Epidemiology, Diagnosis and Management of Alopecia Areata: An Asia‐Pacific Modified Delphi Expert Panel Recommendations

ABSTRACT

Background

Alopecia areata (AA) affects all ages, genders, and ethnicities. AA severely impacts patients' quality of life. Treatments indicated for AA have only been approved since 2022/2023. While some Asia Pacific (APAC) countries/regions have national or regional guidelines, many lack AA‐specific guidance or have not updated existing guidelines to incorporate recently approved treatments.

Methods

To better inform treatment decisions, 18 dermatologists from Australia, China, India, Korea, Malaysia, Singapore, Taiwan, and Thailand completed a three‐round Delphi‐based consensus process involving survey completion, open discussion, and statement voting. A consensus for Likert‐type and multiple‐choice statements was defined as ≥ 70% agreement or disagreement.

Results

Consensus was achieved on 140 statements. The panel recognizes that AA is clinically heterogeneous and imposes a considerable burden on patients and their families. Trichoscopy is deemed essential for diagnosing and monitoring AA, while skin biopsy is reserved for when the cause of hair loss is unclear. In terms of disease severity, moderate AA is defined as 21%–49% hair loss and severe AA as ≥ 50% hair loss. Regarding treatment, topical corticosteroids are recommended in children < 12 years. For patients aged ≥ 12 years, topical and intralesional corticosteroids could be used for mild‐to‐moderate AA, while Janus kinase inhibitors and systemic corticosteroids have a role in moderate‐to‐severe AA. Adjuvant minoxidil could also be used in chronic AA.

Conclusions

This modified Delphi‐based consensus provides a practical, region‐focused framework to standardize the diagnosis and management of AA across diverse APAC healthcare settings in hope of improving patient outcomes.

A panel of 18 dermatologists participated in a three‐round Delphi‐based consensus process to generate a standardized framework for the diagnosis and management of alopecia areata (AA) in Asia Pacific. Recommendations focus on practicality and clinical relevance within the regional context.

1. Introduction

Alopecia areata (AA) is an autoimmune disease that typically presents as one or more round or oval patches of scalp hair loss and could involve eyelashes, eyebrows, beard, and nails [1]. Affecting individuals across all age groups, genders, and ethnicities, a global trend analysis (1990–2021) suggested that AA is more common in females (male‐to‐female ratio of 0.53) and in individuals aged 25–40 years [2, 3]. Observational studies from the United States and United Kingdom found that patients of Asian, Black, and Hispanic/Latino had a higher standardized prevalence and lifetime incidence of AA, compared with those of White ethnicity [4, 5].

The general prevalence of AA in Asia Pacific (APAC) countries is not known due to a lack of regional and national health registries on AA. However, a systematic review on literature published before September 2018 suggested that the overall pooled prevalence of AA among Asians was 1.46% (1.17%–1.79%) [6]. Data from the Global Burden of Disease Study 2019 showed that the age‐standardized disability adjusted life‐year rate of AA across APAC ranged from 6.23 to 9.35 per 1,000,000 [7]. Moreover, compared with other cutaneous conditions such as androgenetic alopecia and psoriasis, patients with AA had a significantly worse quality of life (QoL) [8].

The burden of AA is significant given its unpredictable disease course [1, 9]. While up to 50% of patients with patchy AA may experience spontaneous regrowth within 12 months, the risk of recurrence can be as high as 85% [9]. Moreover, although some might only have one lifetime episode of AA, additional patches of hair loss may develop over time in some patients [1, 10]. There is a 30% and 15% risk for patients with an AA episode > 1 year to progress to alopecia totalis or alopecia universalis, respectively [10].

The management of AA has been a long‐time challenge as there were no approved treatments until 2022/2023 when Janus kinase (JAK) inhibitors, such as baricitinib and ritlecitinib, were subsequently indicated and approved for AA by the United States Food and Drug Administration (US FDA). While international consensus on the management of AA had been published and some East Asian countries/regions (such as China, Japan, Korea, and Taiwan) have their own national guidelines, many countries in the APAC region still lack an AA‐specific clinical reference point or have not updated existing guidelines to include recently approved treatments [11, 12, 13, 14, 15, 16, 17, 18, 19]. Therefore, there is an unmet need for an updated guide that reflects recent research outcomes and treatment options in AA to better inform treatment decisions in APAC.

In view of this, an expert panel of dermatologists cum hair experts from several APAC countries/regions was formed to provide insights and develop recommendations on the management of AA that are specific to the APAC region.

2. Materials and Methods

An expert panel of 18 dermatologists from Australia, China, India, Korea, Malaysia, Singapore, Taiwan, and Thailand came together to formulate a Delphi‐based consensus for the management of patients with AA in APAC. All experts were renowned hair experts in their respective countries/regions with at least 10 years of experience in AA, who have either served as a board member of an academic association, contributed to guideline or high‐level consensus development, or published articles on AA. R.S. and C.C.Y. acted as the co‐chairs of this expert panel. All experts are authors on the manuscript.

A modified Delphi approach was used, with details provided in Figure 1. A consensus for Likert‐type and multiple‐choice statements was defined as a minimum of 70% agreement (i.e., “agree” or “strongly agree” combined) or disagreement (i.e., “disagree” or “strongly disagree” combined).

FIGURE 1.

Details of the three rounds in this Delphi exercise. A flowchart detailing the specifics of all three rounds of this Delphi exercise: Panelists' individual responses to the initial questionnaire were first collected (round 1, in green), followed by a physical meeting to review the initial results and discuss the views of the panelists (round 2, in blue), and lastly, additional discussions and voting were conducted online after the physical meeting (round 3, in pink). AA, alopecia areata.

3. Results

Figure 2 shows the summary of results from all rounds of the Delphi exercise. In the end, 140 statements achieved consensus and 43 statements did not. Key consensus statements on the epidemiology, diagnosis, and management of AA are summarized in Table 1.

FIGURE 2.

Summary of results from all rounds of the Delphi exercise. A flowchart detailing the number of statements that achieved consensus across all three rounds of this Delphi exercise. Results from round 1 (initial online study questionnaire) are indicated in green, results from round 2 (discussions during the 1.5‐day physical meeting) are indicated in blue, and results from round 3 (online discussions after the physical meeting) are indicated in pink. ^aExcluded open‐ended and background‐related questions (n = 43) where percentage of agreement/disagreement cannot be calculated. AA, alopecia areata.

TABLE 1.

Key consensus statements.

Epidemiology of AA

AA is an autoimmune inflammatory condition that produces variable degrees of hair loss, most often presents with hairless patches on normal‐appearing skin and often presents with preserved follicular ostia.

Genetic polymorphism confers susceptibility to AA.

AA is clinically heterogeneous and can be triggered by psychological stress and unknown environmental factors.

AA cases with onset in adulthood have different risk factors than patients with onset in childhood.

Exclamation point hairs at the margins of patches indicate active AA.

All forms of AA cause considerable psychological disorders (e.g., anxiety, mood disorders) and lower the QoL for patients and their families.

Moderate‐to‐severe AA causes significant psychological disorders and dramatically impacts the QoL for patients and their families.

Moderate‐to‐severe AA causes stigmatization in society.

Additional lesions in visible areas beyond the scalp (e.g., eyebrows, eyelashes, beard) impair patients' QoL to a greater extent.

Moderate‐to‐severe AA causes significant work and productivity impairment in adults.

AA is an impairing disease. a

AA patients are perceived as having a disfigurement in our society.

Autoimmune and neuro‐psychiatric comorbidities are more common in AA patients compared to the general population without AA.

The natural course of AA is unpredictable.

Most mild AA cases resolve spontaneously.

The rate of spontaneous resolution appears to be lower in patients with moderate‐to‐severe AA than in patients with mild AA, when the disease duration of AA exceeds 6 months, and in AA patients < 6 years of age.

The risk of progression to AT or AU is higher in patients with early‐onset AA (< 6 years of age).

AA is considered chronic and chronic persistent in patients with the condition for more than 6 and 12 months, respectively.

Severe hair loss (including AT, AU), ophiasis‐pattern AA, medical history of AD, concomitant autoimmune disease, childhood‐onset AA, disease duration (> 1 year), and, nail, eyebrow and eyelash involvement are factors associated with a poor prognosis and/or high likelihood of relapse for AA.

Diagnosis of AA

A positive hair pull test helps distinguish active AA, and a negative hair pull test indicates stable disease.

A positive hair pull test in clinically uninvolved areas is an important sign of progressive disease.

Trichoscopy is the most important tool for the diagnosis of AA and is essential in the assessment of disease activity and severity as well as therapeutic monitoring of AA.

In certain situations, skin biopsies should be considered to exclude other conditions (e.g., when the cause of hair loss is unclear).

Currently, there are no validated biomarkers that aid the diagnosis of AA.

AA patients with a hair loss of 21%–49% can be considered as moderate AA, and those with more than 50% scalp hair loss can be considered as severe AA.

AA patients who have significant eyebrow, eyelash and/or beard involvement, and significantly impaired QoL may be considered as having moderate‐to‐severe AA regardless of hair loss percentage on scalp.

Using systems that allow patients' self‐assessment of disease severity provides an ideal treatment approach by combining the patient and physician's perspective in AA management.

Management of AA

In most cases, AA can be managed by dermatologists alone.

As curative treatment is currently not possible, stopping further hair loss, stimulating the regrowth of hair, and improving QoL are primary goals of AA treatment.

Efficient systemic treatment started at an early stage may prevent the development of disease‐specific comorbidities in AA. b

There is a significant burden of adverse events with the off‐label use of currently available immunosuppressants in AA.

There is a significant unmet need for novel topical and systemic agents that offer prolonged remission and a safe side‐effect profile in long‐term moderate‐to‐severe AA treatment.

In children (< 12 years) with mild‐to‐moderate AA, topical corticosteroids could be a first‐line treatment prior to considering systemic treatment.

Topical corticosteroids could be used as a second‐line treatment in all patients with mild‐to‐moderate AA who cannot tolerate intralesional injections.

Topical corticosteroids should be the first‐line treatment for children < 12 years of age with severe AA.

Intralesional injections are more effective than ultrapotent/potent topical steroids for inducing regrowth and durable remission.

Intralesional corticosteroids alone or in combination with topical corticosteroids should be the primary treatment for all patients aged ≥ 12 years with active mild AA and/or AA with mild isolated patches of hair loss.

Intralesional corticosteroids should be the first‐line treatment for adults with moderate AA.

The optimal interval for intralesional corticosteroid treatment is between 3 and 6 weeks.

The maximum dose of intralesional triamcinolone acetonide treatment should not exceed 40 mg/month.

Intralesional corticosteroids do not sufficiently cover the therapeutic needs of patients with moderate‐to‐severe AA.

Topical therapies (including immunotherapy) do not reliably address the therapeutic needs of patients with moderate‐to‐severe AA.

AA may not place patients at a higher risk for lymphoma due to the consistent use of local, intralesional, or systemic corticosteroids.

Short‐term systemic corticosteroids should be the first‐line treatment for all patients aged ≥ 12 years with active severe AA.

Intravenous pulsed corticosteroids are not considered an acceptable alternative to oral or intramuscular corticosteroids.

Systemic corticosteroids should only be used to temporarily halt disease progression in patients with rapidly progressing, widespread, active disease.

Topical calcineurin inhibitors have lower efficacy than topical corticosteroids in AA.

Topical minoxidil can be used in combination with topical corticosteroid and topical immunotherapy.

Topical or oral minoxidil can be used in combination with other local/systemic treatments for chronic AA.

Steroid‐sparing agents such as cyclosporine, azathioprine and methotrexate should only be used to mitigate the risk of adverse effects associated with prolonged use of systemic corticosteroids.

Potential adverse effects associated with long‐term use and the risk of relapse on dose reduction or treatment cessation limit the use of all conventional systemic therapies for AA.

JAK inhibitors (with or without systemic corticosteroids) can be initiated as a first‐line systemic treatment in all patients aged ≥ 12 years of age with moderate‐to‐severe AA, in whom the disease could not be controlled with optimal topical/local therapies.

JAK inhibitors (with or without systemic corticosteroids) can be initiated as a second‐line systemic treatment in all patients aged ≥ 12 years of age with moderate‐to‐severe AA, in whom the disease could not be controlled with optimal systemic corticosteroid treatment.

JAK inhibitors should not be reserved for patients with moderate‐to‐severe AA who have failed at least two suitable systemic therapies (i.e., systemic corticosteroids, cyclosporine, methotrexate, azathioprine) or as the last resort after all age‐suitable conventional systemic therapies have been used.

Flares and treatment response in AA patients should be assessed by disease severity scores (e.g., SALT, AA‐IGA).

Flares in AA can be defined as an increase in SALT score as noted by the clinician, or an episode requiring escalation of treatment.

Defining an AA flare is a complex process and there is a need for standardization in defining measures of long‐term disease control.

A mild flare could be defined as a relapse of AA that increases the SALT score by ≤ 5 points, a moderate flare by 6–15 points, and severe flare > 15 points or diffuse AA. c

A mild flare does not necessitate additional treatment but could be managed with topical or intralesional therapies.

A moderate flare could be managed with topical or intralesional therapy, and/or additional systemic therapy.

A severe flare should be managed with additional systemic therapy, and/or a switch of JAK inhibitor, and/or adjuvant topical or intralesional therapy.

There are currently no validated biomarkers that would predict treatment response in AA patients.

There are no generally accepted criteria for defining treatment failure in AA.

A SALT score improvement of > 50% is an adequate treatment response for mild‐to‐moderate AA and an improvement of > 75% for severe AA.

Treatment failure can be defined as an inadequate clinical improvement (inadequate response at 3 months with systemic corticosteroids, inadequate response at 6 months with intralesional corticosteroids, methotrexate or once‐weekly topical immunotherapy d , or absence of any treatment response at 12 months with JAK inhibitors) or failure to achieve stable long‐term disease control, despite appropriate dose and duration of, and adherence to a therapeutic agent.

Among those with moderate‐to‐severe AA, 50%–100% of adolescent (aged 12–17 years) and 40%–100% adult patients achieve and maintain adequate treatment response with advanced systemic therapies used alone or in combination with other treatments.

Note: A table summarizing the 140 consensus statements achieved in this study, separated into three categories: the epidemiology, diagnosis, and management of AA.

Abbreviations: AA, alopecia areata; AA‐IGA, Alopecia Areata Investigator Global Assessment scale; AD, atopic dermatitis; AT, alopecia totalis; AU, alopecia universalis; JAK, Janus kinase; QoL, quality of life; SALT, Severity of Alopecia Tool.

^a AA can have a psychological and emotional impact on patients, and can impair their QoL.

^b This does not entail all comorbidities related to AA. Disease‐specific comorbidities mentioned refer to conditions such as psychiatric disorders (e.g., depression, anxiety).

^c The understanding of an increase in SALT score may vary among clinicians and depends on the patient's clinical situation. A flare may occur in patients who demonstrate clinical response. Any modifications to treatment in AA patients who experienced a flare should be subject to the attending clinician's judgment and the individual patient's medical history and clinical condition.

^d Topical immunotherapy refers to diphenylcyclopropenone and squaric acid dibutyl ester.

Details of all statements with consensus are shown in Tables S1–S3. Statements without consensus are listed in Table S4.

4. Discussion

4.1. Epidemiology of AA

Consensus was reached on the clinical presentation and natural history of AA, including triggers, negative prognostic factors, rate of spontaneous resolution, and risk of disease progression, and the definition of chronic and chronic persistent AA based on episode duration.

While the exact pathogenesis of AA remains poorly understood [3], the panel highlighted the association between family history and disease pathogenesis in pediatric patients with AA. The panel also suggested that environmental triggers that stimulate immunogenicity (e.g., vaccination and viral infections), psychological stress, and medical history of other autoimmune diseases are associated with AA disease pathogenesis in adult patients.

Comorbidities are frequent in patients with AA [2]. There was agreement among the panel that autoimmune and neuro‐psychiatric comorbidities were more common in patients with AA compared to the general population without AA. In terms of psychological burden, the panel recognized that AA causes anxiety and mood disorders, impacting both patients and their families [8].

Differences in healthcare systems, access to care, and patient journeys across APAC have contributed to non‐consensus outcomes in this study. Socio‐cultural differences, such as age, gender, and religion, can influence the perception of hair among individuals, leading to varying degrees of impact even in AA patients with the same disease severity [20].

4.2. Diagnosis of AA

While there are currently no validated diagnostic biomarkers for AA, the panel was aligned that trichoscopy is an important tool in diagnosing AA, assessing disease activity and severity, and monitoring treatment response. In contrast, there was no consensus on the usefulness of trichogram and reflectance confocal microscopy in these aspects. In certain situations, the panel concurred that skin biopsies should be considered to exclude other conditions, especially when the cause of hair loss is unclear.

Stratified by the percentage of hair loss, there was agreement on the definition of moderate (21%–49%) and severe AA (≥ 50%), which is consistent with the global, American, and European guidelines/consensuses [11, 13, 21, 22]. In addition, the panel agreed that patients with eyebrows, eyelashes, and/or beard involvement and significantly impaired QoL may be considered as having moderate‐to‐severe AA regardless of the percentage of scalp hair loss.

In daily clinical practice, most panelists would use the Severity of Alopecia Tool (SALT) score to evaluate their patients. The panel agreed that scoring systems that allow patients to self‐assess their disease severity, alongside perspectives from their physicians, would be ideal. Importantly, there is a need for a more practical scoring system that is less time‐consuming and more inclusive of factors such as eyebrow, eyelash, and beard‐specific measures [23].

While the experts would consider patients' QoL when making treatment decisions, there was no consensus on whether QoL indexes must be used. Our panel reckoned the need for comprehensive and easy‐to‐use AA‐specific QoL measures. Alopecia Areata Symptom Impact Scale (AASIS) and Alopecia Areata Quality of Life Index (AA‐QLI) are two AA‐specific health‐related QoL measures recommended by the European Academy of Dermatology and Venereology (EADV) Task Force of Quality of Life and Patient Oriented Outcomes; however, their usage is still limited and further validation is necessary [24].

4.3. Management of AA

Among the experts involved in this study, non‐comprehensive and/or non‐updated local guidelines are seemingly the most used reference point in their management of AA, thereby reinforcing the need for better guidance from an evidence‐based, regional expert‐led perspective.

The panel agreed that dermatologists can manage patients with AA on their own in most cases and provide long‐term follow‐ups, but there was no consensus on the value of adopting a multidisciplinary approach to managing AA. Nonetheless, some studies demonstrated that adjuvant psychological and psychiatric interventions could have a role in improving patients and their families' QoL, which is hence strongly recommended by the British Association of Dermatologists for AA patients experiencing moderate‐to‐severe psychological distress [13, 25, 26].

Figure 3 depicts a simple treatment algorithm based on the statements with consensus achieved in this study. Treatment effectiveness, disease severity, and patient response are the most impactful factors associated with treatment preference among the experts. The panel concurred that starting systemic treatment that is effective at an early stage may prevent the development of disease‐specific comorbidities, such as depression and anxiety, in patients with AA.

FIGURE 3.

Recommended treatment algorithm for patients with AA. A simple treatment algorithm, stratified by age and disease severity, developed based on the statements with consensus achieved in this study to provide a guide for physicians in APAC to manage patients with AA. AA, alopecia areata; ILC, intralesional corticosteroids; JAK, Janus kinase; QoL, quality of life; SALT, Severity of Alopecia Tool; SCS, systemic corticosteroids; TCS, topical corticosteroids. ^aMild AA is defined as a hair loss of < 21% on scalp, moderate AA as 21%–49% of hair loss, and severe AA as ≥ 50% of hair loss. AA patients with eyebrow, eyelash and/or beard involvement, and those who have significantly impaired QoL may be considered as having moderate‐to‐severe AA regardless of hair loss percentage on scalp. ^bAn improvement of > 50% in SALT score is an adequate treatment response for mild‐to‐moderate AA and an improvement of > 75% for severe AA. ^cSystemic corticosteroids should only be used to temporarily halt disease progression in patients with rapidly progressing, widespread, active disease. ^dFlares in AA can be defined as an increase in SALT score as noted by the clinician and as an episode requiring escalation of treatment. ^eThe understanding of an increase in SALT score may vary among clinicians and depends on the patient's clinical situation. A flare may occur in patients who demonstrate clinical response. Any modifications to treatment in AA patients who experienced a flare should be subject to the attending clinician's judgment and individual patient's medical history and clinical condition.

4.3.1. Mild and Mild‐To‐Moderate AA

4.3.1.1. Topical Corticosteroids

Topical corticosteroids are widely used as the first‐line treatment in all patients with mild disease, including children < 12 years, despite the limited number of clinical trials [27, 28, 29]. For patients with mild‐to‐moderate AA, the panel agreed that topical corticosteroids could be the first‐line treatment in children < 12 years and a second‐line treatment in patients who cannot tolerate intralesional injections.

The efficacy results reported for topical corticosteroids were mixed—ranging from 20% to 61% and with higher rates among patients with mild AA—due to inconsistency in the agents, concentrations, and regimens used [29]. While topical corticosteroids are generally safe and well tolerated, the risk of adverse events tends to increase with higher potency formulations, greater doses, and longer periods of use [29]. Discontinuation of topical corticosteroids can also lead to a disease recurrence rate of 38%–63% [29].

4.3.1.2. Intralesional Corticosteroids

In adult patients with moderate AA, the panel agreed that intralesional corticosteroids, with an optimal interval of 3–6 weeks, should be the first‐line treatment. If intralesional triamcinolone acetonide is used, the maximum dose should not exceed 40 mg/month. The panel also agreed that intralesional corticosteroids alone or with topical corticosteroids should be the primary treatment for all patients ≥ 12 years with active mild AA. In addition, the panel agreed that intralesional injections are more effective than ultrapotent/potent topical steroids for inducing regrowth and durable remission because of their ability to penetrate the dermis and reach hair follicles [29].

Although studies on intralesional corticosteroids in patients with AA are mostly limited to case series of small sample sizes in heterogeneous patient populations and with different primary outcome measures, it has been shown that intralesional triamcinolone acetonide significantly improved hair regrowth, density, and caliber across studies [29, 30]. Moreover, due to the local method of drug delivery and limited systemic absorption, intralesional corticosteroids are generally well tolerated with few side effects, where atrophy is commonly reported in patients on intralesional triamcinolone acetonide [29].

It is important to note that steroid phobia is a concern in dermatology in Asia [31], and is observed by the panel in families of pediatric patients and among adult patients who are prescribed topical, intralesional, or systemic corticosteroids. Physicians should always explain the risks and benefits of these medications and take patients' preferences into consideration when prescribing corticosteroids.

4.3.1.3. Other Topical/Local Treatments

While minoxidil is not indicated for AA, the panel agreed that topical minoxidil can be used in combination with topical corticosteroid and topical immunotherapy, whereas topical or oral minoxidil can also be used in combination with other local or systemic treatments for patients with chronic AA (disease duration > 6 months). Although there are only a few studies on the use of topical or oral minoxidil in patients with AA, adjuvant minoxidil may be considered given its role in improving hair density and potentially reducing the risk of relapse [11, 13, 32].

As for other topical/local off‐label treatments—including topical immunotherapy, topical anthralin, and phototherapy (psoralen ultraviolet A), no consensus was reached on their use as they are not widely available in the country/region the experts practice in.

4.3.2. Moderate‐To‐Severe AA

There had been no officially approved treatments that were indicated for patients with severe AA until recent years. The panel agreed that there is an unmet need for novel topical and systemic agents that offer prolonged remission and a safe side‐effect profile, as existing topical therapies (including immunotherapy) and intralesional corticosteroids do not sufficiently cover the therapeutic needs of patients with moderate‐to‐severe AA.

Currently, among the experts, systemic corticosteroids, JAK inhibitors, and cyclosporine (in order of preference) are the most used oral agents in patients ≥ 12 years with moderate‐to‐severe AA who are receiving optimal topical or local therapies.

4.3.2.1. Topical Corticosteroids

For children (< 12 years) with severe AA, the panel was aligned that topical corticosteroids should be the first‐line treatment. Nevertheless, some panelists highlighted the ineffectiveness of topical corticosteroids in controlling disease activity in severe AA, imploring the need for a systemic agent in these children.

4.3.2.2. JAK Inhibitors

There are currently three US FDA‐approved JAK inhibitors for AA: Baricitinib and deuruxolitinib are indicated for adults with severe AA, and ritlecitinib is indicated for adults and adolescents ≥ 12 years with severe AA. The panel agreed unanimously that JAK inhibitors approved for AA should be used as the first‐line systemic treatment in patients ≥ 12 years with severe AA. There was also agreement that such JAK inhibitors should not be reserved as the last resort when considering treatment options for patients with AA.

The efficacy of baricitinib, deuruxolitinib, and ritlecitinib was demonstrated in numerous clinical trials [33, 34, 35]. Moreover, the long‐term efficacy of baricitinib and ritlecitinib was proven through Week 104, with improvements in SALT score and eyebrow and eyelash assessment scores compared to baseline [35, 36]. The safety profiles of baricitinib, ritlecitinib, and deuruxolitinib were consistent, with most treatment‐emergent adverse events being mild or moderate and infrequently requiring treatment interruption or discontinuation [33, 34, 37].

Prior to the development and approvals of these three JAK inhibitors, tofacitinib has also been used as an off‐label alternative. However, there are limited randomized controlled trials investigating its role in AA, and it has not received regulatory approval for the treatment of AA to date [36, 38].

The safety of JAK inhibitors has been a concern since black box warnings for this class of therapeutics were issued following the ORAL Surveillance study [39]. However, reviews and meta‐analyses of dermatology clinical trials (including patients with AA) showed that JAK inhibitors were well tolerated and did not significantly increase the risk of serious infections, major adverse cardiovascular events, venous thromboembolism, and malignancy compared to control/placebo [39, 40, 41]. Discrepancies in findings between these meta‐analyses and the ORAL Surveillance study could be due to the different patient populations included in these studies. Patients with dermatologic conditions are usually of a younger age compared to those with rheumatoid arthritis (i.e., the focus population of the ORAL Surveillance study; a mean age of 61.1 years and had at least one additional cardiovascular risk factor) [39]. Nevertheless, the use of JAK inhibitors in the real world for AA remains limited, and further studies are required to understand the long‐term safety of JAK inhibitors in patients with AA [42].

4.3.2.3. Systemic Corticosteroids

Systemic corticosteroids are often prescribed for patients with severe AA in the real world [27, 28]. The panel agreed that short‐term systemic corticosteroids should be the first‐line treatment for all patients ≥ 12 years with active severe AA. Of note, no consensus was reached among the panel for its use as a first‐line treatment in children < 12 years with severe AA, mainly due to the lack of real‐world evidence and various side effects related to systemic corticosteroids. This differs from the result of an international consensus that recommended oral corticosteroids as a first‐line option in children (7–12 years) with an acute AA episode and SALT score > 50% [43].

The reported efficacy of intravenous pulse corticosteroids remains inconsistent [44, 45]. Corticosteroid therapy is also associated with a higher rate of adverse events versus placebo (55% vs. 13%), where reported adverse events include acne, weight gain, and gastrointestinal symptoms [46]. Moreover, relapse rates after discontinuation of corticosteroids are high (25%–100%) [46]. Another issue with systemic corticosteroids is their side effects when used long term, especially in children, which could lead to growth, immunity, and adrenal suppression [47]. The panel was, therefore, aligned that systemic corticosteroids should only be used to temporarily halt disease progression in patients with rapidly progressing, widespread, active AA.

While systemic corticosteroids can be administered orally, intravenously, or intramuscularly, intravenous corticosteroids are commonly administered in inpatient settings where patients should be carefully monitored, thus limiting their feasibility in busy clinical settings [12, 27]. The panel does not consider intravenous pulsed corticosteroids to be an acceptable alternative to oral or intramuscular corticosteroids.

4.3.2.4. Conventional Disease‐Modifying Antirheumatic Drugs (DMARDs)

DMARDs, including cyclosporine, methotrexate, and azathioprine, are sometimes used as off‐label treatments in AA, especially prior to the approval of AA‐indicated medications [46, 48]. However, side effects were commonly reported, and close monitoring was often required during treatment, which limited their usage [46, 49]. The panel was aligned that these steroid‐sparing agents should only be used to mitigate the risk of adverse effects associated with prolonged use of systemic corticosteroids.

Most importantly, the panel does not support the off‐label use of these medications. With respect to the role of conventional DMARDs, the panelists believe they do not have enough understanding or expertise to recommend such treatments for AA.

4.3.3. Treatment Monitoring

The panel agreed that treatment response and AA flares should be assessed by disease severity scores, where an agreement was reached on the definition of adequate treatment response and AA flares based on the SALT score (Figure 3). An agreement was also reached on the definition of treatment failure in AA.

4.4. Limitations

This study is limited by the participation of select countries in APAC, which do not fully represent all perspectives within a geographically diverse region. In addition, the disease management recommendations presented in this paper are based on the premise that all US FDA/European Medicines Agency (EMA)‐approved treatments for AA are available and accessible to patients across APAC. However, we acknowledge that some of the discussed treatment options are currently not widely available in all countries/regions due to pending regulatory approvals, barriers in treatment access, such as varying healthcare infrastructure and costs.

The panel notes that there is a need for further discourse on the choices of treatment and corresponding doses, monitoring tests, and individualized recommendations for specific patient groups, such as pregnant women or those with prior malignancy and cardiovascular diseases.

5. Conclusion

This expert consensus was developed using a modified Delphi‐based methodology, leveraging the clinical expertise of a panel of experienced dermatologists who practice in APAC. While the disease burden may vary across the region due to differences in population dynamics and healthcare infrastructure, this consensus provides a region‐focused guide to physicians in APAC on the diagnosis and management of AA, which could hopefully improve the outcomes of patients with AA in the long run.

Conflicts of Interest

Rodney Sinclair is the Director and Founder of Samson Medical Pty Ltd. which holds patents on the use of oral minoxidil to treat hair loss disorders; is on the Pharmaceutical advisory board of Eli Lilly, Pfizer Inc., and Leo Pharmaceutical; is on the Speaker bureau of AbbVie, Novartis, Glaxo Smith Kline; is a principal investigator in clinical trials for Amgen, Novartis, Arcutis Biotherapeutics, Aerotech, Merck and Co, Celgene, Coherus BioSciences, Jannsen, Regeneron, MedImmune, Glaxo Smith Kline, Samson Clinical, Boehringer Ingelheim, Oncobiologics, Roche, Ascend, Dermira, AstraZeneca, Akesobio, Reistone Biopharma, UCB Biopharma, Sanofi, Connect, Arena, Sun Pharma, Bristol Myer Squibb, Botanix pharmaceuticals, Pfizer, Eli Lilly, Zai Pharmaceuticals, Jiangsu Hengrui Medicine, Leo Pharma, AbbVie, Astra Zeneca, and Galderma. Chao‐Chun Yang was a clinical trial investigator or consultant for AbbVie, Amgen, Boehringer Ingelheim, Eli Lilly, GSK, Janssen, Novartis, Pfizer, Sanofi, and Takeda. Hyun‐Tae Shin was a clinical trial investigator or consultant for CKD Pharmaceutical Corp., Eli Lilly, Pfizer, and Sanofi. Felix Boon‐Bin Yap has been a speaker and advisor for Pfizer and Eli Lilly; advisor for AbbVie; speaker, advisor, and clinical trial investigator for Novartis and L'Oreal. Leona Yip is a consultant, advisory board member, key opinion leader, and/or speaker for L'Oreal Australia, Galderma, Pierre‐Fabre, Pfizer, Eli Lilly, AbbVie, and Novartis. All other authors have no conflicts of interest.

Supporting information

Table S1: Consensus outcomes on the epidemiology of alopecia areata (AA).

Table S2: Consensus outcomes on the diagnosis of AA.

Table S3: Consensus outcomes on the management of AA.

Table S4: Non‐consensus outcomes.

Data Availability Statement

The data that supports the findings of this study are available in Tables S1–S4 of this article.