Alopecia Areata
Summary
Alopecia areata (AA) is an autoimmune condition causing non-scarring hair loss, characterised by T-cell mediated attack on hair follicles. It presents as well-demarcated patches of hair loss, most commonly on the scalp but potentially affecting any hair-bearing area. The condition ranges from limited patchy involvement to complete scalp hair loss (alopecia totalis) or total body hair loss (alopecia universalis). While not physically harmful, AA carries significant psychological impact. Spontaneous regrowth occurs in 50% of cases within one year, but recurrence is common. Treatment includes topical and intralesional corticosteroids, with JAK inhibitors representing a major therapeutic advance for severe cases.
Key Facts
- Prevalence: Lifetime risk 2%; affects 2 million people in the UK
- Age of onset: Peak age 15-29 years; 60% develop before age 20
- Pattern: Well-circumscribed patches; "exclamation mark" hairs pathognomonic
- Extent variants: Patchy AA, alopecia totalis (scalp), alopecia universalis (entire body)
- Prognosis: 50% spontaneous regrowth within 1 year; high recurrence rate
- Key treatments: Topical steroids, intralesional triamcinolone, JAK inhibitors (baricitinib)
Clinical Pearls
Exclamation Mark Hairs: Short broken hairs that taper toward the scalp are pathognomonic for AA. Finding these at the margins of a patch confirms the diagnosis.
The Nail Sign: Nail pitting (regularly spaced pits) occurs in 10-20% of patients and correlates with more severe or persistent disease.
Autoimmune Associations: Screen for thyroid disease (present in 8-28% of AA patients). Also associated with vitiligo, atopic dermatitis, and pernicious anaemia.
Why This Matters Clinically
Although not medically dangerous, alopecia areata profoundly impacts quality of life and psychological wellbeing. Recognition of the condition, appropriate investigation for associated autoimmune disorders, and supportive management are essential. New treatments (JAK inhibitors) offer hope for severe cases previously considered untreatable.
Incidence & Prevalence
- Lifetime risk: 2%
- Prevalence: 0.1-0.2% at any time
- Annual incidence: 20 per 100,000
- Trend: Stable incidence
Demographics
| Factor | Details |
|---|---|
| Age | Any age; peak 15-29 years; 60% onset before age 20 |
| Sex | Equal male:female ratio |
| Ethnicity | All ethnic groups; possibly higher in Asian populations |
| Geography | Worldwide distribution |
Risk Factors
Non-Modifiable:
- Family history (10-20% have affected first-degree relative)
- Personal history of atopy (hay fever, asthma, eczema)
- Other autoimmune diseases
- Down syndrome (8-10x increased risk)
Modifiable:
| Factor | Association |
|---|---|
| Psychological stress | May trigger episodes (controversial) |
| Viral infections | Possible trigger |
| Smoking | No clear association |
Mechanism
Step 1: Loss of Immune Privilege
- Hair follicles normally have "immune privilege" (protected from immune attack)
- This is maintained by low MHC class I expression and immunosuppressive cytokines
- In AA, this privilege is lost, exposing follicular antigens to immune system
Step 2: T-Cell Mediated Attack
- CD8+ T cells and natural killer cells infiltrate the hair bulb
- IFN-γ upregulates MHC class I and II on follicular keratinocytes
- NKG2D ligands activate cytotoxic T cells
- Melanocyte antigens may be the primary target (explains sparing of grey/white hairs)
Step 3: Hair Follicle Damage
- Attack occurs during anagen (growth phase)
- Premature entry into catagen/telogen
- Dystrophic hairs break easily (exclamation mark hairs)
- Hair shaft miniaturisation
Step 4: Potential Recovery
- Hair follicle stem cells in the bulge are spared
- Regrowth possible when inflammation subsides
- Initial regrowth may be white/depigmented
Classification
| Type | Definition | Prognosis |
|---|---|---|
| Patchy AA | One or more well-defined patches | Best prognosis; 80% spontaneous regrowth |
| Alopecia Totalis (AT) | Complete scalp hair loss | Intermediate prognosis |
| Alopecia Universalis (AU) | Complete body hair loss | Poorest prognosis |
| Ophiasis | Band-like loss at occipital/temporal hairline | Poor response to treatment |
| Sisaipho (Ophiasis Inversus) | Spares occipital/temporal hairline | Better prognosis than ophiasis |
| Diffuse AA | Widespread thinning without patches | May be mistaken for other causes |
Symptoms
Typical Presentation:
Atypical Presentations:
Signs
Nail Changes (10-20%):
Red Flags
[!CAUTION] Red Flags — Requires additional investigation or referral if:
- Scarring or follicular loss (not AA — consider scarring alopecia)
- Signs of secondary syphilis (patchy "moth-eaten" alopecia)
- Signs of systemic lupus erythematosus
- Rapid progression to AT/AU
- Significant psychological distress or depression
Structured Approach
General:
- Hair pull test (positive at active margins)
- Examine all hair-bearing areas (scalp, eyebrows, eyelashes, beard)
- Examine nails (pitting, trachyonychia)
- Look for signs of associated autoimmune disease (vitiligo patches, thyroid abnormalities)
Scalp Examination:
- Distribution and number of patches
- Surface examination (smooth, preserved follicles = non-scarring)
- Hair margins (exclamation mark hairs)
- Signs of regrowth (vellus hairs)
Dermoscopy:
- Yellow dots (empty follicles)
- Black dots (cadaver hairs)
- Short vellus hairs
- Tapered "exclamation mark" hairs
Special Tests
| Test | Technique | Positive Finding | Purpose |
|---|---|---|---|
| Hair pull test | Gently tug 50-60 hairs | More than 10% extracted = active | Assess disease activity |
| Dermoscopy | Examine with dermatoscope | Yellow/black dots, exclamation hairs | Confirm diagnosis |
| Nail examination | Examine all fingernails/toenails | Pitting, ridging | Severity indicator |
First-Line
- Clinical diagnosis — Usually sufficient
- Dermoscopy — Confirms findings if uncertain
Laboratory Tests (to exclude associated conditions)
| Test | Expected Finding | Purpose |
|---|---|---|
| TFTs | Screen for hypo/hyperthyroidism | 8-28% have thyroid disease |
| Anti-TPO antibodies | May be positive | Autoimmune thyroid disease |
| FBC | Exclude anaemia | General health |
| Vitamin D | May be low | Weak association |
| ANA | Only if SLE features | Exclude systemic autoimmunity |
| Syphilis serology | If clinical concern | Exclude secondary syphilis |
Imaging
- Not routinely indicated
Diagnostic Criteria
- Clinical diagnosis based on:
- Well-demarcated patches of non-scarring hair loss
- Exclamation mark hairs at margins
- Preserved follicular openings
- ± Nail pitting
Scalp Biopsy (if diagnostic uncertainty)
- Peribulbar lymphocytic infiltrate ("swarm of bees" pattern)
- Miniaturised hairs
- Increased catagen/telogen hairs
Management Algorithm
ALOPECIA AREATA
↓
┌─────────────────────────────────────────┐
│ ASSESS EXTENT & IMPACT │
│ Surface area, progression, psychology │
└─────────────────────────────────────────┘
↓
┌─────────────────────────────────────────┐
│ LIMITED DISEASE (under 50%) │
├─────────────────────────────────────────┤
│ OBSERVE → 50% spontaneous regrowth │
│ TOPICAL STEROIDS → Potent (Dermovate) │
│ INTRALESIONAL STEROIDS → Triamcinolone │
└─────────────────────────────────────────┘
↓
┌─────────────────────────────────────────┐
│ EXTENSIVE DISEASE (over 50%) │
├─────────────────────────────────────────┤
│ TOPICAL IMMUNOTHERAPY (DPCP/SADBE) │
│ JAK INHIBITORS (Baricitinib) │
│ SYSTEMIC STEROIDS (short course only) │
└─────────────────────────────────────────┘
↓
┌─────────────────────────────────────────┐
│ SUPPORTIVE MEASURES │
│ Camouflage, wigs, counselling │
│ Eyebrow micropigmentation │
└─────────────────────────────────────────┘
Conservative Management
- Observation (50% spontaneous regrowth within 1 year for limited patches)
- Psychological support and counselling
- Patient support groups (Alopecia UK)
- Camouflage cosmetics, wigs, hairpieces
- Eyebrow/eyelash alternatives (stick-on, micropigmentation)
Medical Management
First-Line (Limited Disease):
| Drug | Indication | Dose | Notes |
|---|---|---|---|
| Potent topical steroid | Limited patches | Clobetasol (Dermovate) OD-BD | 12 weeks max, then break |
| Intralesional triamcinolone | Limited patches | 2.5-10mg/ml, 0.1ml per site, monthly | Dermatology-administered |
Second-Line (Extensive or Refractory):
| Drug | Indication | Dose | Notes |
|---|---|---|---|
| Topical immunotherapy | Extensive AA | DPCP or SADBE weekly | Induces allergic contact dermatitis |
| Topical minoxidil | Adjunct | 5% BD | May accelerate regrowth |
| Baricitinib (JAK inhibitor) | Severe AA (≥50% loss) | 2-4mg OD | NICE approved; monitor for infection |
| Short-course oral prednisolone | Acute extensive AA | 0.5mg/kg × 6 weeks | Relapse common on stopping |
JAK Inhibitors:
- Baricitinib approved by NICE (TA792) for adults with ≥50% scalp involvement
- Ritlecitinib approved for adolescents/adults
- Require monitoring: FBC, LFTs, lipids, TB screening
Surgical Management
- Hair transplantation: NOT recommended (disease may recur in grafts)
Disposition
- Refer if: Extensive disease, rapid progression, uncertain diagnosis, psychological distress
- Discharge if: Limited disease with reassurance and topical treatment
- Follow-up: 3-6 monthly to assess response and progression
Immediate
- None (not a systemic disease)
Early (Weeks-Months)
| Complication | Incidence | Presentation | Management |
|---|---|---|---|
| Progression | 30% | Patches enlarge or coalesce | Escalate treatment |
| Psychological impact | 50%+ | Anxiety, depression, social withdrawal | Counselling, psychology referral |
| Steroid atrophy | 5-10% | Skin thinning at injection sites | Stop treatment, usually reversible |
Late (Years)
- Alopecia totalis/universalis: 5-10% progress
- Recurrence: 50% relapse within 5 years after regrowth
- Chronic persistent disease: 10-15%
Natural History
- 50% spontaneous regrowth within 1 year (limited patches)
- 8-10% progress to AT/AU
- High recurrence rate (50% within 5 years)
- Childhood onset may have better or worse prognosis (variable data)
Outcomes with Treatment
| Variable | Outcome |
|---|---|
| Intralesional steroids | 60-70% regrowth in limited patches |
| Topical immunotherapy | 30-40% significant regrowth |
| Baricitinib (JAK inhibitor) | 40% achieve ≥80% regrowth at 36 weeks |
Prognostic Factors
Good Prognosis:
- Limited patches (under 50% scalp)
- Adult onset
- Short duration
- No nail involvement
- No family history
Poor Prognosis:
- Ophiasis pattern
- Alopecia totalis/universalis
- Childhood onset (especially pre-pubertal)
- Long duration (more than 5 years)
- Nail dystrophy
- Atopy
- Family history of AA
Key Guidelines
- BAD Guidelines: Alopecia Areata (2012) — British Association of Dermatologists. BAD
- AAD Guidelines: Alopecia Areata (2020) — American Academy of Dermatology.
- NICE TA792 (2022) — Baricitinib for treating severe alopecia areata. NICE TA792
Landmark Trials
BRAVE-AA1 & BRAVE-AA2 (2022) — Baricitinib for alopecia areata
- Phase 3 RCTs; 1200+ patients with ≥50% scalp involvement
- Key finding: 40% achieved ≥80% scalp coverage (vs 5% placebo) at 36 weeks
- Clinical Impact: First oral treatment approved for severe AA
Ritlecitinib Trials (2023) — JAK3/TEC inhibitor
- Phase 3 trial in adolescents and adults
- Key finding: Significant regrowth vs placebo
- Clinical Impact: FDA approved; additional option for severe AA
Evidence Strength
| Intervention | Level | Key Evidence |
|---|---|---|
| Intralesional steroids | 2b | Cohort studies, expert consensus |
| Topical steroids | 2b | Limited trial data; widely used |
| Baricitinib | 1b | BRAVE-AA1, BRAVE-AA2 |
| Topical immunotherapy | 2a | Systematic reviews |
What is Alopecia Areata?
Alopecia areata is a condition where your immune system mistakenly attacks hair follicles, causing hair to fall out in patches. It is not contagious and is not caused by anything you did wrong. Think of it like a misunderstanding by your body's defence system — it attacks your own hair as if it were a foreign invader.
Why does it matter?
While alopecia areata is not dangerous to your physical health, it can have a significant impact on how you feel about yourself. Hair is closely linked to identity and self-esteem, and losing it can be distressing. The good news is that the hair follicles are not destroyed, so regrowth is often possible.
How is it treated?
- Watch and wait: For small patches, hair often regrows on its own within 6-12 months.
- Steroid treatments: Creams or injections into the scalp can encourage regrowth.
- New medications: For severe cases, tablets called JAK inhibitors (like baricitinib) can help regrow hair.
- Camouflage: Wigs, hairpieces, eyebrow pencils, and micropigmentation can help while waiting for treatment to work.
- Psychological support: Talking therapies and support groups can help you cope.
What to expect
- Hair often regrows, but may initially come back white before returning to its normal colour
- Recurrence is common — about half of people have further episodes
- Some people progress to more extensive hair loss, but this is not the majority
- New treatments offer hope for severe cases
When to seek help
See a dermatologist if you:
- Have rapidly spreading hair loss
- Lose more than half of your scalp hair
- Have signs of scarring (red, scaly, no visible follicles)
- Are experiencing significant distress or depression
- Want to discuss treatment options
Primary Guidelines
- Messenger AG, et al. British Association of Dermatologists' guidelines for the management of alopecia areata 2012. Br J Dermatol. 2012;166(5):916-26. PMID: 22524397
Key Trials
- King B, et al. Two Phase 3 Trials of Baricitinib for Alopecia Areata. N Engl J Med. 2022;386(18):1687-1699. PMID: 35334197
- Gilhar A, et al. Alopecia areata. N Engl J Med. 2012;366(16):1515-25. PMID: 22512484
- Strazzulla LC, et al. Alopecia areata: An appraisal of new treatment approaches and overview of current therapies. J Am Acad Dermatol. 2018;78(1):15-24. PMID: 29241771
Further Resources
- Alopecia UK: alopecia.org.uk
- British Association of Dermatologists: bad.org.uk
- NHS Alopecia Information: nhs.uk/conditions/alopecia
Last Reviewed: 2025-12-24 | MedVellum Editorial Team
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.