2025+澳大利亚专家共识声明：成人中度至重度斑秃的全身治疗（更新版）

ABSTRACT

Over 5000 patients are newly diagnosed with Alopecia areaata(AA) in Australia each year. AA severity varies from a single small patch to complete loss of scalp hair, body hair including eyelashes and eyebrows. Approximately 40% of affected individuals experi-ence only a single patch and achieve spontaneous, complete and durable remission within 6 months(acute AA). A further 27% de-velop additional patches but still attain complete remission within 12months(chronic AA). Chronic persistent AA(CPAA) is defined by an episode duration of>12 months and occurs in approximately 33% of patients. Without systemic treatment, 55% of individuals with CPAA will have persistent multifocal relapsing and remitting disease, 30% will progress to alopecia totalis(AT) and 15% will ultimately develop alopecia universalis(AU). The physical disfigurement, unpredictable course, social isolation and rejection contrib-ute to the psychological distress attributable to AA. A wide range of topical, intralesional and systemic agents used to treat AA were evaluated in the 2018 Australian expert consensus statement. In 2020, the international Alopecia Areata Consensus of Experts(ACE publication stated that if reimbursed,Janus Kinase Inhibitors(JAKi's) would be an ideal systemic treatment for adults with AA.TGA approval of baricitinib in 2023 and rictitibin in 2024 for severe AA is the first step on the pathway for these systemic medications to be reimbursed on the Australian Government Pharmaceutical Benefits Scheme(PBS). Reimbursement would significantly transform the Australian therapeutic landscape for AA. The purpose of this 2025 Update on the Australian Expert Consensus Statement on the treatment of chronic, moderate to severe AA is to augment the 2018 treatment algorithm to include these TGA-approved medications and to address indications for initiation, continuation and dose titration of systemic JAKi treatment, appropriate choice of agent, sat-isfactory outcome measures and to provide guidance on when to discontinue successful or unsuccessful treatment.

Abbreviations:AA,alopecia areaat;AT,alopecia totalis;AU,alopecia universalis;CPAA,chronic persistent alopecia areaata.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

©2025 The Author(s). Australasian Journal of Dermatology published by John Wiley& Sons Australia, Ltd on behalf of Australasian College of Dermatologists.

1| Introduction

Alopeia areaata(AA) is an organ-specific autoimmune disease with a characteristic hististic. Acute, intense peribulbar lym-phocytic inflammation of anagen follicles initiates apoptosis of terminal hair bulb epithelium leading to hair fibre breakage(an-agen effluvium) and premature catagen. Chronic lesions show an increased ratio of catagen and telogen follicles and follicular miniaturisation. Premature catagen, prolonged telogen and re-peated failure to re-establish anagen lead to prolonged baldness.

Until recently there had been no new Therapeutic Goods Administration(TGA) approved treatment for AA in over 50years.In May 2023, Baricitinib, a Janus kinase(JAK)1/2 in-hibitor, was approved under the trade name Olumiant for the treatment of severe AA. In July 2024, Ritlecitinib, a JAK3/TEC kinase inhibitor, was approved under the trade name Litfulo[1,2]. Also in 2024, a third agent, deuruxolitinib, was approved by the U.S. Food and Drug Administration(FDA). Although deuruxolitinib is not yet approved by the TGA, its FDA approval underscores the growing global momentum toward systemic JAK inhibitor therapy for AA. Its potential future availability in Australia may further expand treatment options and inform up-dates to national treatment guidelines. Inclusion of ritlecitinib and baricitinib on the PBS would represent a critical step toward equitable access for Australians living with severe AA and pave the way for potential future reimbursement of emerging agents such as deuruxolitinib. Currently, several other treatments are in phase 2 or phase 3 development.

Treatment of chronic, severe AA with ritlecitinib and barici-tinib results in meaningful hair regrowth in over two-thirds of patients[3, 4]. With ongoing treatment, approximately 90%of responders maintain their response out to 152weeks[5].Most patients who respond within the first 8-24 weeks go on to achieve a SALT score<20 by 52 weeks, whereas fewer than 10%of late responders reach this threshold[6].

Response rates to JAKi are comparable in patients with base-line SALT scores ranging from 20 to 95; however, outcomes are significantly poorer in patients with AT and in those with an episode duration greater than 4years[7,8].

These approvals materially alter the therapeutic landscape for AA and necessitate an update of the 2018 Australian expert consensus guidelines[] to support dermatologists managing patients with AA, who must carefully weigh the safety and ef-ficacy of long-term JAKi therapy against the negative impact of delayed treatment on long-term prognosis.

1.1| Burden of Disease

The global prevalence of AA is 2%[9]. In Australia, the estimated incidence of AA is 0.28 per 1000 patient-years, with the peak age of onset occurring between 19 and 34 years. The point prevalence of AA in 2020 was estimated at 0.13%(1.26 per 1000 individuals)[10].

Amongst patients with newly diagnosed AA,17% were prescribed antidepressant and 9% aniolytic medication. This is more than double the national average for the prescription of these therapies

[10]. Individuals with AA frequent their primary care provider more than matched controls, particularly women, rural dwellers and those of lower socioeconomic status. The proportion of indi-viduals with AA referred to secondary care has increased over time from 19.4% in 2009 to 27.9% in 2017[11]. Significant anxiety,stress and a substantial negative impact on self-perception and quality of life is prevalent amongst these individuals. Psychosocial impact is greatest amongst individuals with SALT score 50%-94%, and stigma is linearly correlated with AA severity[12].

Patients' self-perception of disease severity and involvement of eyebrows/eyelash loss have been identified as the strongest predictors of diminished quality of life rather than physician-recorded SALT scores[13, 14]. Although quality of life impact assessment in AA can be established using the Dermatology Life Quality Index[15] and specific quality of life questionnaires for use in AA have been developed, there remains no standardised health-related quality of life(HRQoL) outcome measure for use in AA[15].

1.2| Aetiology and Pathogenesis

AA pathogenesis involves interferon-gamma mediated collapse of hair follicle immune privilege or privilege. Immune privilege is characterised by down-regulation of classical human leukocyte antigen(HLA)expression and up-regulation of non-classical HLA expression on the lower portion of the follicle, from the bulb to the bulge[16].

Hair follicle immune privilege is a requirement for long hair.Ageing hair bulbs increasingly express cell surface antigens such as MICA and ULBP-3 as a marker of senescence. In non-immune privileged tissues, co-expression of these senescent antigens together with classical HLA antigens triggers immune-mediated apoptosis and/or necroptosis[16, 17]. In immune priv-legied anagen follicles, apoptosis is not triggered in senescent matrix cells and catagen is prevented. The lack of cell surface expression of HLA-C and B(combined with the up-regulation of HLA E, F and G) antigens masks senescent antigens and pre-vents them from triggering immune-mediated apoptosis and necroptosis. Collapse of immune privilege, with cell surface expression of classical HLA-A, B and C and loss of HLA-E, F and G antigens unmasks previously hidden senescent antigens to antigen presenting T cells(APC)[16,18-19].

APCs recruit and activate CD8+NKG2D+ effector T cells that induce apoptosis in follicle outer root sheath cells, resulting in anagen arrest and the initiation of catagen within the proband hair follicle[20,21].

Local factors transmit immune privilege collapse and T cell me-diated anagen arrest to neighbouring follicles, producing circu-lar patches of alopecia.The subsequent appearance of secondary patches of AA suggests systemic as well as local factors are in-volved in patients with multifocal disease. The demonstration of an altered inflammasome in non-lesional hair bulbs using RT-PCR further supports the role of systemic factors in the patho-genesis of AA[22, 23].

Genetic aetiology is conferred as a complex polygenic trait. A genome-wide association study identified 139 single nucleotide

polymorphisms from eight genomic regions that are signifi-cantly associated with AA. Each of these genomic regions con-tains several genes controlling: the activation and proliferation of regulatory T cells(Treg cells); cytotoxic T-lymphocyte-associated antigen 4(CTLA4); interleukin(IL)-2/IL-21, IL-2 receptor A(IL-2RA; CD25); Eos(also known as Ikaros family zinc finger 4;IKZF4); HLA; PRDX5 and STX17 genes expressed in the hair follicle itself; as well as ULBP(cytomegalovirus UL16-binding protein) gene cluster on chromosome 6q25 that encodes activating ligands of the natural killer cell receptor NKG2D[24].

Although AA was previously considered a Th1-driven disease,there is increasing recognition that Th2 cytokine activation has a role in the disease[25]. Highlighting that the underlying mechanisms of AA are not yet fully understood.

1.3| Natural History

Non-scarring hair loss most commonly involves the scalp and face but can affect any terminal hair follicle. Episode duration is the dominant predictor of the natural history of AA[26] with longer episodes being associated with a lower likelihood of spon-taneous regrowth. Approximately two-thirds of affected individ-uals experience acute, self-limiting AA, whereas the remaining one-third develop CPAA. About 40% of episodes present as a single patch that undergoes spontaneous, complete and durable remission within 6 months. A further 27% of episodes involve secondary patches that appear sequentially but still achieve complete and durable remission within 12 months. Fewer than 5% of patients develop acute multifocal and/or diffuse AA that progresses rapidly over weeks to months to AT or AU. CPAA,defined by an episode duration>12 months, occurs in approx-imately 33% of patients. Consistent with the placebo response rate below 3% observed in phase 3 clinical trials, spontaneous remission in CPAA is rare, and nearly 50% of cases ultimately progress to AT or AU[27-29].

1.4| Currently Available Treatments

Chronic persistent AA and moderate to severe AA generally require systemic therapy[30]. Systemic corticosteroids are only suitable for short-term use due to accumulated toxicity.A number of systemic non-steroidal anti-inflammatory med-ications are used off-label in combinations with systemic ste-roids as steroid-sparing agents. Their efficacy in this context is uncertain, and with the exception of ciclosporin, none have been investigated in a high-quality study as a monotherapy. In a placebo-controlled, randomised, double-blind trial investi-gating ciclosporin 4mg/kg in patients with moderate to severe AA, 31.3% of patients achieved a 50% reduction in SALT score(SALT50) and 6.3% of patients achieved 100% reduction in SALT score(SALT100) at 12 weeks[26-29].

The cost per cure is a metric used to compare the price of differ-ent treatments. It takes into account the cost of that treatment and the number of patients who need to be treated for 1 patient to achieve a positive treatment outcome.

The PBS dispensed price for thirty ciclosporin 100mg cap-sules is$373.80[31,32]. According to the Australian Bureau of Statistics in 2017-2018, the average weight for Australian men was 87kg and Australian women 72kg[33]. For an 87kg man,the estimated monthly cost of ciclosporin at 4 mg/kg is$4329.15 per SALT50 response and$31,674.41 per SALT100 response.

In comparison, the dispensed price for twenty-eight baricitin 4mg tablets is$1046.01. The published SALT≤20 response is 51.9% at 36 weeks. The cost per‘cure’(defined as SALT≤20)with baricitinib for severe AA is$2695.87. The published SALT≤20 response rate to ritlecitinib 50 mg daily is 43% at 48 weeks[34]. The cost of ritlecitinib in Australia has not yet been estab-lished. The cost of 30 ritlecitinib capsules based on the United Kingdom National Health Service is£949.41, which is approxi-mately$1981.00 AUD[35]. The approximate cost per‘cure’ for ritlecitinib 50mg is$2693.87 per month at current exchange rates. Although most ciclosporin responders eventually lose re-sponse, most responders to ritlecitinib sustain clinical response at 24 months with treatment[36, 37].

1.5| Definition of Moderate to Severe Alopecia Areta

The Severity of Alopecia Tool(SALT) is the standard metric used to quantify the extent of hair loss in phase 2 and phase 3 clinical trials of AA[15]. A SALT score of 0 indicates no scalp hair loss, whereas a score of 100 represents complete loss of scalp hair[38, 39]. Subscript numerals are used to denote percentage improvement from baseline. For example, SALT50 reflects a 50%reduction in hair loss compared to baseline.

The Alopecia Areatita Investigator Global Assessment scale(AA-IGA)(Table 1) uses SALT as a singular measure to define disease severity. Specifically, a SALT score from 1 to 20 corre-sponds to limited disease; 21-49 to moderate disease; 50-94 to severe disease; and 95-100 to very severe disease(Table 1)[40].These severity thresholds have been endorsed by a global expert consensus statement[26].

There is expert consensus that AA patients with moderate to very severe disease are candidates for systemic therapy, and that systemic corticosteroids reduce the risk of disease progression and disease relapse[30, 41-42].

In the pivotal phase 3 trials for patients with a baseline SALT>50 treated with either baricitin or ritlecitinib, the primary outcome measure that was used to define a favourable treatment outcome was a SALT score of≤20[40].

Various visual aids are available to facilitate calculation of the SALT score. The original aid created by Olsen et al. allows cli-nicians to map the area of hair loss in each quadrant. It is most useful for patients with moderate to very severe disease. The Sinclair SALT seven score card(Figure 1) is a transparent busi-ness card with markings representing SALT scores of 0.125, 1,2,3 and 7, which can be placed on the scalp. It is particularly useful for rapid scoring of patients with limited or moderate dis-ease[43].

TABLE 1| The Alopecia Areata Investigator Global Assessment scale.

||None Limited Limited 0|Moderate 2|Severe|Very severe|| |---|---|---|---|---|---| ||0|1|2|3|4| |Extent of scalp hair loss(%)a|0|1-20|21-49|50-94|95-100|

aSALT is recommended to assess the extent of hair loss[40].

 B

 FIGURE 1|(A) SALT Seven Score Card.(B) Demonstration of the SALT SEVEN score card being used in clinical practice(Score=2).

2| Methods

An initial exercise on reviewing current international and Australian guidelines for management of severe alocia area was conducted as well as a review of current literature. The grade of each therapy type was determined based on current data availability and assessed using the National Health and Medical Research Council(NHMRC) Body of Evidence Matrix(Table 2)[44]. Subsequently, a summary of treatment types was categorised according to the NHMRC grading(Table 3).

Following this exercise, discussions with local Australian der-matologists with specific expertise in treating AA were held,and key areas of need were identified.

An updated consensus statement for the management of chronic,moderate-to-severe AA was drafted from these discussions and

TABLE 2| Definition of NHMRC grades of recommendations.

|Grade of recommendation|Description| |---|---| |A|Body of evidence can be trusted to guide practice| |B|Body of evidence can be trusted to guide practice in most situations| |C|Body of evidence provides some support for recommendation(s) but care should be taken in its application| |D|Body of evidence is weak and recommendation must be applied with caution|

disseminated to Australian dermatologists with a subspecialty in hair and scalp disorders for input.

Treatment algorithms were developed to guide clinical decision-making in alopecia areaata(AA),incorporating current evidence,clinical experience and key disease characteristics.

Two separate algorithms are presented: one for acute AA(dis-ease duration<6 months)(Figure 2A) and one for chronic or chronic persistent AA(Figure 2B). Both provide a stepwise ap-proach to treatment, considering disease severity, duration and prior treatment response.

3| JAK Inhibitors(Level of Evidence A)

JAK inhibitors(JAKi), which block intracellular signalling of multiple pro-inflammatory cytokines including interferon-y and interleukins involved in T-cell activation, have demonstrated promising therapeutic potential in the treatment of AA. In a 2023 systematic review and meta-analysis of seven randomised clinical trials with 1710 patients, JAK inhibitors were associ-ated with patients achieving a 30%, 50% or 90% improvement in SALT scores from baseline compared with placebo. Results from notable large RCTs are outlined below.

3.1| Baricitinb

Baricitinib is a selective inhibitor of JAK1 and 2 that is approved by the Therapeutic Goods Administration(TGA) for the treat-ment of severe and very severe alopecia areata in adults[45]. It

TABLE 3| Summary of therapeutic type and grade of recommendation per NHMRC definition.

|Therapy type|Grade of recommendation| |---|---| |Systemic therapy|| |Baricitinib|Level A| |Ritlecitinib|Level A| |Prednisolone|Level B| |Tofacitinib|Level C| |Ciclosporin|Level C| |Methotrexate|Level C| |Contact immunotherapy|Level C| |Phototherapy|Level D| |Azathioprine|Level D| |Sulfasalazine|Level D| |Topical and adjunctive therapy|| |Intralesional|Level B| |triamcinolone|| |Topical corticosteroids|Level B| |Topical prostaglandin analogues|Level C| |Oral/Sublingual minoxidil|Level C| |Topical minoxidil|Level C| |Topical JAKis|Level D| |Topical calcineurin|Level D| |inhibitors|| |Platelet rich plasma(PRP)|Level D|

is also TGA approved for the treatment of atopic dermatitis and rheumatoid arthritis[46].

In severe AA, Baricitinib is administered orally or a dos-age of 2mg once daily, which can be increased to 4mg once daily in case of inadequate response. In very severe AA,therapy should be initiated at a dosage of 4 mg once daily, re-duced to 2mg once daily when an adequate response has been achieved[46].

3.1.1| Efficacy

In the BRAVE-AA1 and AA2 Phase 3 randomised clinical tri-als,36.8%-40.9% of participants with severe or very severe AA treated with baricitinib 4mg and 21.2%-24.4% of those treated with baricitinib 2mg achieved a SALT score of≤20 at 52 weeks.With continued treatment, that response(SALT score of≤20)was maintained through to 152 weeks in 89.1% of participants treated with 4mg daily and 83.6% of those who received 2mg daily. A SALT score≤10 was achieved by 27.8%-29.9% of partic-ipants treated with 4mg and 14.1%-16.7% of those treated with 2mg at 52 weeks[3, 5, 47].

Outcome measures continued to improve after 18 and 26 months of treatment implying that long-term therapy could be especially important for patients with extensive disease at baseline[47]. A re-cent real-world study found 61.5%(59 out of 96 patients) achieved a SALT score of≤20 at the end of a 52-week treatment period[48].

3.2| Ritlecitinib

Ritlecitinib is a selective inhibitor of Janus kinase 3(JAK3)and the tyrosine kinase expressed in hepatocellular carcinoma(TEC) family of kinases. It inhibits cytokine-induced phos-phorylation of signal transducer and activator of transcription(STAT) mediated by JAK3-dependent cytokines, as well as blocking signalling of B and T-cell receptors dependent on TEC kinase family members[49].

Ritleitinib was approved by the TGA for the treatment of severe AA in June 2024 in adults and adolescents 12years and older.Ritlecitinib is administered orally at a dosage of 50mg once daily[2,50].

3.2.1| Efficacy

An integrated analysis of the ALLEGRO Phase 2b/3 and long-term Phase 3 studies found 45.1% of participants who received ritlecitinib 50mg and 45.9% of those receiving 200mg/50mg(200mg daily loading dose for 4weeks followed by 50mg daily dose) achieved a SALT score of≤20 at Year 1. Additionally, a SALT score of≤10 was achieved by 34.2% of participants on 50mg and 39.4% on the 200mg/50mg regimen in the first year[4]. A higher proportion of participants achieved a SALT score of≤20 by Year 2.

Participants with AT or AU or with longer episodes of severe disease, showed lower response rates. These findings suggest that earlier initiation of treatment may result in better outcomes[34,51].

A recent systematic review evaluated the efficacy and safety of ritlecitinib versus baricitinib, showing comparable efficacy of ritlecitinib 50mg daily and baricitinib 4mg[52]. A comparison of side effects and laboratory investigation alterations reported with baricitinib and ritlecitinib in AA patients is described in Table 4.

3.3| Assessment of Response to JAKi Treatment

Response to treatment is defined in current studies as achiev-ing a SALT≤20 with a secondary objective of achieving SALT≤10. Response to treatment can also be evaluated by percent-age of change from baseline. AT and AU patients might perceive achieving eyebrow, eyelash and beard regrowth as a reason-able treatment response despite the SALT score remaining un-changed. The area of scalp involvement, whether it be easy to conceal by parting hair a certain way or through adopting a dif-ferent hairsple, can significantly influence patient satisfaction.This cosmetic impact may determine whether a patient feels content or distressed, regardless of their SALT score.

A

Treatment algorithm

Moderate, severe and very severe acute alocia area

 *Defined as less than 50% improvement in SALT score from baseline LDOM; Low Dose Oral Minoxidil

B

Treatment algorithm Moderate, severe and very severe chronic and chronic persistent alocia area

 *Defined as less than 50% improvement in SALT score from baseline LDOM; Low Dose Oral Minoxidil

FIGURE 2|(A) Treatment algorithm for moderate, severe and very severe acute alopectia area. Solid arrows indicate the preferred treatment sequence. Dashed arrows indicate alternative treatment pathways or modifications based on clinical response or contraindications.(B) Treatment al-gorithm for moderate, severe and very severe chronic and chronic persistent alopectia area. Solid arrows indicate the preferred treatment sequence.Dashed arrows indicate alternative treatment pathways or modifications based on clinical response or contraindications.

TABLE 4| Side effects reported with baricitinib and ritlecitinib in alocia areaata patients[47].

|Reported percentage of side effects(%)|Baricitinib(N=1303)|Ritlecitinib(N=1294)| |---|---|---| |Adverse events occurring in≥5% of patientsa||| |Nasopharyngitis|6.8%|12.4%| |Acne|6.7%|10.4%| |Headache|8.2%|17.7%| |Upper respiratory tract infection|10.9%|10.2%| |COVID-19|11%|15.5%| |Urticaria|NR|6.8%| |Urinary tract infection|6.1%|NR| |Pyrexia|NR|7.6%| |Cough|NR|7.4%| |Fatigue|NR|7%| |Adverse events of special interest||| |Herpes Zoster|3.4%|1.5%| |GI perforation|0.1%d|NR| |Sensorineural hearing loss|NR|1.1%| |MACE|0.1%|0.2%| |Malignancy|0.3%|0.5%| |Opportunistic infection|0.1%|<0.1%| |Death|NR|0.2%| |DVT/PE|0.2%|<0.1%| |Laboratory abnormalities||| |Platelets||| |>600X109/L|0.8%|NR| |Anaemia||| |Hg<8g/dL|0.2%|<0.1%| |Neutropenia||| |1000 to<1500/mm3|NR|5.1%| |<1000/mm3|1.6%|0.8%| |Lymphopenia||| |<500/mm3|0.3%|2.2%| |Blood creatine phosphokinase increase||| |>5*ULN|6.6%|5.9%| |HDL cholesterol|53.3%(<1.55 mmol/L)|0.6%(<0.8*LLN)| |LDL cholesterol|36.8%>(> 3.36mmol/L)|1.6%>(> 1.2*ULN)| |Triglecyrides|1%>(> 5.7mmol/L)|8.2%>(> 2.2mmol/L)| |ALT||| |>3*ULN|3.7%|2.5%| |AST||| |$$>3^{\ast} ULN$$|2.9%|2.3%|

Abbreviations:ALT,alanine aminotransferase;AST,aspartate aminotransferase;HDL,high-density lipoprotein;LLD,low-density lipoprotein;LLN,lower limit of normal; MACE,major adverse cardiovascular events; NR,not reported; ULN,upper limit of normal.

With one or both treatments.

bIn the rilebitinb study, four cases of breast cancer, one testicular cancer, one papillary thyroid cancer and one adjudicated malignant melanoma were reported. Time to onset of the event ranged from 68 to 299 days(median 156 days) after starting ritleitinib.

Two reported deaths during the study period that were determined by the investigator to be unrelated to the study treatment(breast cancer and acute respiratory failure/cardiorespiratory arrest).

One case of chronic lymphocytic leukaemia, one case of B-cell lymphoma, one case of breast cancer and one case of melanoma in situ were reported.

One case of chronic lymphocytic leukaemia, one case of B-cell lymphoma, one case of breast cancer and one case of melanoma in situ were reported.

3.4| Effect of Episode Duration on Response to Treatment

Nearly 50% of patients with patchy alopecia area persisting for over a year(CPAA) progress to develop AT or AU and have an estimated 0% chance of spontaneous recovery[29]. Longer disease duration confers a reduced response to treatment with JAKi, though the response to treatment is seen even in patients with a disease episode of over 4 years. The duration of the AA episode does not appear to affect the speed of response to treat-ment[6].

3.5| When to Stop or Titrate Down Treatment

A study evaluating relapse rates following treatment withdrawal in patients who achieved a SALT score of≤20 with baricitinib(n=40) and maintained their response for 1 year found that 20% of patients sustained their response 3 years after discontin-uation. Upon retreatment, most patients regained clinical re-sponse. Notably, patients who remained in remission for 3 years had a shorter current episode duration and shorter disease du-ration[5].

Similarly, for patients who were successfully treated with ritilei-tinib for 6 months, defined as a 30% improvement in SALT score(n=22), 18%(4/22) of patients maintained response 28 weeks post-discontinuation[53].

As approximately one-fifth of patients remain in remission after treatment withdrawal, discontinuation of JAK inhibitor therapy may be considered after 6-12 months of treatment in patients who have achieved their target response. Alternatively, gradual dose tapering can be considered where feasible. The decision should be made in discussion with the patient, ensuring they are fully informed of the potential consequences of continuing stopping or reducing the dose.

3.5.1| Interclass Switching

Treatment failure with one JAKi does not necessarily predict treatment failure with a another. Emerging evidence has shown that patients that failed to respond to the pan JAKi, tofacitinib,may respond to treatment with baricitinib or ruxolitinib. These findings support the feasibility of interclass switching and sug-gest that trialling a different JAKi may be a reasonable strategy in non-responders[51, 52, 54].

4| Guidelines for Treatment Initiation,Monitoring and Management With JAK Inhibitors

Prior to initiating JAK inhibitor(JAKi) therapy, patients should be assessed for risk factors that may increase the likelihood of morbidity or mortality with JAKi therapy(see Table 5). Although the only absolute contraindications in current drug prescribing information to JAKis are hypersensitivity to the drug or its ex-cipients and active serious or opportunistic infections, other clinical conditions may warrant caution or even avoidance of

TABLE 5| Recommended pretreatment evaluation[55, 56].

Patients at increased risk for morbidity or mortality

Age≥50 with at least one cardiovascular risk factor

History of PE, VTE, retinal artery occlusion, stroke

Current or past long-time smoking

Patient undergoing surgery or immobilisation

History of malignancy-consider type, stage, duration and prior treatment

${}^{a}$ Current smoker, high-density lipoprotein level<40mg/dL, history of hypertension,diabetes,myocardial infarction or coronary heart disease.

bExcluding resolved non-melanoma skin cancer.

TABLE 6| Contraindications[46, 57].

Contraindications

Serious active infection

Hypersensitivity to therapeutic agenta

Active malignancy(not including resolved non-melanoma skin cancer)

Low platelet count<100,000 cells/mm3

Haemoglobin<8g/dL

Absolute neutrophil count<1000 cells/mm3

Lymphocyte count< 500 cells/mm3

Therapy with interacting medication

History of thromboembolism or pulmonary embolism

Pregnancy or intent to become pregnant ${}^{a,b}$

Lactating womena

eGFR<30mL/min/1.73m2a(30<eGFR<60mL/

min/1.73m2 requires dose adjustment)(baricitinb)

Severe hepatic impairment(Child-Pugh C, ritlecitinib)

Immunosuppressed patient

Note: Some contraindications listed above are relative, some absolute."Absolute.

bWomen of childbearing potential should take appropriate precautions to avoid becoming pregnant during treatment with baricitin and for at least 1 week after the final treatment and at least 1 month for ritleitinib.

treatment(Table 6). Although not explicitly listed as absolute contraindications in the current prescribing information, their presence should prompt a careful individualised risk-benefit as-sessment. Recommended laboratory testing before and during JAKi therapy is outlined in Table 7.

4.1| Vaccinations

Live vaccines are generally contraindicated immediately before and after treatment with JAKi, and if indicated should be re-ceived at least 1 month before starting immunosuppressive ther-apy[59].

TABLE 7| Laboratory testing[46,57-58].

|Test|Prior to initiating treatment|During treatment| |---|---|---| |FBC|$+$|Within 1 month and then every 3 months| |CMP|$+$|Within 1 month and then every 3 months| |Hepatitis B and C virus serologic panel|$+$|| |HIV serology|Consider|| |Lipid profile|$+$|Within 1 month and then every 3 months(baricitinb)| |PPD/QuantiFERON-TB Gold assay and (In immune- suppressed or history of tuberculosis) chest-X ray|$+$|Be alert for symptoms such as chronic cough, weight loss, fever or night sweats and consider further evaluation if these occur during treatment|

Abbreviations:CMP,complete metabolic profile;FBC,full blood count;PPD,purified protein derivative(Mantoux test).

Completion of all age-appropriate immunisation is recom-mended prior to treatment initiation, as well as:

4.3| AA Flare-Up During Treatment

During treatment, some patients may experience disease flare-up with new onset of discrete alopecic patches. Such cases can be managed by increasing the dose of JAKi if on baricitin 2mg daily dose(increase to 4mg daily). Intralesional steroid injections if limited involvement, or in cases of extensive exac-erbation, initiation of a short course of concomitant systemic corticosteroids, with gradual tapering.

● Recombinant herpes zoster vaccine

● Influenza vaccine

● Pneumococcal vaccine

● COVID-19 vaccine

For vaccines given as a series(Shingrix), the first dose should ideally be given before starting therapy to ensure the best re-sponse, unless this would cause a significant delay in the start of a necessary treatment. All non-live vaccinations recommended prior to treatment can be given safely during therapy if neces-sary. Administration of adjuvanted recombinant zoster vaccine in rheumatoid arthritis patients treated with JAKi resulted in significant increases in anti-varicella-zoster virus immunoglob-ulin G titers[59-62].

4.2| Indications for Interruption of Treatment

Treatment should be interrupted and restarted when values/sta-tus return to normal[46, 57].

• Absolute lymphocyte count<500/mm3

● Haemoglobin<8g/dL

• Absolute neutrophil count<1000 cells/mm3

● Serious infection or opportunistic infection

● Liver function tests show elevations of≥3 times the upper limit of normal

● In case of herpes zoster infection developing while on treatment, temporary interruption of treatment may be considered

Treatment should be discontinued:

$$\text{- Platelet count}<50,000/ mm^{3}$$

4.4| Adjuvant Minoxidil Therapy

A synergistic effect has been demonstrated when incorporating minoxidil with JAKi treatment[63, 64]. A recent systematic re-view, found increased efficacy when combining oral minoxidil with JAKi(85%)[65].

5| Systemic Corticosteroids(Level of Evidence B)

Prednisolone or similar systemic corticosteroids are currently considered first-line treatment for acute moderate to very se-vere AA.

Treatment can be administered orally, intramuscularly or intra-venously as pulse therapy[66-69]. A trial of systemic steroids can be considered for chronic moderate to very severe AA.Relapse on dose reduction or cessation of treatment is common;however, severe short-term and cumulative toxicity preclude their use for more than 3 months.

Therapeutic protocols and effectiveness vary across studies and there is no evidence to clearly rank the various systemic steroid agents or therapeutic protocols.

In the Alopeia Areata Consensus of Experts(ACE) study,prednisolone was the preferred systemic corticosteroid, with once daily mane administration[41] starting with a dose of 0.4-0.6mg/kg/day with gradual tapering off over 6-12weeks.

Pre-screening investigations for untreated infections should be considered to minimise the steroid-related complications.Patients on treatment should be monitored regularly for sleep and mood disturbance, diabetes, hypertension, peptic ulcer dis-ease, ocular toxicity and acute infections. Prophylaxis against osteopenia should also be considered.

6| Ciclosporin(Level of Evidence C)

To date, there is only one RCT that has investigated the efficacy of ciclosporin(CSA) monotherapy in AA[31]. In this double-blind, randomised, placebo-controlled study, 32 patients(18-65 years) with moderate-severe AA were randomised to receive either CSA(4 mg/kg/day) or placebo for 3 months. Although the proportion of patients achieving a 50% reduction in the SALT score was higher in the ciclosporin group(31.3%) compared to the placebo group(6.3%), the results were not statistically signif-icant(p=0.07).

A 2021 meta-analysis assessing the therapeutic efficacy of CSA in AA incorporated seven studies evaluating CSA monotherapy and eight studies examining combination with systemic cortico-steroids. The authors' assessment was that CSA exhibits a ben-eficial therapeutic impact on AA. The overall mean proportion of responders, defined as terminal hair growth exceeding 50%,was 73%(95% CI, 57%-85%), with a mean recurrence rate of 39%(95% CI,10%-78%).

The mean response rate for CSA monotherapy was 66%(95% CI,50%-79%), whereas combination therapy with corticosteroids showed a response rate of 78%(95% CI, 48%-93%). Recurrence rates were 55%(95% CI, 6%-96%) for monotherapy and 28%(95%CI,6%-72%) for combination therapy[70].

In the ACE study, it was agreed that CSA is an effective mono-therapy agent in AA, with a recommended dose of 3-5mg/kg/day for a maximum treatment duration of 6-12 months[41].CSA, however, is not TGA-approved for the treatment of AA and based on the current evidence, its use as a first-line therapy is not recommended by this group. Where other first-line ther-apies are not available, or contraindicated, it can be used as a second-line(off-label) treatment, either as a monotherapy or in combination with systemic steroids as a steroid-saring agent in patients who respond initially to systemic steroids but relapse on dose reduction.

7| Methotrexate(Level of Evidence C)

There have been no randomised, placebo-controlled studies in-vestigating methotrexate(MTX) in AA. In view of the signifi-cant rate of spontaneous remission seen in patients with acute and chronic AA, it cannot be assumed that MTX is superior to placebo. Nevertheless, a 2019 meta-analysis of 16 studies con-cluded that MTX was an effective treatment for AA[71].

The overall rate of complete hair regrowth with MTX was 35.8%(95% CI, 25.0%-48.3%). Subgroup analysis revealed that the pooled complete response rate in adults was 44.7%(95%CI, 32.9%-57.1%), significantly higher than the 11.6%(95% CI,

5.1%-24.5%) observed in the paediatric population(p=0.001).A recent 2023 double-blinded RCT of 89 patients with chronic and refractory AT and AU evaluated the efficacy and tolerance of MTX, both as monotherapy(25mg/week) and in combina-tion with low-dose prednisone(20mg/day for 3months, then 15mg/day for 3months)[72]. At the end of the 12-month period,the authors concluded that while MTX alone generally resulted in partial hair regrowth in patients with chronic AT or AU,whereas combining it with low-dose prednisone led to complete hair regrowth in up to 31% of patients.

In the ACE study, it was agreed that the recommended MTX dose for the treatment of AA is 15-20 mg once weekly[41].

8| Azathioprine(Level of Evidence D)

An open-label RCT involving 50 patients with AA(SALT score≥10) compared 300mg weekly azathioprine(AZA) pulse therapy(WAP) to 5mg betamethasone on 2 consecutive days every week(mini-pulse therapy) for 4 months[73]. The authors concluded both treatments to be effective for AA, with 44.52%of patients who received WAP therapy demonstrating hair regrowth.

In a Cochrane analysis, these results were of low certainty[74].AZA has also been used with success in the paediatric AA pop-ulation; however, its benefits must be considered against its po-tential risks[75].

9| Topical Therapy

Topical therapy can be used as monotherapy or as an adjunctive treatment.

9.1| Topical and Intralesional Steroid Therapy

Topical corticosteroids(TCS) are used in cases of limited area of involvement. They can be used as monotherapy or as an ad-junctive treatment[76]. High-potency TCS have been shown to be more efficacious than low-potency formulations[77].Intralesional triamcinolone acetonide(ILK) is a well-established treatment for limited-type AA, with response rates ranging from 60% to 95% across 12 studies[78]. A systematic review and meta-analysis identified that the optimal regimen for the admin-istration of ILK is at 3-4 weekly intervals for up to 6 months, at concentrations of 2.5-10 mg/mL for the scalp and 2.5-5 mg/mL for the face[79].

Potential side effects of TCS and ILK include folliculitis, atrophy,striae, telangiectasia and acneiform eruptions[80].

9.2| Contact Immunotherapy

Topical contact immunotherapy with diphenylcycloprope-none or squoric acid dibutyl ester can promote hair regrowth in patients with AA. A meta-analysis of 45 studies(n=22,227)found that 65% of patients showed some improvement, with

32.3% achieving complete regrowth with a 49% recurrence rate.However, most studies were not randomised, placebo-controlled trials, which limit the strength of the evidence[81].

As the mechanism of action relies on inducing allergic contact dermatitis, side effects are common. These include local ery-thema, eczematous reactions(e.g., blistering, scaling, exuda-tion), pruritus, regional lymphadenopathy, generalised eczema,hyperpigmentation and flu-like symptoms[76, 81].

9.3| Topical Calcineurin Inhibitors

Topical calcineurin inhibitors are not considered a first-line treatment for AA at present, as there is no evidence of clinical benefit[82-84].

9.4| Topical JAK Inhibitors

Topical JAK inhibitors are a potential new treatment for AA with limited effectiveness[85]. A study conducted by Bokhari et al. involved applying 2% tofacitinib, 1% ruxolitinib, 0.005%topical clobetasol dipropionate and a placebo to the four scalp quadrants of 16 patients with AU for 28 weeks. Partial hair re-growth was observed in the tofacitinib(6/16), ruxolitinib(5/16)and clobetasol(10/16) groups, but not in the placebo group(0/16)[86].

In an open-label, single-arm pilot study, Liu et al. assessed the efficacy and safety of topical to factinib 10 patients with AA.Regrowth occurred in 3 patients(significant regrowth in 1 pa-tient with 61% regrowth and partial regrowth of 35% in 2 pa-tients), whereas seven patients experienced no regrowth[87].Topical ruxolitinib and delocitinib were investigated with un-satisfactory results[88, 89]. We currently do not advocate using topical JAKi for scalp AA.

9.5| Topical Minoxidil

Topical minoxidil can induce accelerated hair regrowth in al-opicia patches and reduce disease activity in AA cases by lowering periflicular lymphocytic infiltration[90]. The most common side effect is skin irritation[76, 91]. Topical minoxidil has inconclusive evidence to support its use as an adjunct ther-apy in AA[41].

9.6| Topical Prostaglandin Analogues

Several studies have explored the efficacy of bimatoprost and la-tonoprost for scalp aloeta area, with mixed results[92, 93].Improved efficacy was seen when combined with topical beta-methasone or clobetasol[94, 95].

10| Emerging Treatments for AA

Several JAK inhibitors are in phase 1, 2 and 3 clinical trials for chronic severe and very severe AA. Notable agents under

investigation include tofacitinib, brepopitinib, deuruxoli-tinib, ruxolitin, deucravacitinib, upadacitinib, jaktinib and ivarmacitinib.

Tofacitinib, a pan-JAK inhibitor, is used in both oral and sublin-gual preparations for AA. A meta-analysis showed a 54% signif-icant hair regrowth rate, but a high relapse rate after cessation[96]. Oral to factitinib is given at a twice-daily dose. Sublingual tofacitinib offers pharmacokinetic benefits and a longer half-life, potentially allowing once-daily dosing[97].

Brepocitinib, a selective TYK2 and JAK1 inhibitor, was evalu-ated against ritleitinib in a phase 2a RCT with 142 participants[98]. At 24 weeks, 60% of repocitinib users and 50% of ritleci-tinib users achieved a 30% improvement in SALT scores, versus 2% in the placebo group. In addition, 81% reported eyelash re-growth and 72% observed improvements in eyebrows.

Ruxolitinib, a selective reversible JAK1/2 inhibitor, has shown effectiveness in treating moderate-to-severe AA across various case series[99, 100]. In an open-label study of 75 patients, both ruxolitinib and tofacitinib achieved similar rates of complete re-mission(21%). However,84.2% of patients on ruxolitinib reached SALT50 or better, versus 78.4% on tofacitinib[99].

Deuruxolitinib, a deuterated form of ruxolitinib, approved by the FDA since July 2024 for treatment of severe AA, demonstrated significant improvements in SALT scores in phase 3 studies. At 24 weeks, 42% of patients in the 12mg group achieved a SALT score of<20[101].

Upadacitinib, a JAK1 inhibitor, is being evaluated in a phase 3 trial in adults and adolescents[96]. Data from case reports and retrospective cohort studies suggest upadacitinib is effec-tive in treating AA, particularly in patients with concurrent atopic dermatitis[102-104]. One study involving 25 patients demonstrated a median SALT score improving from 50 to 5 after 24 weeks of treatment[105]. Another study with 19 pa-tients showed that 57.1% achieved complete hair regrowth at 28 weeks[106].

Jaktinib, a novel JAK1/2 inhibitor previously evaluated for my-efibrosis, is in a phase 3 RCT for severe AA[107].

Ivarmacitinib, a JAK1 inhibitor, has shown promising outcomes in a phase 2 RCT involving adults with moderate-to-severe AA[108]. After 24 weeks, the percentage reduction in SALT score from baseline was 19% in the placebo group compared to 56% in patients receiving 4mg ivarmacitinib daily.

Filgotinib is a JAKi with high selectivity for JAK-1. It is ap-proved by the FDA and EMA(European Medicines Agency) for the treatment of rheumatoid arthritis and has also been investi-gated for use in Crohn's disease. Complete scalp hair regrowth was reported in a patient with severe alopecia areata who re-ceived filgotinib as part of a clinical trial evaluating its efficacy in Crohn's disease[109].

Deucravacitinib, a TYK2 inhibitor, approved by the TGA for the treatment of psoriasis, is undergoing phase 2 clinical trials to assess its effectiveness in treating AA[110].

10.1| Biologics

Dupilumab, an IL-4Rα blocker approved for atopic dermatitis,may exert therapeutic effects in alopearia area through mod-ulating the Th2-pathway signalling[23]. In a phase 2a RCT involving 60 patients(23 patients with AD), 32.5% achieved SALT30,22.5% SALT50 and 15% SALT75 by week 48. A signif-icant correlation was observed between elevated baseline IgE levels and response to treatment[111]. In contrast, there are also case reports suggesting that dupilumab may paradoxically in-duce or exacerbate AA in certain individuals[112-114].

Tralokinumab, an IL-13 inhibitor, has shown effectiveness in a case study in mild to moderate AA patients with AD treat-ment[115].

Several immunomodulating agents are in phase 2 trials for AA,including daxidimilab(ILT7 target), rosnilimab(PD-1 agonist),etrasimod (SJP receptor modulator), EQ101(tri-specific IL-2,IL-9, IL-15 antagonist) and bempibartil(IL-7/TSLP receptor an-tagonist)[116-120].

Apremilast, a PDE-4 inhibitor that reduces IFN-y activity, has been described in the treatment of AA; however, case series in which its use in AA has been described have revealed inconsis-tent effectiveness[121-125].

10.2| Off Label Indications for Systemic Treatment-Facial Alopecia Areaata

Baricitinib, ritleitinib and brepicitin have shown efficacy in promoting eyebrow and eyelash regrowth through phase 2-3 RCTs[34, 47, 126]. Tofacitinib has also shown effectiveness in a large case series[127]. Interestingly, the duration of eyebrow and eyelash did not significantly impact treatment outcomes,indicating these hair follicles may remain viable even after ex-tended periods of inactivity. Topofitacitinib and ruxitibin have shown promise in smaller studies [128-131]. An eDelphi study found that systemic therapy is warranted for AA affecting eyebrows or eyelashes if it leads to functional or occupational impairment[26]. Beard apecteraa(BAA) can have pro-found psychosocial effects[132]. Baricitinib, tofacitinib and rux-itionalib have been used successfully in case reports and small case series, though their efficacy in BAA has not been studied in RCTs[127,132-133].

Prostaglandin analogues including bimatoprost and prolatanoprost have been shown to induce eyelash regrowth in several studies[93,94,134-138].

10.3| Patient Registries

Given the need to understand the safety profile of emerging ther-apies and better describe the real-world effectiveness of exist-ing and emerging mono and combination treatment regimens,the group strongly advocates for the registration of patients in high-quality patient registries. This concept has been supported internationally and has led to the development of the Global Registry of Alopeia Areatis Disease Severity and Treatment

Safety(GRASS)[139, 140]. The pilot phase of this project has been led by the Australasian Hair and Wool Research Society and National and International Registry Solutions(NISR), an Irish charity, in Australia over the past 3years, but has also es-tablished sites in Ireland and Italy, with multiple other interna-tional centres in the process of joining to provide comparable,harmonised data that will facilitate the development of valuable networks to help gather and interpret data from the use of ther-apies in AA.

11| Conclusion

Guidelines for the management of moderate to very severe al-opeia area in paediatric and adolescent populations are needed; however, this was beyond the scope of the current work.

Given the accumulating evidence demonstrating the limited efficacy, higher cost and unfavourable side effect profiles of immunosuppressants such as MTX,CSA and AZA, we recom-mend reserving these treatments for cases in which systemic treatment is warranted but JAKi are contraindicated. Emerging data suggest that early initiation of treatment is associated with improved response rates and prognosis. Therefore, JAKi should be considered for patients with a SALT score of 21 and higher corresponding with moderate-to-severe severity. In cases of eyelash or eyebrow involvement, initiation of JAKi therapy may also be appropriate at lower SALT scores.

Conflicts of Interest

Dr. Kushnir-Grinbaum has served as an investigator for AbbVie, Eli Lilly,Merck,Pfizer,DermAbio,Sanofi,Novartis,Eli Lilly,Samson.She has received honoraria for professional services from AbbVie and Eli Lilly. Dr. Yip has been a consultant and/or advisory board member for L'oreal, Galderma, Eli Lilly, Pfizer, LEO Pharma, CryoMed. Dr. Wall reports receiving honoraria for consultancy from Bristol Myers Squibb,Eli Lilly, Pfizer, AbbVie and Sun Pharma; has received speaker fees from Almirall, Lilly and L'real; and received support from AbbVie to attend conferences. He is a shareholder in Samson Clinical. He is an employee of National and International Skin Registry Solutions(NISR)and a director of Hair Restoration Blackrock. He is a steering committee member of the Global Registry of Alopeia Aarea Disease Severity and Treatment Safety(GRASS) International and PI of GRASS Ireland.

Dr.Eisman is a member of the Australian Dermatology Advisory Board of Eli Lilly and is a principal investigator in clinical trials for Pfizer Inc.,AbbVie,Arena Pharmaceuticals,Boston Pharmaceuticals,Bristol-Myers Squibb, Botanic, Dermira,Eli Lilly and Company,LEO Pharma,Novartis, Regeneron, Tigermed, Suzhou Connect Pharmaceuticals,Janssen,Kymab Ltd.,Evelo Biojosciences,KoBiolabs and Avance Clinical.Prof. Sinclair has been an investigator for and/or provided professional services to AbbVie, Aerotek Scientific, Akeso Biopharma, Amgen,Arcutis, Arena Pharmaceuticals, Ascend Laboratories, AstraZeneca,Bayer Pharma- ceuticals, Boehringer Ingelheim, Bristol Myers Squibb,Celgene Co-herus BioSciences, Connect Biopharma,Cutaneana, Dermira,Eli Lilly and Company, Galderma, GlaxoSmithKline, Janssen, LEO Pharma,MedImmune/AstraZeneca, Merck Sharp& Dohme, Novartis,On- cobiologics, Pfizer, Regeneron, Reistone Biopharma, Roche,Samson Medical Technologies, Sanofi, Sun Pharma and UCB Pharma.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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