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Patient guide · Prescription Per TDA 2024 + BAD 2025 living guideline · Updated 2026-05-08

Alopecia areata — complete patient guide
Autoimmune hair loss, SALT grading, the JAK inhibitor era

TL;DR:Alopecia areata is autoimmune patchy hair loss — not 'scared off' by stress — and often regrows by itself or with treatment. For extensive or recurrent cases, JAK inhibitors are an effective new option.

Alopecia areata (AA) is an autoimmune-driven hair loss. Lifetime risk in Taiwan is ~1.7-2.1%, and 85.5% of patients develop disease before age 40. Mild cases can recover spontaneously, but severe or chronic cases need active treatment. From 2024 onward, JAK inhibitors (baricitinib, ritlecitinib) have become the new first-line therapy for severe AA, though access in Taiwan still hinges on NHI criteria and out-of-pocket costs.

Note:This article is a patient-education summary. Actual drug selection, dosing, and Taiwan NHI coverage criteria must be evaluated by a specialist based on your individual situation.
SALT severity grading (TDA 2024)
Mild
≤ 20%
Hair loss ≤ 20% of scalp surface
Moderate
21-50%
Hair loss 20–50% of scalp
Severe
> 50%
Hair loss > 50%, including alopecia totalis and universalis

Upgrade criteria (any one promotes the severity by one tier): psychosocial impact, eyebrow / eyelash loss, ≥ 6 months treatment non-response, rapid progression with positive hair-pull test.

What is Alopecia Areata?

Alopecia areata (AA) is an autoimmune disease — the immune system mistakenly attacks hair follicles, producing well-demarcated round/oval patches of hair loss. Onset is sudden; patients often discover it while shampooing or are told by their hairdresser.

Alopecia areataAndrogenetic alopeciaTelogen effluvium
MechanismAutoimmuneAndrogens / geneticsStress / postpartum / illness
PatternSharply demarcated patches, smooth scalpReceding hairline, vertex thinningDiffuse global thinning
OnsetSuddenSlow (years)2-3 mo after trigger
Hair pull testPositive in active phaseNegativePositive
RecoveryMild self-resolves; severe needs treatmentNo spontaneous recovery6-12 mo after trigger removal

Taiwan TDA 2024 consensus: lifetime risk 1.7-2.1%; 66% onset before 30, 85.5% before 40. Pediatric/adolescent prevalence ~0.2-0.3%.

Why Does It Happen?

  • Environmental triggers: infection (viral, bacterial), drugs, vaccines (rarely)
  • Major psychological trauma or acute stress (bereavement, accident, surgery)
  • Family history of AA or other autoimmune disease
  • Coexisting autoimmunity: thyroid, vitiligo, atopic dermatitis, lupus
  • Lifestyle (Taiwan studies): smokers 1.88× risk; obstructive sleep apnea bidirectional association

Note: stress is often overstated as the sole cause. ~50% of patients have a major stressor in the prior 6 months; the other 50% don't. AA is multifactorial.

Clinical Subtypes

  • Patchy AA: most common; round/oval patches
  • Ophiasis: band along temporal/occipital hairline; treatment-resistant
  • Alopecia totalis: complete scalp hair loss (~30% of chronic cases progress)
  • Alopecia universalis: complete body hair loss including eyebrows, eyelashes (~15% of chronic cases)
  • Rapidly progressive AA: spreading to > 80% scalp within 3 months — emergency, needs steroid pulse
  • Acute diffuse and total alopecia (ADTA): similar presentation but better prognosis (~80% recover within 6 months)

Diagnosis

Most cases diagnosed by clinical exam + trichoscopy:

  • Exclamation-mark hairs — pathognomonic for active AA
  • Black dots — broken hair shafts at scalp
  • Sharply demarcated patches, smooth skin without erythema or scale
  • Positive pull test (≥ 6 hairs released by gentle traction = active)
  • Nail pitting — supportive evidence

Scalp biopsy needed only when distinguishing from tinea capitis, trichotillomania, primary scarring alopecia.

SALT Severity Assessment

  • Mild: SALT ≤ 20%
  • Moderate: SALT 20-50%
  • Severe: SALT > 50%

TDA 2024 escalates severity by one grade if any of: psychological/social impact, eyebrow/eyelash involvement, ≥ 6 months of inadequate response, rapid progression with positive pull test.

Treatment Ladder (TDA 2024 + EU Consensus 2024)

Children < 12 years

SeverityRecommended
All severitiesTopical corticosteroid ± topical 5% Minoxidil
Severe (3-11 yo, off-label)Systemic GC; tofacitinib 2.5-10 mg/d (off-label); MTX 0.3-0.6 mg/kg/wk

Adolescents (12-18) and Adults

Severity1st-line2nd-line
Mild-moderate (SALT ≤ 50%)Potent topical CS or intralesional triamcinolone ± topical Minoxidil 5%± topical DPCP immunotherapy
± UV / excimer laser
Severe (SALT > 50%)Oral / IV CS pulse ororal JAK inhibitor (Baricitinib, Ritlecitinib)Oral MTX or Cyclosporine + UV / excimer ± topical DPCP

JAK Inhibitor Era (key 2024 update)

Baricitinib (Olumiant)Ritlecitinib (Litfulo)
IndicationAdults ≥ 18, severe AA (SALT > 50%)≥ 12 yo severe AA
MechanismJAK1 / JAK2JAK3 / TEC
Dose4 mg/d (2 mg if ≥75 yo or infection-prone)200 mg/d × 4 wk loading → 50 mg/d maintenance
Phase-3 efficacyBRAVE-AA1/2 (n=1200): 36-wk SALT ≤ 20: 4 mg = 38.8% / 2 mg = 22.8% / placebo = 6.2%ALLEGRO 2b/3 (n=718): 24-wk SALT ≤ 20: 31% (200/50) / 23% (50) / 2% placebo
Pre-treatment screeningTB (IGRA + CXR), HBV/HCV, HIV, CBC, lipids, LFTTB, hepatitis, platelets, lymphocytes
Common AEsURI, headache, acne, CK rise, HSV reactivationHeadache, folliculitis, acne, diarrhea

EU 2024 Core Treatment Principles

  • "Wait-and-see" is NOT advisable for severe AA — natural recovery only 0-16.7%; earlier treatment responds better
  • Treatment goal: SALT ≤ 10 or SALT improvement ≥ 90% (replaces older SALT 20)
  • Adjustment trigger: change/dose-modify if no goal achievement at 24-36 weeks
  • Long-term maintenance: continue 6-12 months after complete regrowth; often required 3-7 years or even lifelong
  • Re-treatment after relapse: ritlecitinib 2nd course only 57% respond — avoid premature discontinuation
  • Combination: JAK + oral CS may enhance effect (small studies support)
  • Adjuvant: low-dose oral minoxidil consider (not monotherapy); biotin not recommended unless deficiency confirmed

Comorbidities (Taiwan NHIRD studies)

  • Anxiety, depression — elevated; some psychiatric disorders precede AA
  • Stroke risk: 1.61× elevated
  • Sensorineural hearing loss — cochlear melanocyte involvement
  • Sleep apnea — 3.89× AA risk; bidirectional
  • Other autoimmune: thyroid, atopic dermatitis, vitiligo, lupus, allergic rhinitis
  • Cancer: overall slightly reduced (SIR 0.89, only male significant); but lymphoma, breast (especially < 50 yo women), kidney, bladder cancers elevated — periodic screening recommended

Summary

AA is not a death sentence, but neither is it "wait until you're happier and it'll go away." TDA 2024 + EU Rudnicka 2024 + BAD 2025 living guideline (Nov 2025, second iteration) give a clear pathway: mild = intralesional CS + topical; severe = oral JAK inhibitor (now ↑↑ strong recommendation for adults AND adolescents ≥ 12 per BAD 2025 R40 / R41), with oral CS often used as a bridge. Reassess at 36 weeks; some patients may need up to 18 months before declaring failure (R42/R44). Long-term treatment is usually required; abrupt cessation increases relapse risk (R45). Counsel on MHRA/FDA black-box warnings: VTE, MACE, cancer, death — caution if > 65 or with risk factors (R47). Long-term safety in adolescents is still unknown — registry enrollment encouraged (R48). JAK inhibitors are the biggest treatment breakthrough in 5 years, but not a cure-all. If a patch persists > 1 month, spreads rapidly, or affects eyebrows/eyelashes — see a dermatologist promptly.