Alopecia areata is a non-scarring, autoimmune hair loss disorder characterized by sudden, well-circumscribed patches of hair loss that can progress to total scalp (AT) or universal body hair loss (AU). Breakdown of hair follicle immune privilege with IFN-γ and JAK-STAT pathway activation drives disease. Severity and course are variable; spontaneous regrowth can occur. Management ranges from intralesional steroids for limited disease to topical immunotherapy and systemic JAK inhibitors for extensive or refractory cases. Psychosocial burden is substantial and warrants support.
Epidemiology
- Lifetime risk ~2%; any age; peaks in childhood and young adulthood.
- Associations: atopy, thyroid disease, vitiligo, Down syndrome, other autoimmune diseases.
- Nail changes (trachyonychia, pitting) occur in ~10–20%.
Pathophysiology
- Autoimmune CD8+ NKG2D+ T cells target anagen follicles; IFN-γ and IL-15 signaling with JAK-STAT activation.
- Genetic predisposition (HLA, immune genes); triggers include stress, infection.
Clinical Features
- Sudden round/oval patches of non-scarring alopecia; exclamation point hairs at margins, positive hair pull test in active disease.
- Variants: ophiasis (temporal-occipital band-like), sisaipho (reverse ophiasis), diffuse AA, AT, AU.
- Eyebrows/eyelashes may be involved; nail ridging/pitting; alopecia incognita in adults.
Diagnosis
- Clinical; dermoscopy: yellow dots, black dots, broken hairs, exclamation hairs.
- Consider screening TSH based on history/symptoms; rule out tinea capitis in children with scaling/adenopathy.
- Biopsy rarely needed; peribulbar “swarm of bees” lymphocytes.
Severity Assessment
- SALT score (Scalp Alopecia Tool) for extent; eyebrow/eyelash scales for facial involvement; patient-reported outcomes for impact.
Management
- Limited patchy AA (adults)
- Intralesional triamcinolone acetonide 2.5–10 mg/mL every 4–6 weeks (max total volume per session); monitor for atrophy.
- Topicals: high-potency steroids, minoxidil 5% foam/solution as adjunct; anthralin short-contact for irritation-induced regrowth.
- Children: avoid IL steroids; use topical steroids, minoxidil, anthralin.
- Extensive or rapidly progressive AA
- Topical immunotherapy: DPCP or SADBE applied weekly to induce contact dermatitis and regrowth; requires experienced centers.
- Systemic therapies:
- JAK inhibitors: baricitinib (adults; FDA approved), ritlecitinib (adults/adolescents; FDA approved), deuruxolitinib (region-specific/under review) show meaningful SALT responses; monitor for infections, lipids, cytopenias, acne, VTE risks as per label; vaccination review before therapy.
- Oral corticosteroids (pulse regimens) for short-term rescue; relapse common on taper.
- Methotrexate ± low-dose steroids, cyclosporine as alternatives with monitoring.
- Eyebrows/eyelashes
- Bimatoprost/latanoprost topical; intralesional steroids with care; JAK inhibitors can improve brows/lashes.
- Adjunctive measures
- Camouflage, wigs, scalp prostheses; eyebrow microblading/tattooing after stabilization.
- Psychosocial support: screening for anxiety/depression; support groups.
- Special populations
- Pediatrics: prioritize topical therapy and counseling; JAKs are being studied and some approved for adolescents (e.g., ritlecitinib ≥12 years in some regions).
- Pregnancy: avoid JAK inhibitors; use topical steroids/minoxidil cautiously (minoxidil often avoided); IL steroids localized if necessary.
Prognosis
- Variable; up to 50% regrow within a year for limited AA; relapses frequent.
- Poor prognostic factors: AT/AU, ophiasis, early onset, nail disease, long duration.
References (recent guidelines and key reviews)
- International alopecia areata consensus statements, 2022–2024.
- Phase 2/3 trials of baricitinib, ritlecitinib, and other JAK inhibitors, 2021–2024.
- Dermoscopy and outcome measure updates (SALT), 2022–2024.
- Psychosocial impact and QoL literature, 2021–2024.