Key Facts

Alopecia areata (AA) is the most common autoimmune cause of hair loss. It can range from a single small patch to total body hair loss. Understanding the natural history and prognosis is essential for appropriate counselling.

Epidemiology

• Lifetime prevalence: ~2%
• Equal sex distribution
• Any age; peak onset 20–40 years
• ~20% onset in childhood
• Family history in ~10–20% (polygenic)

Aetiology

• Autoimmune: CD8+ T-lymphocyte attack on hair follicle bulb — collapse of hair follicle immune privilege
• Genetic: polygenic; HLA associations (HLA-DQB1*03); increased risk in first-degree relatives
• Environmental triggers: emotional stress (debated), infection, vaccination (rare reports)
• Autoimmune associations: thyroid disease, vitiligo, pernicious anaemia, Addison's disease, coeliac disease, type 1 diabetes

Pathophysiology

• Normal hair follicles have 'immune privilege' — protected from immune surveillance
• In AA: collapse of immune privilege → CD8+ NKG2D+ T-cells recognise follicular autoantigens → attack hair bulb during anagen (growth) phase
• IFN-gamma and IL-15 signalling → JAK-STAT pathway activation → sustained inflammation
• Follicle enters premature catagen/telogen → hair shedding
• Follicle is NOT destroyed → regrowth potential preserved (non-scarring)

Typical Presentation

• Well-circumscribed patches of complete hair loss on scalp
• Smooth, skin-coloured scalp (no scarring, no scale)
• Exclamation mark hairs at periphery: short (3–4 mm), tapered proximally
• Single or multiple patches
• May affect beard, eyebrows, eyelashes, body hair

Subtypes

• Patchy: most common — one or more patches
• Alopecia totalis: complete scalp hair loss
• Alopecia universalis: complete body hair loss
• Ophiasis: band-like pattern along occipital and temporal scalp — poor prognosis
• Sisaipho (ophiasis inversus): spares the periphery; hair loss centrally
• Diffuse alopecia areata: diffuse thinning without discrete patches — can mimic telogen effluvium

Nail Changes (~10–20%)

• Fine pitting (most common)
• Trachyonychia (sandpaper-like roughness)
• Longitudinal ridging, brittleness

Red Flags

• Rapid progression to totalis/universalis
• Childhood onset with extensive disease — poor prognosis
• Associated autoimmune features (thyroid, vitiligo) — screen appropriately

Bedside

• Clinical examination: characteristic smooth patches with exclamation mark hairs — often diagnostic
• Dermoscopy (trichoscopy): exclamation mark hairs, yellow dots (empty follicles), black dots (broken hairs), short vellus hairs (regrowth)
• Pull test: may be positive at active edges

Bloods

• TFTs: thyroid autoimmune disease (~20% association)
• Ferritin, FBC: exclude iron deficiency contributing to hair loss
• Vitamin D: commonly low; may contribute
• Anti-TPO antibodies: screen for autoimmune thyroid disease
• Coeliac screen (tTG IgA): if GI symptoms or suspicion

Biopsy

• Scalp punch biopsy: not usually required for typical AA; consider if diagnostic uncertainty
• Histology: peribulbar lymphocytic infiltrate ('swarm of bees'), increased catagen/telogen hairs, miniaturisation

Special Tests

• Not routinely required
• SALT score (Severity of Alopecia Tool): quantifies scalp hair loss — used in clinical trials and for monitoring

Non-Pharmacological

• Reassurance and support: ~50% with limited disease recover within 1 year
• Alopecia UK: patient support charity
• Wigs/hairpieces: available on NHS prescription
• Camouflage techniques: eyebrow pencils, microblading
• Psychological support: CBT, counselling — hair loss significantly impacts quality of life

Pharmacological — Limited Disease (≤50% Scalp)

• Intralesional triamcinolone acetonide 5–10 mg/mL: first-line — injected into affected areas every 4–6 weeks; effective for limited patches
• Potent topical corticosteroids: clobetasol propionate 0.05% OD — alternative/adjunct
• Topical minoxidil 5%: may promote regrowth; adjunctive

Pharmacological — Extensive Disease (>50% Scalp)

• Baricitinib 4 mg OD (JAK inhibitor): NICE TA913 — for severe alopecia areata in adults who have not responded to other treatments
  • BRAVE-AA1 and BRAVE-AA2 trials: 35–39% achieved SALT ≤20 at 36 weeks vs 3–6% placebo
  • Monitor: FBC, LFTs, lipids, infection screening
• Ritlecitinib (JAK3/TEC inhibitor): NICE-approved for adolescents and adults with severe AA
• Contact immunotherapy (diphencyprone/DPCP): specialist centres — induce allergic contact dermatitis to redirect immune response; ~30–40% response
• Short-course oral prednisolone: pulse therapy (e.g. prednisolone 0.5 mg/kg for 3 months tapering) — may halt rapid progression but relapse common
• Oral methotrexate 15–25 mg weekly: specialist use for refractory disease

Referral Criteria

• Dermatology: extensive disease, rapid progression, diagnostic uncertainty
• Psychology: significant psychological impact, children with AA
• Trichology clinic: specialist hair loss centres

• Limited patchy AA: ~50% recover within 1 year; ~80–90% at some point
• Alopecia totalis/universalis: <10% achieve full recovery
• Poor prognostic factors: extensive disease (>50%), ophiasis pattern, childhood onset, >1 year duration, associated autoimmune disease, family history
• Relapse: common (~50% relapse after initial recovery)
• Baricitinib: sustained response in ~35% at 52 weeks (BRAVE trials); regrowth lost on stopping
• Psychological impact: significant — associated with depression, anxiety, social isolation

Alopecia Areata Severity Classification

BRAVE Trial Results (Baricitinib)

Prognostic Factors