Alopecia Areata (Adult)

1. Clinical Overview

Summary

Alopecia areata (AA) is a common, T-cell mediated autoimmune disorder characterised by non-scarring hair loss manifesting as well-demarcated, round or oval patches of complete alopecia. The condition affects approximately 2% of the general population during their lifetime, with equal sex distribution and peak onset before 30 years of age. [1] The pathogenesis involves collapse of hair follicle immune privilege and subsequent CD8+ T-cell mediated attack on anagen follicles, driven primarily by the IFN-γ/JAK-STAT signalling pathway. [2,3]

The disease spectrum ranges from localised patchy AA (80-90% of cases) to alopecia totalis (complete scalp hair loss) and alopecia universalis (complete body hair loss). Pathognomonic clinical features include "exclamation mark" hairs at active patch margins and yellow dots on dermoscopy. [4] Nail involvement occurs in 10-66% of patients, with geometric pitting being most characteristic. [5]

Spontaneous remission occurs in 34-50% of patients with limited disease within 12 months, though recurrence affects greater than 80% of patients over their lifetime. [1,6] Poor prognostic indicators include extensive disease (greater than 50% scalp), ophiasis pattern, early childhood onset, prolonged duration, atopic diathesis, and family history. [7]

Treatment is stratified by disease extent. For limited patchy AA (less than 50% scalp), first-line therapy is intralesional corticosteroids (triamcinolone 5-10 mg/mL) with 60-67% showing cosmetically acceptable regrowth. [8] For extensive AA (greater than 50% scalp), the recent FDA and NICE approval of oral JAK inhibitors (baricitinib, ritlecitinib) represents a paradigm shift, with BRAVE-AA trials demonstrating 35-39% achieving SALT score ≤20 (≥80% coverage) at 36 weeks compared to 6% with placebo. [9,10] Contact immunotherapy (DPCP/SADBE) remains an alternative for moderate-severe disease, with 40-60% response rates in specialist centres. [11]

Psychological morbidity is substantial, with 39-74% of patients experiencing anxiety or depression, necessitating routine screening and psychological support as integral components of care. [12,13]

Key Facts

Clinical Pearls

"Exclamation Mark Hairs": Pathognomonic for active AA. Short (3-4mm) broken hairs that taper at the proximal end (base). Found at expanding patch margins.

"Yellow Dots on Dermoscopy": Highly specific for AA. Represent empty follicular ostia filled with keratinous debris and sebum. Differentiate from black dots (also seen in tinea, trichotillomania).

"Non-Scarring = Reversibility": Follicular stem cells in bulge region are preserved. Hair follicles can regenerate even after years. Distinguishes AA from cicatricial alopecias where follicles are permanently destroyed.

"Ophiasis Pattern = Poor Prognosis": Band-like hair loss along temporal-occipital margins. Treatment-resistant. Greater than 75% do not achieve complete regrowth. [7]

"JAK Inhibitors: Game-Changer for Severe AA": Baricitinib (Olumiant) approved 2022. First systemic agent with Level 1a RCT evidence. 35-39% achieve ≥80% coverage vs 6% placebo. [9,10]

"Nail Geometric Pitting": Regular, uniform pitting in geometric pattern. Seen in 10-66% AA patients. Correlates with disease severity and poorer prognosis. [5]

"White Regrowth": Initial regrowth often white/depigmented due to melanocyte destruction during immune attack. Usually repigments within 3-6 months.

"Thyroid Screening Essential": 8-28% of AA patients have thyroid disease (mostly autoimmune thyroiditis). Check TFTs at baseline and annually. [14]

Why This Matters Clinically

Alopecia areata is the second most common cause of alopecia presenting to dermatology (after androgenetic alopecia), accounting for approximately 2-3% of new dermatology consultations. [1] Its clinical significance extends beyond mere cosmetic impact:

Diagnostic Imperative: Distinguishing AA from cicatricial (scarring) alopecias is critical, as the latter cause irreversible follicular destruction requiring urgent biopsy and aggressive immunosuppression. Clinical features (smooth non-scarred scalp, exclamation mark hairs, yellow dots on dermoscopy) enable bedside diagnosis in 90% of cases. [4]

Therapeutic Revolution: The 2022 FDA and NICE approval of oral JAK inhibitors for severe AA represents the first evidence-based systemic therapy, ending decades of reliance on off-label immunosuppressants with limited efficacy. The BRAVE-AA trials demonstrated unprecedented 35-39% complete/near-complete response rates, fundamentally changing treatment algorithms. [9,10]

Psychological Burden: AA causes profound psychosocial morbidity comparable to chronic systemic diseases. Studies demonstrate 39-74% prevalence of anxiety/depression, with quality of life impairment equivalent to psoriasis or atopic dermatitis. [12,13] Hair loss affecting socially visible areas (eyebrows, eyelashes) carries particularly high distress. Recognition and addressing of psychological comorbidity is now considered standard of care.

Autoimmune Screening Window: AA frequently coexists with other autoimmune conditions, particularly thyroid disease (8-28%), vitiligo (3-8%), and atopic dermatitis (10-39%). [14,15] Diagnosis of AA should prompt autoimmune screening, potentially identifying subclinical thyroid dysfunction or other treatable conditions.

Examination Relevance: AA is a high-yield examination topic across MRCP PACES, FRCS vivas, and dermatology OSCEs due to:

• Pathognomonic clinical signs (exclamation mark hairs)
• Well-defined autoimmune pathophysiology (JAK-STAT pathway)
• Recent therapeutic advances (JAK inhibitors)
• Differential diagnosis reasoning (scarring vs non-scarring)
• Communication challenges (managing expectations, psychological support)

Prognostic Counselling: Accurate prognosis stratification based on disease extent, pattern (ophiasis), age of onset, duration, and nail involvement enables realistic patient counselling. Limited patchy AA has 34-50% spontaneous remission within 12 months, whereas alopecia totalis/universalis has less than 10% complete long-term regrowth. [1,6,7]

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2. Epidemiology

Incidence & Prevalence

Age and Sex Distribution

Ethnicity and Geography

Genetic Epidemiology

Associated Conditions

Autoimmune Associations:

Genetic Syndromes:

Atopic Associations:

Risk Factors

Established Risk Factors:

Putative Triggers (Evidence Limited):

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3. Pathophysiology

Overview: Collapse of Hair Follicle Immune Privilege

The hair follicle bulb during anagen (growth phase) is an immune-privileged site, similar to the eye, testis, and brain. This privilege is actively maintained through:

• Low MHC class I/II expression
• Local immunosuppressive factors (TGF-β, α-MSH, IGF-1)
• Fas ligand-mediated deletion of infiltrating lymphocytes [2]

In AA, this immune privilege collapses, exposing follicular autoantigens to cytotoxic CD8+ T cells. The central pathogenic cytokine is IFN-γ, which signals via JAK1/JAK2 to upregulate MHC expression, perpetuating the autoimmune attack. [2,3]

Genetic Susceptibility

Genome-Wide Association Studies (GWAS) Findings: [18]

Key Insight: Greater than 100 susceptibility loci identified, with 60% overlap with other autoimmune diseases (vitiligo, rheumatoid arthritis, type 1 diabetes), confirming shared autoimmune mechanisms. [18]

Immunopathogenesis: Step-by-Step

Step 1: Loss of Immune Privilege

Triggering Events (hypothesised):

• Viral infection → IFN-α/β production → MHC upregulation
• Stress → Cortisol/catecholamines → Immune dysregulation
• Trauma (Koebner) → Local inflammation → Antigen release [20]

Step 2: Autoimmune T-Cell Attack

Step 3: Autoantigens - The Targets

Clinical Correlation: Predominance of melanocyte-associated antigens explains why initial regrowth is often white/depigmented (melanocyte destruction) before repigmentation occurs. [22,23]

Step 4: JAK-STAT Pathway - The Central Engine

The IFN-γ/JAK-STAT pathway is the critical signalling axis in AA pathogenesis: [2,3]

IFN-γ (from Th1 cells and CD8+ T cells)
   ↓
IFN-γ Receptor (on follicular keratinocytes and melanocytes)
   ↓
JAK1 + JAK2 activation (phosphorylation)
   ↓
STAT1 phosphorylation and dimerisation
   ↓
Nuclear translocation
   ↓
Transcription of:
   - MHC class I and II (antigen presentation)
   - CXCL9, CXCL10, CXCL11 (T-cell chemotaxis)
   - Pro-apoptotic genes
   - Inflammatory mediators

Why JAK Inhibitors Work: By blocking JAK1/JAK2, these drugs prevent IFN-γ signalling, halt MHC upregulation, reduce T-cell recruitment, and allow restoration of immune privilege. [9,10]

Step 5: Disruption of Hair Cycle

"Exclamation Mark" Hair Formation:

• Immune attack causes proximal hair shaft narrowing (reduced matrix cell proliferation)
• Distal (older) portion remains normal calibre
• Hair breaks, leaving short (3-4mm) tapered hair
• Pathognomonic sign of active disease [4]

Step 6: Reversibility - Stem Cell Preservation

This preservation of regenerative capacity is the fundamental difference between AA (non-scarring) and cicatricial alopecias (irreversible follicular destruction). It is the biological basis for therapeutic optimism. [2]

Histopathology

Active/Acute Alopecia Areata:

Chronic/Stable Alopecia Areata:

Triggering and Perpetuating Factors

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4. Clinical Presentation

Classification Systems

By Extent (Most Clinically Useful):

By Pattern (Prognostic Significance):

Typical Presentation

Chief Complaint: "I've noticed bald patches on my scalp" or "My hair is falling out in patches"

History Features:

Physical Examination Findings

Scalp:

Dermoscopy (Trichoscopy) - Essential Diagnostic Aid: [4]

Other Hair-Bearing Sites:

Nail Examination: [5]

Clinical Correlation: Nail changes occur in 10-66% of AA patients (prevalence varies by cohort), with higher rates in extensive disease and childhood onset. [5]

Disease Activity Assessment

Active Disease Indicators:

• Positive pull test at patch margins
• Exclamation mark hairs present
• Expanding patch size (patient report or serial photos)
• New patches appearing
• Black dots on dermoscopy
• Patient-reported tingling/burning

Stable/Inactive Disease:

• Negative pull test
• No new patches for greater than 3-6 months
• Stable patch size
• White/vellus hair regrowth at periphery
• Absence of exclamation mark hairs

Severity Assessment: SALT Score

SALT (Severity of Alopecia Tool): [26]

Scalp divided into 4 quadrants:

• Top: 40% (0.4 × % loss in this area)
• Right: 18% (0.18 × % loss)
• Left: 18% (0.18 × % loss)
• Back: 24% (0.24 × % loss)

SALT Score = Sum of (% loss in each quadrant × quadrant coefficient)

Clinical Use: SALT score ≤20 (≥80% coverage) is the primary endpoint in JAK inhibitor trials (BRAVE-AA, ALLEGRO). [9,10]

Psychological and Quality of Life Impact

Screening Tools:

• PHQ-9 (depression)
• GAD-7 (anxiety)
• DLQI (dermatology-specific QoL)
• Skindex (skin-specific QoL)

Red Flags

[!CAUTION] Red Flags Requiring Urgent Action or Alternative Diagnosis:

• Scarring: Loss of follicular openings, atrophy, smooth shiny skin → Urgent biopsy for cicatricial alopecia (irreversible)
• Scaling, Erythema, Pustules: Consider tinea capitis, folliculitis decalvans, dissecting cellulitis → KOH, culture, biopsy
• Systemic Symptoms: Fever, weight loss, fatigue, rash → Screen for lupus, syphilis, sarcoidosis
• Unilateral or Asymmetric Scarring: Morphea (en coup de sabre), linear scleroderma → Biopsy
• Diffuse Thinning with Scalp Tenderness: Telogen effluvium, loose anagen syndrome, trichotillomania
• Rapid Total Loss in Hours/Days: Anagen effluvium (chemotherapy, toxins)
• Child with Extensive AA and Growth Delay: Screen for polyglandular autoimmune syndrome
• Significant Suicidal Ideation: Urgent psychiatric referral

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5. Differential Diagnosis

Comprehensive Differential

Dermoscopy Differential

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6. Investigations

Core Principle: Clinical Diagnosis

Alopecia areata is primarily a clinical diagnosis. In classic presentations (well-demarcated round patches, smooth scalp, exclamation mark hairs, yellow dots on dermoscopy), no investigations are required. [4]

Investigation Algorithm

Typical Patchy AA (less than 50% scalp, classic features):

• No investigations required
• Consider: TFTs (high autoimmune thyroid association)
• If available: Dermoscopy (confirms diagnosis)

Atypical Presentation or Diagnostic Uncertainty:

• Scalp biopsy (4mm punch from active edge)
• TFTs, ANA (autoimmune screen)
• Consider: Syphilis serology (VDRL/RPR) if sexually active/at-risk

Suspected Scarring Alopecia:

• Urgent scalp biopsy (horizontal sectioning preferred)
• DIF biopsy if lupus suspected

Diffuse Alopecia Areata (Alopecia Areata Incognita):

• Scalp biopsy (distinguish from telogen effluvium)
• TFTs, FBC, ferritin, vitamin D

Scaling/Inflammatory Features:

• KOH preparation and fungal culture (exclude tinea capitis)

Pre-Treatment for JAK Inhibitors:

• Full pre-treatment screening panel (see below)

Laboratory Investigations

Thyroid Function Tests (Recommended for All AA Patients): [14]

Rationale: 8-28% of AA patients have thyroid disease, predominantly autoimmune thyroiditis. [14] Screen at baseline and consider annual monitoring.

Other Investigations (As Indicated):

Dermoscopy (Trichoscopy)

Essential in Modern Practice - Point-of-Care Diagnostic Tool: [4]

Dermoscopy increases diagnostic confidence and reduces need for biopsy in 70-80% of cases. [4]

Scalp Biopsy

Indications:

1. Diagnostic uncertainty (atypical pattern or features)
2. Suspected scarring alopecia (urgent to prevent irreversible loss)
3. Diffuse alopecia (distinguish from telogen effluvium)
4. Non-response to treatment (exclude cicatricial component)

Technique:

• 4mm punch biopsy from active patch edge
• Include adjacent normal scalp for comparison
• Horizontal sectioning preferred (follicle count, follicular architecture assessment)
• +/- Vertical sectioning for DIF if lupus suspected

Histopathology Findings:

Active AA: [24]

• "Swarm of bees" peribulbar lymphocytic infiltrate (pathognomonic)
• CD4+ and CD8+ T cells around anagen hair bulbs
• Pigment incontinence (melanin in dermis)
• Increased catagen/telogen follicles
• Preserved follicular units (non-scarring)

Chronic AA:

• Sparse peribulbar inflammation
• Increased telogen proportion (greater than 50%)
• Miniaturised (nanogen) follicles
• Fibrous streamers (not true scar - follicular units preserved)

JAK Inhibitor Pre-Treatment Screening Panel [9,10]

MANDATORY Before Starting Baricitinib or Ritlecitinib:

Monitoring on JAK Inhibitors:

• FBC: 4 weeks, 12 weeks, then every 3 months
• LFTs: Every 3 months
• Lipids: 12 weeks, then annually
• Clinical assessment: Every 3-6 months for efficacy and side effects

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7. Management

General Principles

Treatment Algorithm by Disease Extent

Step 1: Assess Disease Extent (SALT Score or Clinical Estimation)

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1. Intralesional Corticosteroids (ILC) - First-Line for Limited Disease

Evidence: Level 2b (cohort studies). Response rate 60-67% cosmetically acceptable regrowth in limited AA. [8]

Technique:

Response Rates: [8]

• Limited AA (less than 50% scalp): 60-67% cosmetically acceptable regrowth
• Better response: Smaller patches, fewer patches, shorter duration
• Poorer response: Ophiasis, extensive disease, long-standing AA

Side Effects:

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2. Topical Corticosteroids

Evidence: Level 2b. Less effective than ILC; useful adjunct or for children/needle-phobic patients. [8]

Options:

Protocol:

• Apply to affected areas ± 0.5-1cm margin
• Can use under occlusion (shower cap overnight) for enhanced penetration
• Trial for 3-6 months
• Taper if successful (e.g., alternate days, then twice weekly maintenance)

Side Effects: Folliculitis (common), skin atrophy (prolonged use), telangiectasia

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3. Topical Minoxidil

Evidence: Level 3 (case series). Not effective as monotherapy; use as adjunct.

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4. Topical Immunotherapy (DPCP/SADBE) - Moderate-Severe AA

Evidence: Level 2a (systematic reviews). Response rate 40-60% in specialist centres. [11]

Agents:

• DPCP (Diphenylcyclopropenone): Most widely used
• SADBE (Squaric Acid Dibutylester): Alternative
• DNCB: No longer used (mutagenic concerns)

Mechanism: Induce allergic contact dermatitis → shift immune response away from follicle destruction (antigenic competition hypothesis).

Protocol (DPCP): [11]

Response Predictors:

• Better: Patchy AA, moderate extent
• Poorer: AT/AU, ophiasis, children

Side Effects:

Contraindications: Pregnancy (teratogenic potential), inability to attend weekly appointments

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5. JAK Inhibitors - PARADIGM SHIFT for Severe AA

The Only Systemic Agents with Level 1a RCT Evidence

Baricitinib (Olumiant) - FDA/NICE Approved 2022 [9,10]

Indication: Adults with severe AA (≥50% scalp hair loss or SALT ≥50)

Efficacy (BRAVE-AA1 and BRAVE-AA2 Trials, n=1200): [9,10]

NICE Recommendation (TA875, 2022): Baricitinib recommended for adults with ≥50% scalp hair loss who have not responded to contact immunotherapy or for whom contact immunotherapy is unsuitable.

Response Maintenance: Continued treatment required; relapse occurs in 70-80% within 6 months of stopping. [9]

Ritlecitinib (Litfulo) - FDA Approved 2023 [28]

Indication: Severe AA in adults and adolescents ≥12 years

Off-Label JAK Inhibitors

Pre-Treatment Screening and Monitoring

See Investigations Section for Full Panel

Key Contraindications:

• Active serious infection (including TB)
• Pregnancy/breastfeeding
• Severe hepatic impairment (Child-Pugh C)
• Severe renal impairment (eGFR less than 30)
• Uncontrolled cytopenias
• Recent venous thromboembolism (relative)

FDA Boxed Warnings (All JAK Inhibitors): [27]

• Serious infections (including TB, herpes zoster)
• Malignancy (lymphoma, lung cancer, skin cancer)
• Major adverse cardiovascular events (MACE)
• Thrombosis (deep vein thrombosis, pulmonary embolism)
• Death (in rheumatoid arthritis patients ≥50 years with ≥1 CV risk factor)

Monitoring:

• FBC: 4 weeks, 12 weeks, then 3-monthly
• LFTs: Every 3 months
• Lipids: 12 weeks, then annually (statins if indicated)
• Clinical: 3-6 monthly; assess response, side effects, psychological wellbeing

Side Effects:

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6. Systemic Corticosteroids

Evidence: Level 2b. Short-term use only; high relapse rate on stopping; side effects preclude long-term use.

Regimens:

Indications: Rapidly progressive AA (bridge to other therapy); not for long-term use

Side Effects: Cushingoid features, weight gain, hyperglycaemia, hypertension, osteoporosis, adrenal suppression, mood changes

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7. Other Systemic Agents (Off-Label, Limited Evidence)

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Treatment Algorithm Summary

ALOPECIA AREATA CONFIRMED
         ↓
┌────────┴────────┐
│  ASSESS EXTENT  │
└────────┬────────┘
         │
    ┌────┴────┬────────────┬──────────┐
    ↓         ↓            ↓          ↓
 less than 50%      50-75%       75-99%      100% (AT/AU)
    │         │            │          │
    ↓         ↓            ↓          ↓
┌───────┐ ┌─────────┐ ┌──────────┐ ┌──────────┐
│  ILC  │ │ Topical │ │   JAK    │ │   JAK    │
│  ±    │ │ Immuno  │ │ Inhibitor│ │ Inhibitor│
│Topical│ │   OR    │ │ (First-  │ │ (First-  │
│Steroid│ │   JAK   │ │  Line)   │ │  Line)   │
│± Minox│ │ Inhibit │ │    OR    │ │    OR    │
│       │ │         │ │ Topical  │ │ Topical  │
│       │ │         │ │ Immuno   │ │ Immuno   │
└───────┘ └─────────┘ └──────────┘ └──────────┘
    │         │            │          │
    └─────────┴────────────┴──────────┘
                   ↓
        ┌──────────────────────┐
        │ ALL PATIENTS:        │
        │ - Psychological      │
        │   support            │
        │ - Cosmetic options   │
        │ - Patient education  │
        │ - Autoimmune screen  │
        └──────────────────────┘

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Special Populations and Sites

Children:

• Higher spontaneous remission rate; watch and wait often appropriate for limited disease
• Topical steroids first-line
• Intralesional steroids from ~10 years (if cooperative)
• Topical immunotherapy from ~8 years (requires parental commitment)
• JAK inhibitors: Ritlecitinib approved ≥12 years [28]
• Psychological support essential (bullying, self-esteem)

Eyebrow/Eyelash Alopecia:

• Intralesional triamcinolone 2.5-5 mg/mL (careful technique, avoid periorbital atrophy)
• Bimatoprost 0.03% (off-label; prostaglandin analogue for eyelashes)
• Cosmetic options: Eyebrow pencil, microblading, false lashes

Beard (Alopecia Barbae):

• Intralesional triamcinolone 5 mg/mL (as per scalp)
• Topical corticosteroids
• JAK inhibitors for extensive

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Cosmetic and Psychological Support

Cosmetic Options:

Psychological Support:

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8. Prognosis & Outcomes

Natural History

Prognostic Factors

Good Prognosis (Favourable for Regrowth):

• Limited number of patches (1-3)
• Small patch size (less than 5cm diameter)
• Adult onset (greater than 30 years)
• Short duration (less than 6 months)
• No nail involvement
• No family history
• No atopic diathesis

Poor Prognosis (Unfavourable for Regrowth): [7]

• Extensive disease (greater than 50% scalp, AT, AU)
• Ophiasis pattern (band-like occipital/temporal)
• Early childhood onset (less than 10 years)
• Long duration (greater than 1 year)
• Nail involvement (pitting, trachyonychia)
• Atopic diathesis (eczema, asthma, allergic rhinitis)
• Strong family history (multiple affected FDRs)
• Associated autoimmune disease
• Down syndrome

Response to Treatment

Intralesional Corticosteroids (Limited AA): [8]

• 60-67% cosmetically acceptable regrowth
• Better response if fewer, smaller, newer patches
• Response visible 4-8 weeks; assess 3-6 months

Topical Immunotherapy (DPCP): [11]

• 40-60% cosmetically acceptable regrowth (specialist centres)
• Higher response in patchy AA; lower in AT/AU
• Requires 6-12 months to assess

JAK Inhibitors (Baricitinib 4mg for Severe AA): [9,10]

• 35-39% achieve SALT ≤20 (≥80% coverage) at 36 weeks
• Response begins 12-24 weeks; maximal 36-52 weeks
• Maintenance therapy required (relapse 70-80% on stopping)

Relapse Rates

• Overall: Greater than 80% of patients experience recurrence at some point in life [1]
• Post-Treatment Relapse: 30-50% within 12 months of stopping treatment
• Post-JAK Inhibitor Cessation: 70-80% relapse within 6 months [9]

Quality of Life and Psychological Outcomes

• With Treatment and Psychological Support: Significant improvement in DLQI, anxiety, and depression scores [12,13]
• Eyebrow/Eyelash Regrowth: Disproportionately high QoL impact (socially visible areas)
• Children: Early intervention and psychological support improve long-term adjustment

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9. Evidence & Guidelines

Key Guidelines

Landmark Clinical Trials

BRAVE-AA1 and BRAVE-AA2 (2022) - Baricitinib Phase 3 RCTs: [9,10]

• Design: Randomised, double-blind, placebo-controlled
• N: 1200 adults with severe AA (≥50% scalp loss)
• Intervention: Baricitinib 4mg, 2mg, or placebo daily for 36 weeks
• Primary Endpoint: SALT ≤20 (≥80% coverage) at 36 weeks
• Results:
  • Baricitinib 4 mg: 35-39% achieved SALT ≤20
  • Baricitinib 2 mg: 20-22%
  • "Placebo: 3-6%"
  • NNT = 3 for SALT ≤20 (4mg vs placebo)
• Significance: First Level 1a evidence for systemic AA therapy; led to FDA/NICE approval

ALLEGRO-2b/3 (2023) - Ritlecitinib Phase 3: [28]

• Design: Randomised, placebo-controlled
• N: 718 adults and adolescents ≥12 years
• Intervention: Ritlecitinib 50mg daily vs placebo
• Results: 23-31% achieved SALT ≤20 at 24 weeks (vs 2% placebo)
• Significance: First JAK inhibitor approved for adolescents (≥12 years)

Evidence Quality Summary

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10. Patient/Layperson Explanation

What is Alopecia Areata?

Alopecia areata is a condition where your immune system mistakenly attacks your hair follicles, causing hair to fall out in round, smooth patches. It is not contagious - you cannot catch it from someone else or pass it to others.

Why Does It Happen?

Your immune system normally protects you from infections. In alopecia areata, it mistakenly sees hair follicles as a threat and attacks them. We don't know exactly why this happens, but it can run in families and is more common in people with other immune conditions like thyroid disease.

Possible triggers (in some people):

• Stress or emotional trauma
• Viral infections
• Family history

Who Gets It?

• About 2 in 100 people (1 in 50) develop it at some point
• Can happen at any age, but usually starts before age 30
• Men and women equally affected
• Runs in families in about 10-20% of cases

Will My Hair Grow Back?

For Small Patches (Less Than Half Your Scalp):

• Good news: 34-50% of people see regrowth within a year, even without treatment
• Hair may initially grow back white, then return to normal colour
• Recurrence is common - hair may fall out again later

For Extensive Hair Loss (Total Loss of Scalp or Body Hair):

• More challenging; full regrowth less common without treatment
• New treatments (JAK inhibitors) are helping more people regrow hair
• About 35-40% achieve significant regrowth with these new medicines

What Treatments Are Available?

For Small Patches:

For Extensive Hair Loss:

Important: Treatments need to be continued. Hair often falls out again when treatment stops.

Wigs and Hairpieces

Options:

• Synthetic wigs: Affordable, pre-styled, less natural
• Human hair wigs: More natural, can be styled, more expensive
• Scalp micropigmentation: Tattoo technique to simulate hair follicles (permanent)

In the UK: Wigs can be prescribed on the NHS for medical hair loss. Ask your GP or dermatologist.

Eyebrows and Eyelashes

If you've lost eyebrows or eyelashes:

• Eyebrow pencils and makeup help with daily appearance
• Microblading: Semi-permanent eyebrow tattoo (lasts 1-2 years)
• False eyelashes: Magnetic or adhesive
• Some treatments may help - discuss with your doctor

Psychological Support

Losing hair can be very distressing, even though it is not medically dangerous. Your feelings are valid.

Where to Get Help:

• Your GP: Can refer for counselling or prescribe medication for anxiety/depression if needed
• Alopecia UK (www.alopecia.org.uk): Support groups (online and in-person), peer support
• Therapy (CBT): Effective for body image concerns and anxiety

Children with Alopecia:

• Schools should be informed to prevent bullying
• Child psychology services can help
• Specialist wigs for children available

Frequently Asked Questions

Q: Is alopecia areata contagious? A: No. You cannot catch it from someone or pass it to others.

Q: Will I lose all my hair? A: Most people do not. Only 5-10% progress to total hair loss.

Q: Can stress cause it? A: Stress may trigger it in some people, but stress alone does not cause alopecia areata.

Q: Is there a cure? A: There is no permanent cure yet, but treatments can help regrow hair. New JAK inhibitor tablets (approved 2022) are the most effective treatment available.

Q: Are the new JAK inhibitor treatments available on the NHS? A: Yes. Baricitinib was approved by NICE in 2022 for severe alopecia areata (≥50% scalp hair loss). Ask your dermatologist if you qualify.

Q: What should I eat to help my hair? A: A balanced diet is important, but no specific diet cures alopecia areata. Ensure adequate protein, iron, and vitamins.

Q: Can I colour my remaining hair? A: Yes. Hair dye does not affect alopecia areata or make it worse.

Q: Should I use special shampoos? A: Normal shampoo is fine. Specialised anti-hair-loss shampoos do not help alopecia areata.

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References

1. Pratt CH, King LE Jr, Messenger AG, Christiano AM, Sundberg JP. Alopecia areata. Nat Rev Dis Primers. 2017;3:17011. doi:10.1038/nrdp.2017.11 PMID: 28300084

2. Gilhar A, Etzioni A, Paus R. Alopecia areata. N Engl J Med. 2012;366(16):1515-1525. doi:10.1056/NEJMra1103442 PMID: 22512484

3. Xing L, Dai Z, Jabbari A, et al. Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition. Nat Med. 2014;20(9):1043-1049. doi:10.1038/nm.3645 PMID: 25129481

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