Chinese Guidelines for the Diagnosis and Treatment of Alopecia Areata (2026 Edition)

Journal：Skin, 2026, DOI:10.2738/SKIN.2026.0002 Lead authors: Wu Wen‑yu, Zhou Cheng; drafted by Lin Jin‑ran, Li Xiang‑qian; Hair Research Group, Chinese Society of Dermatology Disclaimer: This is structured abstract‑key recommendations excerpt, for professional learning only, not substitute for clinical practice.

Abstract

Alopecia areata (AA) is a T‑cell‑mediated autoimmune non‑scarring hair‑loss disorder caused by collapse of follicular immune privilege. It occurs across all age groups and imposes substantial psychosocial burden. This guideline was developed via systematic literature review, GRADE evidence grading and Delphi expert consensus. It updates definition, classification, diagnostic workflow, severity assessment, step‑wise treatment algorithm, special‑population management and long‑term follow‑up strategies, with special emphasis on JAK‑inhibitor‑based systemic therapy and psychological intervention for AA patients.

1 Definition & Clinical Phenotypes

Alopecia areata (AA): Autoimmune‑mediated non‑scarring alopecia characterized by well‑demarcated patches of hair loss; exclamation‑mark hairs are a classic clinical sign. Nail changes (pitting, trachyonychia) may co‑occur.

• Patchy AA: Localized bald patches
• Alopecia totalis (AT): Complete scalp hair loss
• Alopecia universalis (AU): Loss of all scalp‑ and body hair
• Diffuse AA: Widespread, non‑patchy hair shedding; easily misdiagnosed as telogen effluvium
• Ophiasis pattern: Band‑like hair loss along scalp periphery, generally poor‑prognosis phenotype

2 Severity Assessment

1. SALT (Severity of Alopecia Tool) score (baseline metric)
   • SALT 0: 0 % hair loss
   • SALT 1: 1‑24 % (mild)
   • SALT 2: 25‑49 % (mild‑moderate)
   • SALT 3: 50‑74 % (moderate‑severe)
   • SALT 4: 75‑99 % (severe)
   • SALT 5: 100 % (AT/AU)PMC
2. Severity‑upgrading criteria (any one present → upgrade severity by one grade)
   1. Complete loss of eyebrows/eyelashes
   2. Ophiasis‑type distribution
   3. Diffuse‑active disease (positive hair‑pull test)
   4. Nail severe involvement
   5. Poor response to prior adequate therapy
   6. Early‑childhood onset (<6 years old)
   7. Significant patient‑reported psychosocial impairment

3 Diagnostic Work‑up

3.1 Core diagnostic steps

1. Detailed history: onset, progression, hair‑pull test, personal/family atopy/autoimmune disease history, psychological stress, prior treatments.
2. Physical examination: scalp, eyebrows, eyelashes, body hair, nail examination.
3. Trichoscopy (dermoscopy): recommended routine examination. Typical findings: exclamation‑mark hairs, yellow dots, black dots, broken hairs.
4. Scalp biopsy: not routine. Reserved for ambiguous cases to differentiate from other non‑scarring / early scarring alopecias.

3.2 Laboratory screening

• Routine screening for comorbid autoimmune diseases: thyroid function + thyroid autoantibodies.
• Additional tests guided only by clinical clues: ANA, complete blood count, atopy‑related markers.

3.3 Differential diagnosis

Telogen effluvium, trichotillomania, androgenetic alopecia, syphilitic alopecia, scarring alopecias, alopecia caused by nutritional deficiency.

4 Step‑wise Therapeutic Recommendations

Therapeutic goals: halt disease progression, hair regrowth, reduce relapse, improve quality‑of‑life; stratified by age, severity, activity, phenotype.

4.1 Mild AA (SALT ≤24 %)

‑ First‑line: topical corticosteroids, intralesional corticosteroid injection (for limited stable patches). ‑ Adjuvant: topical minoxidil 2‑5 %. ‑ Observation is acceptable for small‑size, stable lesions with minimal psychological impact.

4.2 Mild‑to‑moderate AA (SALT 25‑49 %)

‑ Local therapy: topical / intralesional corticosteroids plus topical minoxidil. ‑ If upgrading‑criteria present or progressive disease: initiate systemic therapy.

4.3 Moderate‑severe / severe AA (SALT ≥50 %); age ≥ 12 years

‑ First‑line systemic therapy: oral JAK inhibitors (baricitinib, ritlecitinib, ivarmacitinib). Also recommended for rapidly‑progressive acute diffuse AA, when systemic corticosteroids are ineffective, contraindicated or declined by patients. ‑ Systemic corticosteroids: suitable for acute‑phase disease induction; long‑term maintenance oral steroids are not recommended. ‑ Adjuvant: low‑dose oral minoxidil. ‑ Dupilumab: option for patients with concomitant type‑2 inflammatory comorbidities (atopic dermatitis, asthma).

4.4 Children under 12 years old

‑ First‑line: topical / intralesional corticosteroids + topical minoxidil. ‑ JAK inhibitors: only use under specialist supervision when benefits outweigh risks, strictly follow age‑labelling restrictions. ‑ Systemic corticosteroids: avoid long‑term use, caution for growth‑related adverse effects.

4.5 Physical / adjuvant therapy

‑ Phototherapy (NB‑UVB): alternative for patients intolerant to pharmacotherapy. ‑ Psychological assessment and intervention: mandatory for patients with obvious anxiety/depression.

5 Safety Monitoring

1. JAK‑inhibitor monitoring: baseline complete blood count, liver function, lipid panel, tuberculosis screening; periodic follow‑up during treatment. Screen thromboembolic risk factors.
2. Corticosteroid‑related adverse‑effect surveillance (local atrophy for intralesional injection; glucose, bone metabolism for systemic steroids).

6 Relapse Prevention & Long‑term Management

‑ After achieving satisfactory hair regrowth: gradual tapering of systemic agents; maintain topical therapy. ‑ Inform patients of high relapse risk; regular follow‑up. ‑ Screen for associated atopic and autoimmune comorbidities throughout disease course.

7 Key Guideline Take‑home Messages

1. Combine SALT score plus seven upgrading criteria for comprehensive severity evaluation, not merely hair‑loss area. Psychosocial burden is formally included in severity judgement.
2. Trichoscopy is essential for diagnosis and activity monitoring; biopsy is not routine.
3. For patients ≥12 years with moderate‑severe AA, JAK inhibitors are first‑line systemic therapy.
4. Systemic corticosteroids are only for acute‑phase induction; long‑term maintenance is discouraged.
5. Comorbidity screening and psychological support are integral parts of AA management.

Note: This is manually structured excerpt of the original English guideline paper, for medical‑professional study purpose, cannot replace full‑text original article or clinical physician judgement.