tofacitinib, two had complete regrowth of scalp hair, one had partial regrowth, and one failed to respond [74]. Responses occurred within three to six months. The three responders received 5 mg twice daily, and the child who failed treatment received 5 mg once daily, which was subsequently increased to 5 mg twice daily after three months. In another series, partial hair regrowth occurred in all of eight adolescents with alopecia universalis treated with tofacitinib 5 mg twice daily for 5 to 18 months [73]. Initial signs of regrowth occurred within the first three months. No adverse events occurred in either series.

Tofacitinib therapy is associated with increased risk for infection, including serious infections [75,76]. The development of malignancy and laboratory abnormalities has also been reported in patients receiving tofacitinib therapy for other diseases [77]. Further study is necessary to confirm the efficacy of this treatment, and large clinical trials of JAK inhibitor therapy are underway.

Oral ruxolitinib – Further support for a potential role for JAK inhibitors in the treatment of alopecia areata stems from an open-label pilot study, case series, and case reports describing the use of oral ruxolitinib [63,78-81]. In the open-label study, 9 of 12 patients (75 percent) with moderate to severe alopecia areata treated with 20 mg of ruxolitinib twice daily for three to six months achieved at least 50 percent hair regrowth by the end of treatment [81].

Other oral Janus kinase inhibitors – Phase 2 trial data suggest efficacy of investigational oral JAK inhibitors, such as brepocitinib and CTP-543 [82,83].

Topical Janus kinase inhibitors – The efficacy of topical JAK inhibitors in alopecia areata is uncertain. A 24-week trial in which 39 adults with alopecia areata (25 to 100 percent hair loss) were randomly assigned to either ruxolitinib 1.5% cream twice daily or vehicle found no significant difference in the proportion of patients achieving 50 percent improvement in the SALT scores between the two groups [84]. Topical delgocitinib, an investigational JAK inhibitor, did not appear more effective than vehicle in a small, randomized trial (n = 31) [85]. Moreover, several topical JAK inhibitor trials have been terminated prematurely for reasons such as inefficacy, futility, or sponsor decision [86].

Other studies suggest potential benefit [87-92]. A 28-week, phase 1 trial in which 16 adults with alopecia universalis applied tofacitinib 2% ointment, ruxolitinib 1% ointment, clobetasol dipropionate 0.05% ointment, or vehicle to one of four randomly assigned areas of the scalp and eyebrows twice daily found hair regrowth in the treated area in 6, 5, 10, and 0 patients, respectively [87]. In addition, in a 24-week, open-label study, hair regrowth occurred in 3 of 10 adults with alopecia areata or alopecia totalis during use of tofacitinib 2% ointment [88]. In a case series, tofacitinib 2% ointment therapy in 11 children with alopecia areata, alopecia totalis, or alopecia universalis refractory to oral and topical corticosteroids was associated with improvement in the SALT score in eight children, including three children who had sufficient hair regrowth to cover the scalp or conceal residual areas of hair loss [89].

Dupilumab — Cases of improvement, onset, reactivation, and exacerbation of alopecia areata during treatment with dupilumab have been reported [93,94]. Additional study is necessary to determine efficacy of dupilumab for alopecia areata.

A phase 2 trial suggests benefit of dupilumab therapy [95]. In the trial, 60 adults with alopecia areata (≥30 percent scalp hair loss) were randomly assigned in a 2:1 ratio to receive either dupilumab (300 mg once weekly) or placebo for 24 weeks. At week 24, seven patients (18 percent) in the dupilumab group achieved at least 30 percent improvement in the SALT score compared with two patients (10 percent) in the placebo group. However, the differences between the two groups were not statistically significant. After an additional 24 weeks of dupilumab therapy given in a subsequent open-label phase, 13 patients (33 percent) in the original dupilumab group achieved at least 30 percent improvement in the SALT score, suggesting that a longer, larger trial may be beneficial for assessing efficacy of dupilumab. Factors associated with a higher likelihood of response included a baseline serum immunoglobulin E (IgE) level of at least 200 international units/mL, a personal or family history of atopy, and a shorter period of time since last hair regrowth.

Benefit of dupilumab has also been reported in case reports and case series [93,96,97]. In a series of 16 children with both alopecia areata and atopic dermatitis treated with dupilumab (300 mg every two weeks), four of six children with active disease at the time of dupilumab initiation and at least four months of clinical follow-up had improvement in disease severity [96]. The children who improved had ophiasis pattern (two children), alopecia universalis (one child), or patchy alopecia areata (one child); the two children who did not respond had alopecia universalis.

Oral immunosuppressants — Immunosuppressants occasionally used for refractory alopecia areata include methotrexate, azathioprine, and cyclosporine. Efficacy data for these therapies are limited, and treatment with these drugs requires close laboratory monitoring due to potential toxicities.

Methotrexate – A systematic review and meta-analysis of primarily retrospective, observational studies suggests benefit of methotrexate, particularly when used in adults or in conjunction with systemic glucocorticoids [98]. Patients were generally treated with methotrexate doses between 7.5 and 25 mg per week. The pooled rate of good or complete response (at least 50 percent hair regrowth) was 63 percent. Initial hair regrowth with methotrexate may be evident after approximately 3 months, and 6 to 12 months of therapy may be necessary for complete regrowth. However, recurrence appears common upon tapering of methotrexate. (See "Major side effects of low-dose methotrexate".)

In a randomized trial, combination therapy with methotrexate and a systemic glucocorticoid was associated with improvement in some patients with the most severe forms of alopecia areata [99]. In the trial, adults with chronic alopecia universalis (n = 88) or alopecia totalis (n = 1) refractory to other treatments received either oral methotrexate (dose of 20 or 25 mg per week depending on weight) or placebo for six months. After month 6, patients who had more than 25 percent hair growth (three patients in the methotrexate group and one patient in the placebo group) continued their assigned treatment. Patients who had not achieved this endpoint were rerandomized to either combination therapy with methotrexate (same dose) plus oral prednisone (20 mg per day for three months, then 15 mg per day for three months) or methotrexate plus a placebo from month 6 to month 12. Thirty patients dropped out over the course of the study (including 10 in the methotrexate group and 6 in the placebo group prior to rerandomization), mostly because of lack of response.

At month 12, complete or almost complete hair regrowth (SALT score <10) occurred in 7 of 35 patients (20 percent) who received both methotrexate (for 6 or 12 months) and prednisone (for 6 months), including 5 of 16 patients (31 percent) who had received methotrexate for 12 months and prednisone for 6 months. This endpoint occurred in only 1 of 35 patients who were either rerandomized to methotrexate alone (32 patients) or continued methotrexate alone throughout the study (3 patients). One additional patient taking methotrexate alone achieved complete or almost complete hair regrowth after 9 months but did not return for assessment at 12 months. Adverse events were more frequent during treatment with methotrexate or methotrexate plus prednisone than during receipt of placebo, but no severe, treatment-related adverse events occurred.

Azathioprine – Data from small, uncontrolled studies suggest that azathioprine induces hair regrowth in some patients with moderate to severe alopecia areata [100,101]. In a prospective study of 14 adult patients with alopecia universalis, six patients regrew hair during treatment with azathioprine (2.5 mg/kg per day adjusted according to thiopurine methyltransferase [TPMT] levels), all achieving regrowth on 75 percent or more of the scalp [100]. Responses occurred four to six months after the start of treatment, and four of the six responders had persistent improvement after the discontinuation of treatment. Adverse effects (diarrhea, liver enzyme elevation, pancreatitis, or bone marrow suppression) occurred in 5 of the 14 treated patients, resulting in treatment cessation in four patients. (See "Overview of pharmacogenomics", section on 'Thiopurines and polymorphisms in TPMT and NUDT15'.)

CyclosporineCyclosporine may induce hair growth in patients with alopecia areata. However, cyclosporine therapy is associated with the potential for serious adverse effects that preclude long-term therapy. Therefore, we tend to avoid use of cyclosporine for alopecia areata.

Efficacy data for cyclosporine are limited. In a 12-week trial that randomly assigned 36 adults with moderate to severe alopecia areata (including 21 adults with alopecia totalis or alopecia universalis) to either cyclosporine (4 mg/kg per day) or placebo, at least 50 percent improvement in the SALT score occurred in 31 and 6 percent of patients, respectively [102]. The difference was not statistically significant. Additional studies with larger sample sizes or longer treatment durations may be useful for confirming benefit of cyclosporine.

Data from case series and uncontrolled studies also suggest benefit of cyclosporine given with or without systemic glucocorticoids [103-106]. Cyclosporine doses higher than 4 mg/kg have also been utilized [103]. (See "Pharmacology of cyclosporine and tacrolimus", section on 'Side effects'.)

The development of alopecia areata during cyclosporine therapy has also been reported [107-110].

Topical anthralin — Anthralin is a topical irritant agent. Evidence of its effectiveness for alopecia areata is limited to case series without adequate controls [10,111]. Compared with intralesional corticosteroids and topical immunotherapy, anthralin appears to be less effective. Children may also have difficultly tolerating the irritation caused by anthralin.

Short-contact therapy with anthralin is performed by applying anthralin 0.5 or 1% cream to the affected areas for 20 to 30 minutes daily, followed by rinsing the cream off with cool to lukewarm water, and washing the treated area with any shampoo [11]. The time of contact is increased by 10 minutes every two weeks up to one hour or to the time required to elicit a mild dermatitis. Therapy is then continued at that exposure time.

Alternatively, treatment can be initiated with application of a 0.1% concentration of anthralin to the scalp for 10 to 20 minutes. Tolerance to irritation is built up by gradually increasing (over a period of days) the time that the anthralin is left on the affected area, eventually reaching tolerance for leaving anthralin on overnight. The concentration of anthralin can be increased up to 2% as tolerated.

An irritant reaction with erythema and scaling is desired but should not be allowed to become frankly vesicular. Mild irritation is expected and preferred over severe irritation. Anthralin should be used for at least three months before re-evaluating for treatment effectiveness.

Anthralin will stain hair, skin, and fabrics brown. Patients should wash their hands with cool to lukewarm water immediately after application.

OTHER THERAPIES

Local therapies — Additional local therapies evaluated for alopecia areata include topical minoxidil, excimer laser, platelet-rich plasma, and photochemotherapy. The efficacy of these therapies is unclear.

Topical minoxidil – Randomized trials of minoxidil have been small, and some, but not all, trials have found evidence of benefit, at least for patients with limited alopecia areata [112-114]. Minoxidil does not appear to be effective in patients with total loss of scalp hair [114].

Topical minoxidil is used twice daily alone or in combination with intralesional or topical corticosteroids. While there may be a dose-response effect, with the 5% solution being more effective than the 2% solution [115], few patients achieve cosmetically significant regrowth. If used, minoxidil should be tried for three months before evaluating effectiveness.

Topical minoxidil is generally well tolerated but can lead to unwanted growth of facial hair in approximately 3 percent of women [116]. Pruritus or dermatitis is an occasional adverse event [117]; a foam formulation is less likely to induce these symptoms [118]. Unlike the solution formulation, propylene glycol (a common allergen and irritant) is not present in minoxidil foam.

Excimer laser – The excimer laser emits monochromatic ultraviolet B (UVB) light at a wavelength of 308 nm. Its mechanism of action in alopecia areata is thought to involve the induction of T cell apoptosis [119,120]. In a few small studies and case reports, treatment with the excimer laser was associated with improvement in patchy alopecia areata of the scalp [119,121-124]. Patients with lesions on the extremities, alopecia totalis, or alopecia universalis have not responded to therapy [119,121,124].

Platelet-rich plasma – Platelet-rich plasma, which contains growth factors that are important for cell proliferation and differentiation and has anti-inflammatory properties, may be beneficial in alopecia areata [125]. In a trial in which 45 patients with chronic, recurring alopecia areata of at least two years duration were randomly assigned to intralesional injections of autologous platelet-rich plasma, triamcinolone acetonide, or placebo administered once per month for three months, platelet-rich plasma injection was most effective for inducing hair regrowth [126]. Platelet-rich plasma therapy also was associated with reductions in symptoms of burning or itching in affected areas. Additional studies are necessary to validate the findings of this trial.

Photochemotherapy – Psoralen plus ultraviolet A (PUVA) photochemotherapy involves topical or oral administration of a psoralen, a photosensitizing agent, followed by exposure to ultraviolet A (UVA) light. Several uncontrolled series suggest efficacy rates of 60 to 65 percent, though with a high relapse rate [127-130]. Other series have found efficacy rates no higher than what might be expected without therapy [131,132]. PUVA photochemotherapy has the potential for long-term adverse effects, including cutaneous malignancy. PUVA is generally avoided in children for this reason. In our practices, we avoid PUVA photochemotherapy for both adult and pediatric patients. (See "Psoralen plus ultraviolet A (PUVA) photochemotherapy".)

Topical pimecrolimus [133], topical tacrolimus [134,135], topical cyclosporine [136,137], and photodynamic therapy [138-140] have not demonstrated efficacy for alopecia areata.

Systemic therapies — Uncontrolled studies suggest benefit of sulfasalazine, a drug with immunomodulatory properties, in some patients with alopecia areata [141-143]. Other systemic therapies that have been proposed for alopecia areata include ezetimibe-simvastatin [144-146], oral minoxidil [147-149], and low-dose recombinant interleukin (IL) 2 [150,151]. Efficacy data for these therapies are limited, precluding recommendations for routine use. Data on the efficacy of hydroxychloroquine are limited and conflicting [152-154].

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

Overview – Alopecia areata is a chronic, relapsing disorder that results in nonscarring hair loss. The clinical course of alopecia areata varies; the disease may spontaneously resolve, persist, recur, or progress. The management of patients with alopecia areata includes several components (algorithm 1) (see 'Approach to treatment' above):

Education about the course and prognosis of alopecia areata

Consideration of whether to proceed with medical treatment

Treatment selection (for patients who elect to proceed with treatment)

Provision of resources for psychologic support

Discussion of cosmetic options

Decision to treat – The decision to treat is a shared decision with the patient that involves careful consideration of the patient's preferences and the risks and benefits of treatment. Some patients may elect to defer treatment because of factors such as the uncertainty of regaining long-term, cosmetically satisfactory hair regrowth; the absence of a curative treatment; a desire to avoid the potential adverse effects of treatment; or the achievement of psychologic acceptance of hair loss. (See 'Decision to treat' above.)

Approach to treatment – The response of alopecia areata to treatment varies. The extent of disease and rate of hair loss influence the initial approach to treatment (algorithm 1). Limited, patchy hair loss and extensive hair loss may be loosely defined as loss of less than 50 percent of scalp hair and loss of greater than 50 percent of scalp hair, respectively. (See 'Preferred initial therapies' above.)

Limited, patchy hair loss – For adults with limited, patchy hair loss, we suggest intralesional corticosteroid injections rather than other treatments (Grade 2C). High-potency topical corticosteroids are an acceptable alternative for adults who are unlikely to tolerate intralesional therapy. For the initial treatment of children with limited, patchy hair loss, we suggest topical corticosteroids, given better tolerability (Grade 2C). (See 'Limited, patchy hair loss' above.)

Extensive hair loss in adults – For the initial treatment of most adults with extensive hair loss, we suggest oral baricitinib or oral ritlecitinib rather than other therapies (Grade 2C).

An exception is those patients presenting with rapidly progressive, extensive hair loss. In such patients, an initial, short course of systemic glucocorticoids may be beneficial for halting progression. These patients can subsequently transfer to baricitinib, ritlecitinib, or the selected therapy. (See 'Extensive hair loss' above and 'Oral baricitinib' above and 'Rapidly progressing hair loss' above.)

Topical immunotherapy is an acceptable alternative for patients who cannot receive or access baricitinib or ritlecitinib or prefer to avoid systemic therapy. Some uncertainty remains about the long-term efficacy and safety of Janus kinase (JAK) inhibitors. (See 'Treatment selection' above and 'Oral baricitinib' above and 'Topical immunotherapy' above.)

Psychosocial support – Hair loss from alopecia areata is often distressing for patients. Clinician sensitivity to the psychologic impact of hair loss is an important component of the clinical encounter. Provision of resources for psychosocial support, such as a clinical or behavioral health psychologist or psychiatrist and the National Alopecia Areata Foundation, can also be helpful. (See 'Psychosocial support' above.)

Cosmetic interventions – Cosmetic interventions are helpful for some patients. Wigs, hairpieces, shaving of the scalp, and other interventions are options for scalp hair loss. Temporary tattooing can be helpful for loss of eyebrows. False eyelashes can be helpful for alopecia of the eyelashes. (See 'Cosmetic options' above.)

  1. Vallerand IA, Lewinson RT, Parsons LM, et al. Assessment of a Bidirectional Association Between Major Depressive Disorder and Alopecia Areata. JAMA Dermatol 2019; 155:475.
  2. Villasante Fricke AC, Miteva M. Epidemiology and burden of alopecia areata: a systematic review. Clin Cosmet Investig Dermatol 2015; 8:397.
  3. Davey L, Clarke V, Jenkinson E. Living with alopecia areata: an online qualitative survey study. Br J Dermatol 2019; 180:1377.
  4. Mesinkovska N, King B, Mirmirani P, et al. Burden of Illness in Alopecia Areata: A Cross-Sectional Online Survey Study. J Investig Dermatol Symp Proc 2020; 20:S62.
  5. Liakopoulou M, Alifieraki T, Katideniou A, et al. Children with alopecia areata: psychiatric symptomatology and life events. J Am Acad Child Adolesc Psychiatry 1997; 36:678.
  6. Ghanizadeh A. Comorbidity of psychiatric disorders in children and adolescents with alopecia areata in a child and adolescent psychiatry clinical sample. Int J Dermatol 2008; 47:1118.
  7. Aschenbeck KA, McFarland SL, Hordinsky MK, et al. Importance of Group Therapeutic Support for Family Members of Children with Alopecia Areata: A Cross-Sectional Survey Study. Pediatr Dermatol 2017; 34:427.
  8. Montgomery K, White C, Thompson A. A mixed methods survey of social anxiety, anxiety, depression and wig use in alopecia. BMJ Open 2017; 7:e015468.
  9. Barton VR, Toussi A, Awasthi S, Kiuru M. Treatment of pediatric alopecia areata: A systematic review. J Am Acad Dermatol 2022; 86:1318.
  10. Messenger AG, McKillop J, Farrant P, et al. British Association of Dermatologists' guidelines for the management of alopecia areata 2012. Br J Dermatol 2012; 166:916.
  11. Alkhalifah A, Alsantali A, Wang E, et al. Alopecia areata update: part II. Treatment. J Am Acad Dermatol 2010; 62:191.
  12. Porter D, Burton JL. A comparison of intra-lesional triamcinolone hexacetonide and triamcinolone acetonide in alopecia areata. Br J Dermatol 1971; 85:272.
  13. Kubeyinje EP. Intralesional triamcinolone acetonide in alopecia areata amongst 62 Saudi Arabs. East Afr Med J 1994; 71:674.
  14. Tan E, Tay YK, Giam YC. A clinical study of childhood alopecia areata in Singapore. Pediatr Dermatol 2002; 19:298.
  15. Kuldeep C, Singhal H, Khare AK, et al. Randomized comparison of topical betamethasone valerate foam, intralesional triamcinolone acetonide and tacrolimus ointment in management of localized alopecia areata. Int J Trichology 2011; 3:20.
  16. Chu TW, AlJasser M, Alharbi A, et al. Benefit of different concentrations of intralesional triamcinolone acetonide in alopecia areata: An intrasubject pilot study. J Am Acad Dermatol 2015; 73:338.
  17. Ustuner P, Balevi A, Özdemir M. Best dilution of the best corticosteroid for intralesional injection in the treatment of localized alopecia areata in adults. J Dermatolog Treat 2017; 28:753.
  18. Muhaidat JM, Al-Qarqaz F, Khader Y, et al. A Retrospective Comparative Study of Two Concentrations of Intralesional Triamcinolone Acetonide in the Treatment of Patchy Alopecia Areata on the Scalp. Clin Cosmet Investig Dermatol 2020; 13:795.
  19. Lenane P, Macarthur C, Parkin PC, et al. Clobetasol propionate, 0.05%, vs hydrocortisone, 1%, for alopecia areata in children: a randomized clinical trial. JAMA Dermatol 2014; 150:47.
  20. Harrison S, Sinclair R. Optimal management of hair loss (alopecia) in children. Am J Clin Dermatol 2003; 4:757.
  21. Hawit F, Silverberg NB. Alopecia areata in children. Cutis 2008; 82:104.
  22. Cervantes J, Fertig RM, Maddy A, Tosti A. Alopecia Areata of the Beard: A Review of the Literature. Am J Clin Dermatol 2017; 18:789.
  23. Charuwichitratana S, Wattanakrai P, Tanrattanakorn S. Randomized double-blind placebo-controlled trial in the treatment of alopecia areata with 0.25% desoximetasone cream. Arch Dermatol 2000; 136:1276.
  24. Campbell LS, Chevalier M, Levy RA, Rhodes A. Hypothalamic-pituitary-adrenal axis suppression related to topical glucocorticoid therapy in a child with psoriatic exfoliative erythroderma. Pediatr Dermatol 2012; 29:101.
  25. Walsh P, Aeling JL, Huff L, Weston WL. Hypothalamus-pituitary-adrenal axis suppression by superpotent topical steroids. J Am Acad Dermatol 1993; 29:501.
  26. Keipert JA, Kelly R. Temporary Cushing's syndrome from percutaneous absorption of betamethasone 17-valerate. Med J Aust 1971; 1:542.
  27. King B, Ohyama M, Kwon O, et al. Two Phase 3 Trials of Baricitinib for Alopecia Areata. N Engl J Med 2022; 386:1687.
  28. Olumiant (baricitinib) tablets, for oral use. US FDA approved product information; Indianapolis, IN: Eli Lilly and Company; July 2020. https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/207924s002lbl.pdf (Accessed on June 22, 2022).
  29. Moussa A, Eisman S, Kazmi A, et al. Treatment of moderate-to-severe alopecia areata in adolescents with baricitinib: A retrospective review of 29 patients. J Am Acad Dermatol 2023; 88:1194.
  30. US Food and Drug Administration. FDA requires warnings about increased risk of serious heart-related events, cancer, blood clots, and death for JAK inhibitors that treat certain chronic inflammatory conditions. https://www.fda.gov/drugs/drug-safety-and-availability/fda-requires-warnings-about-increased-risk-serious-heart-related-events-cancer-blood-clots-and-death (Accessed on June 16, 2022).
  31. King B, Mostaghimi A, Shimomura Y, et al. Integrated safety analysis of baricitinib in adults with severe alopecia areata from two randomized clinical trials. Br J Dermatol 2023; 188:218.
  32. King B, Zhang X, Harcha WG, et al. Efficacy and safety of ritlecitinib in adults and adolescents with alopecia areata: a randomised, double-blind, multicentre, phase 2b-3 trial. Lancet 2023; 401:1518.
  33. Hordinsky M, Hebert AA, Gooderham M, et al. Efficacy and safety of ritlecitinib in adolescents with alopecia areata: Results from the ALLEGRO phase 2b/3 randomized, double-blind, placebo-controlled trial. Pediatr Dermatol 2023; 40:1003.
  34. Rokhsar CK, Shupack JL, Vafai JJ, Washenik K. Efficacy of topical sensitizers in the treatment of alopecia areata. J Am Acad Dermatol 1998; 39:751.
  35. van der Steen PH, van Baar HM, Perret CM, Happle R. Treatment of alopecia areata with diphenylcyclopropenone. J Am Acad Dermatol 1991; 24:253.
  36. Happle R. Antigenic competition as a therapeutic concept for alopecia areata. Arch Dermatol Res 1980; 267:109.
  37. Herbst V, Zöller M, Kissling S, et al. Diphenylcyclopropenone treatment of alopecia areata induces apoptosis of perifollicular lymphocytes. Eur J Dermatol 2006; 16:537.
  38. Happle R, Klein HM, Macher E. Topical immunotherapy changes the composition of the peribulbar infiltrate in alopecia areata. Arch Dermatol Res 1986; 278:214.
  39. Wasyłyszyn T, Kozłowski W, Zabielski SL. Changes in distribution pattern of CD8 lymphocytes in the scalp in alopecia areata during treatment with diphencyprone. Arch Dermatol Res 2007; 299:231.
  40. Hoffmann R, Wenzel E, Huth A, et al. Cytokine mRNA levels in Alopecia areata before and after treatment with the contact allergen diphenylcyclopropenone. J Invest Dermatol 1994; 103:530.
  41. Choe SJ, Lee S, Pi LQ, et al. Subclinical sensitization with diphenylcyclopropenone is sufficient for the treatment of alopecia areata: Retrospective analysis of 159 cases. J Am Acad Dermatol 2018; 78:515.
  42. Wiseman MC, Shapiro J, MacDonald N, Lui H. Predictive model for immunotherapy of alopecia areata with diphencyprone. Arch Dermatol 2001; 137:1063.
  43. Garg S, Messenger AG. Alopecia areata: evidence-based treatments. Semin Cutan Med Surg 2009; 28:15.
  44. Karanovic S, Harries M, Kaur MR. Diphenylcyclopropenone for alopecia areata: a U.K. survey. Br J Dermatol 2018; 179:514.
  45. Vedak P, Kroshinsky D. Squaric acid sensitization is not required for response in the treatment of alopecia areata. J Am Acad Dermatol 2015; 73:471.
  46. Lee S, Lee WS. Home-based contact immunotherapy with diphenylcyclopropenone for alopecia areata is as effective and safe as clinic-based treatment in patients with stable disease: A retrospective study of 40 patients. J Am Acad Dermatol 2018; 78:599.
  47. Lee S, Kim BJ, Lee YB, Lee WS. Hair Regrowth Outcomes of Contact Immunotherapy for Patients With Alopecia Areata: A Systematic Review and Meta-analysis. JAMA Dermatol 2018; 154:1145.
  48. Tosti A, Iorizzo M, Botta GL, Milani M. Efficacy and safety of a new clobetasol propionate 0.05% foam in alopecia areata: a randomized, double-blind placebo-controlled trial. J Eur Acad Dermatol Venereol 2006; 20:1243.
  49. 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; 49:96.
  50. Chang KH, Rojhirunsakool S, Goldberg LJ. Treatment of severe alopecia areata with intralesional steroid injections. J Drugs Dermatol 2009; 8:909.
  51. Ro BI. Alopecia areata in Korea (1982-1994). J Dermatol 1995; 22:858.
  52. Winter RJ, Kern F, Blizzard RM. Prednisone therapy for alopecia areata. A follow-up report. Arch Dermatol 1976; 112:1549.
  53. Alabdulkareem AS, Abahussein AA, Okoro A. Severe alopecia areata treated with systemic corticosteroids. Int J Dermatol 1998; 37:622.
  54. Kar BR, Handa S, Dogra S, Kumar B. Placebo-controlled oral pulse prednisolone therapy in alopecia areata. J Am Acad Dermatol 2005; 52:287.
  55. Vañó-Galván S, Hermosa-Gelbard Á, Sánchez-Neila N, et al. Pulse corticosteroid therapy with oral dexamethasone for the treatment of adult alopecia totalis and universalis. J Am Acad Dermatol 2016; 74:1005.
  56. Sladden MJ, Hutchinson PE. Is oral pulsed prednisolone useful in alopecia areata? Critical appraisal of a randomized trial. J Am Acad Dermatol 2005; 53:1100.
  57. Gallaga NM, Carrillo B, Good A, et al. Pediatric pulse dose corticosteroid therapy dosing and administration in the treatment of alopecia areata: A review of literature. Pediatr Dermatol 2023; 40:276.
  58. Olsen EA, Carson SC, Turney EA. Systemic steroids with or without 2% topical minoxidil in the treatment of alopecia areata. Arch Dermatol 1992; 128:1467.
  59. Roseborough I, Lee H, Chwalek J, et al. Lack of efficacy of topical latanoprost and bimatoprost ophthalmic solutions in promoting eyelash growth in patients with alopecia areata. J Am Acad Dermatol 2009; 60:705.
  60. Faghihi G, Andalib F, Asilian A. The efficacy of latanoprost in the treatment of alopecia areata of eyelashes and eyebrows. Eur J Dermatol 2009; 19:586.
  61. 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; 53:1095.
  62. 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; 24:481.
  63. Xing L, Dai Z, Jabbari A, et al. Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition. Nat Med 2014; 20:1043.
  64. Phan K, Sebaratnam DF. JAK inhibitors for alopecia areata: a systematic review and meta-analysis. J Eur Acad Dermatol Venereol 2019; 33:850.
  65. Liu LY, Craiglow BG, Dai F, King BA. Tofacitinib for the treatment of severe alopecia areata and variants: A study of 90 patients. J Am Acad Dermatol 2017; 76:22.
  66. 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; 134:2988.
  67. Dhayalan A, King BA. Tofacitinib Citrate for the Treatment of Nail Dystrophy Associated With Alopecia Universalis. JAMA Dermatol 2016; 152:492.
  68. Craiglow BG, Liu LY, King BA. Tofacitinib for the treatment of alopecia areata and variants in adolescents. J Am Acad Dermatol 2017; 76:29.
  69. Gupta AK, Carviel JL, Abramovits W. Efficacy of tofacitinib in treatment of alopecia universalis in two patients. J Eur Acad Dermatol Venereol 2016; 30:1373.
  70. Ibrahim O, Bayart CB, Hogan S, et al. Treatment of Alopecia Areata With Tofacitinib. JAMA Dermatol 2017; 153:600.
  71. Jabbari A, Sansaricq F, Cerise J, et al. An Open-Label Pilot Study to Evaluate the Efficacy of Tofacitinib in Moderate to Severe Patch-Type Alopecia Areata, Totalis, and Universalis. J Invest Dermatol 2018; 138:1539.
  72. Kennedy Crispin M, Ko JM, Craiglow BG, et al. Safety and efficacy of the JAK inhibitor tofacitinib citrate in patients with alopecia areata. JCI Insight 2016; 1:e89776.
  73. Castelo-Soccio L. Experience with oral tofacitinib in 8 adolescent patients with alopecia universalis. J Am Acad Dermatol 2017; 76:754.
  74. Craiglow BG, King BA. Tofacitinib for the treatment of alopecia areata in preadolescent children. J Am Acad Dermatol 2019; 80:568.
  75. Papp KA, Menter A, Strober B, et al. Efficacy and safety of tofacitinib, an oral Janus kinase inhibitor, in the treatment of psoriasis: a Phase 2b randomized placebo-controlled dose-ranging study. Br J Dermatol 2012; 167:668.
  76. Wollenhaupt J, Silverfield J, Lee EB, et al. Safety and efficacy of tofacitinib, an oral janus kinase inhibitor, for the treatment of rheumatoid arthritis in open-label, longterm extension studies. J Rheumatol 2014; 41:837.
  77. www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm327152.htm (Accessed on July 01, 2014).
  78. Harris JE, Rashighi M, Nguyen N, et al. Rapid skin repigmentation on oral ruxolitinib in a patient with coexistent vitiligo and alopecia areata (AA). J Am Acad Dermatol 2016; 74:370.
  79. Pieri L, Guglielmelli P, Vannucchi AM. Ruxolitinib-induced reversal of alopecia universalis in a patient with essential thrombocythemia. Am J Hematol 2015; 90:82.
  80. Liu LY, King BA. Ruxolitinib for the treatment of severe alopecia areata. J Am Acad Dermatol 2019; 80:566.
  81. Mackay-Wiggan J, Jabbari A, Nguyen N, et al. Oral ruxolitinib induces hair regrowth in patients with moderate-to-severe alopecia areata. JCI Insight 2016; 1:e89790.
  82. King B, Guttman-Yassky E, Peeva E, et al. A phase 2a randomized, placebo-controlled study to evaluate the efficacy and safety of the oral Janus kinase inhibitors ritlecitinib and brepocitinib in alopecia areata: 24-week results. J Am Acad Dermatol 2021; 85:379.
  83. King B, Mesinkovska N, Mirmirani P, et al. Phase 2 randomized, dose-ranging trial of CTP-543, a selective Janus Kinase inhibitor, in moderate-to-severe alopecia areata. J Am Acad Dermatol 2022; 87:306.
  84. Olsen EA, Kornacki D, Sun K, Hordinsky MK. Ruxolitinib cream for the treatment of patients with alopecia areata: A 2-part, double-blind, randomized, vehicle-controlled phase 2 study. J Am Acad Dermatol 2020; 82:412.
  85. Mikhaylov D, Glickman JW, Del Duca E, et al. A phase 2a randomized vehicle-controlled multi-center study of the safety and efficacy of delgocitinib in subjects with moderate-to-severe alopecia areata. Arch Dermatol Res 2023; 315:181.
  86. Steele L, Lee HL, Maruthappu T, O'Toole EA. The status and outcomes of registered clinical trials for Janus kinase inhibitors in alopecia areata: are unpublished trials being overlooked? Clin Exp Dermatol 2021; 46:1290.
  87. Bokhari L, Sinclair R. Treatment of alopecia universalis with topical Janus kinase inhibitors - a double blind, placebo, and active controlled pilot study. Int J Dermatol 2018; 57:1464.
  88. Liu LY, Craiglow BG, King BA. Tofacitinib 2% ointment, a topical Janus kinase inhibitor, for the treatment of alopecia areata: A pilot study of 10 patients. J Am Acad Dermatol 2018; 78:403.
  89. Putterman E, Castelo-Soccio L. Topical 2% tofacitinib for children with alopecia areata, alopecia totalis, and alopecia universalis. J Am Acad Dermatol 2018; 78:1207.
  90. Craiglow BG, Tavares D, King BA. Topical Ruxolitinib for the Treatment of Alopecia Universalis. JAMA Dermatol 2016; 152:490.
  91. Cheng MW, Kehl A, Worswick S, Goh C. Successful Treatment of Severe Alopecia Areata With Oral or Topical Tofacitinib. J Drugs Dermatol 2018; 17:800.
  92. Bayart CB, DeNiro KL, Brichta L, et al. Topical Janus kinase inhibitors for the treatment of pediatric alopecia areata. J Am Acad Dermatol 2017; 77:167.
  93. Sachdeva M, Witol A, Mufti A, et al. Alopecia Areata Related Paradoxical Reactions in Patients on Dupilumab Therapy: A Systematic Review. J Cutan Med Surg 2021; 25:451.
  94. Jin P, Wei L, Zhang Q, et al. Dupilumab for alopecia areata treatment: A double-edged sword? J Cosmet Dermatol 2022; 21:5546.
  95. Guttman-Yassky E, Renert-Yuval Y, Bares J, et al. Phase 2a randomized clinical trial of dupilumab (anti-IL-4Rα) for alopecia areata patients. Allergy 2022; 77:897.
  96. McKenzie PL, Castelo-Soccio L. Dupilumab therapy for alopecia areata in pediatric patients with concomitant atopic dermatitis. J Am Acad Dermatol 2021; 84:1691.
  97. Harada K, Irisawa R, Ito T, et al. The effectiveness of dupilumab in patients with alopecia areata who have atopic dermatitis: a case series of seven patients. Br J Dermatol 2020; 183:396.
  98. Phan K, Ramachandran V, Sebaratnam DF. Methotrexate for alopecia areata: A systematic review and meta-analysis. J Am Acad Dermatol 2019; 80:120.
  99. Joly P, Lafon A, Houivet E, et al. Efficacy of Methotrexate Alone vs Methotrexate Plus Low-Dose Prednisone in Patients With Alopecia Areata Totalis or Universalis: A 2-Step Double-Blind Randomized Clinical Trial. JAMA Dermatol 2023; 159:403.
  100. Vañó-Galván S, Hermosa-Gelbard Á, Sánchez-Neila N, et al. Treatment of recalcitrant adult alopecia areata universalis with oral azathioprine. J Am Acad Dermatol 2016; 74:1007.
  101. Farshi S, Mansouri P, Safar F, Khiabanloo SR. Could azathioprine be considered as a therapeutic alternative in the treatment of alopecia areata? A pilot study. Int J Dermatol 2010; 49:1188.
  102. Lai VWY, Chen G, Gin D, Sinclair R. Cyclosporine for moderate-to-severe alopecia areata: A double-blind, randomized, placebo-controlled clinical trial of efficacy and safety. J Am Acad Dermatol 2019; 81:694.
  103. Açıkgöz G, Calışkan E, Tunca M, et al. The effect of oral cyclosporine in the treatment of severe alopecia areata. Cutan Ocul Toxicol 2014; 33:247.
  104. Yeo IK, Ko EJ, No YA, et al. Comparison of High-Dose Corticosteroid Pulse Therapy and Combination Therapy Using Oral Cyclosporine with Low-Dose Corticosteroid in Severe Alopecia Areata. Ann Dermatol 2015; 27:676.
  105. Jang YH, Kim SL, Lee KC, et al. A Comparative Study of Oral Cyclosporine and Betamethasone Minipulse Therapy in the Treatment of Alopecia Areata. Ann Dermatol 2016; 28:569.
  106. Kim BJ, Min SU, Park KY, et al. Combination therapy of cyclosporine and methylprednisolone on severe alopecia areata. J Dermatolog Treat 2008; 19:216.
  107. Phillips MA, Graves JE, Nunley JR. Alopecia areata presenting in 2 kidney-pancreas transplant recipients taking cyclosporine. J Am Acad Dermatol 2005; 53:S252.
  108. Dyall-Smith D. Alopecia areata in a renal transplant recipient on cyclosporin. Australas J Dermatol 1996; 37:226.
  109. Cerottini JP, Panizzon RG, de Viragh PA. Multifocal alopecia areata during systemic cyclosporine A therapy. Dermatology 1999; 198:415.
  110. Davies MG, Bowers PW. Alopecia areata arising in patients receiving cyclosporin immunosuppression. Br J Dermatol 1995; 132:835.
  111. Wu SZ, Wang S, Ratnaparkhi R, Bergfeld WF. Treatment of pediatric alopecia areata with anthralin: A retrospective study of 37 patients. Pediatr Dermatol 2018; 35:817.
  112. Price VH. Double-blind, placebo-controlled evaluation of topical minoxidil in extensive alopecia areata. J Am Acad Dermatol 1987; 16:730.
  113. Fenton DA, Wilkinson JD. Topical minoxidil in the treatment of alopecia areata. Br Med J (Clin Res Ed) 1983; 287:1015.
  114. Vestey JP, Savin JA. A trial of 1% minoxidil used topically for severe alopecia areata. Acta Derm Venereol 1986; 66:179.
  115. Fiedler-Weiss VC. Topical minoxidil solution (1% and 5%) in the treatment of alopecia areata. J Am Acad Dermatol 1987; 16:745.
  116. Lucky AW, Piacquadio DJ, Ditre CM, et al. A randomized, placebo-controlled trial of 5% and 2% topical minoxidil solutions in the treatment of female pattern hair loss. J Am Acad Dermatol 2004; 50:541.
  117. Olsen EA, Dunlap FE, Funicella T, et al. A randomized clinical trial of 5% topical minoxidil versus 2% topical minoxidil and placebo in the treatment of androgenetic alopecia in men. J Am Acad Dermatol 2002; 47:377.
  118. Olsen EA, Whiting D, Bergfeld W, et al. A multicenter, randomized, placebo-controlled, double-blind clinical trial of a novel formulation of 5% minoxidil topical foam versus placebo in the treatment of androgenetic alopecia in men. J Am Acad Dermatol 2007; 57:767.
  119. Zakaria W, Passeron T, Ostovari N, et al. 308-nm excimer laser therapy in alopecia areata. J Am Acad Dermatol 2004; 51:837.
  120. Novák Z, Bónis B, Baltás E, et al. Xenon chloride ultraviolet B laser is more effective in treating psoriasis and in inducing T cell apoptosis than narrow-band ultraviolet B. J Photochem Photobiol B 2002; 67:32.
  121. Al-Mutairi N. 308-nm excimer laser for the treatment of alopecia areata. Dermatol Surg 2007; 33:1483.
  122. Raulin C, Gündogan C, Greve B, Gebert S. [Excimer laser therapy of alopecia areata--side-by-side evaluation of a representative area]. J Dtsch Dermatol Ges 2005; 3:524.
  123. Gundogan C, Greve B, Raulin C. Treatment of alopecia areata with the 308-nm xenon chloride excimer laser: case report of two successful treatments with the excimer laser. Lasers Surg Med 2004; 34:86.
  124. Al-Mutairi N. 308-nm excimer laser for the treatment of alopecia areata in children. Pediatr Dermatol 2009; 26:547.
  125. Almohanna HM, Ahmed AA, Griggs JW, Tosti A. Platelet-Rich Plasma in the Treatment of Alopecia Areata: A Review. J Investig Dermatol Symp Proc 2020; 20:S45.
  126. Trink A, Sorbellini E, Bezzola P, 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; 169:690.
  127. Claudy AL, Gagnaire D. PUVA treatment of alopecia areata. Arch Dermatol 1983; 119:975.
  128. Lassus A, Eskelinen A, Johansson E. Treatment of alopecia areata with three different PUVA modalities. Photodermatol 1984; 1:141.
  129. Mitchell AJ, Douglass MC. Topical photochemotherapy for alopecia areata. J Am Acad Dermatol 1985; 12:644.
  130. van der Schaar WW, Sillevis Smith JH. An evaluation of PUVA-therapy for alopecia areata. Dermatologica 1984; 168:250.
  131. 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; 133:914.
  132. Healy E, Rogers S. PUVA treatment for alopecia areata--does it work? A retrospective review of 102 cases. Br J Dermatol 1993; 129:42.
  133. Rigopoulos D, Gregoriou S, Korfitis C, et al. Lack of response of alopecia areata to pimecrolimus cream. Clin Exp Dermatol 2007; 32:456.
  134. Price VH, Willey A, Chen BK. Topical tacrolimus in alopecia areata. J Am Acad Dermatol 2005; 52:138.
  135. Feldmann KA, Kunte C, Wollenberg A, Wolfe H. Is topical tacrolimus effective in alopecia areata universalis? Br J Dermatol 2002; 147:1031.
  136. Gilhar A, Pillar T, Etzioni A. Topical cyclosporin A in alopecia areata. Acta Derm Venereol 1989; 69:252.
  137. Mauduit G, Lenvers P, Barthélémy H, Thivolet J. [Treatment of severe alopecia areata with topical applications of cyclosporin A]. Ann Dermatol Venereol 1987; 114:507.
  138. Lee JW, Yoo KH, Kim BJ, Kim MN. Photodynamic therapy with methyl 5-aminolevulinate acid combined with microneedle treatment in patients with extensive alopecia areata. Clin Exp Dermatol 2010; 35:548.
  139. Fernández-Guarino M, Harto A, García-Morales I, et al. Failure to treat alopecia areata with photodynamic therapy. Clin Exp Dermatol 2008; 33:585.
  140. Bissonnette R, Shapiro J, Zeng H, et al. Topical photodynamic therapy with 5-aminolaevulinic acid does not induce hair regrowth in patients with extensive alopecia areata. Br J Dermatol 2000; 143:1032.
  141. Ellis CN, Brown MF, Voorhees JJ. Sulfasalazine for alopecia areata. J Am Acad Dermatol 2002; 46:541.
  142. Aghaei S. An uncontrolled, open label study of sulfasalazine in severe alopecia areata. Indian J Dermatol Venereol Leprol 2008; 74:611.
  143. Rashidi T, Mahd AA. Treatment of persistent alopecia areata with sulfasalazine. Int J Dermatol 2008; 47:850.
  144. Lattouf C, Jimenez JJ, Tosti A, et al. Treatment of alopecia areata with simvastatin/ezetimibe. J Am Acad Dermatol 2015; 72:359.
  145. Ali A, Martin JM 4th. Hair growth in patients alopecia areata totalis after treatment with simvastatin and ezetimibe. J Drugs Dermatol 2010; 9:62.
  146. Robins DN. Case reports: alopecia universalis: hair growth following initiation of simvastatin and ezetimibe therapy. J Drugs Dermatol 2007; 6:946.
  147. Sharma AN, Michelle L, Juhasz M, et al. Low-dose oral minoxidil as treatment for non-scarring alopecia: a systematic review. Int J Dermatol 2020; 59:1013.
  148. Villani A, Fabbrocini G, Ocampo-Candiani J, et al. Review of oral minoxidil as treatment of hair disorders: in search of the perfect dose. J Eur Acad Dermatol Venereol 2021; 35:1485.
  149. Wambier CG, Craiglow BG, King BA. Combination tofacitinib and oral minoxidil treatment for severe alopecia areata. J Am Acad Dermatol 2021; 85:743.
  150. Shin BS, Furuhashi T, Nakamura M, et al. Impaired inhibitory function of circulating CD4+CD25+ regulatory T cells in alopecia areata. J Dermatol Sci 2013; 70:141.
  151. Castela E, Le Duff F, Butori C, et al. Effects of low-dose recombinant interleukin 2 to promote T-regulatory cells in alopecia areata. JAMA Dermatol 2014; 150:748.
  152. Stephan F, Habre M, Tomb R. Successful treatment of alopecia totalis with hydroxychloroquine: report of 2 cases. J Am Acad Dermatol 2013; 68:1048.
  153. Nissen CV, Wulf HC. Hydroxychloroquine is ineffective in treatment of alopecia totalis and extensive alopecia areata: A case series of 8 patients. JAAD Case Rep 2016; 2:117.
  154. Yun D, Silverberg NB, Stein SL. Alopecia areata treated with hydroxychloroquine: A retrospective study of nine pediatric cases. Pediatr Dermatol 2018; 35:361.
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