Alopecia Areata (Adult)
Summary
Alopecia areata (AA) is a Common, Autoimmune, Non-Scarring Hair Loss Disorder characterised by Patchy Hair Loss with well-demarcated, Smooth, Coin-shaped bald patches. It can affect the Scalp, Beard, Eyebrows, Eyelashes, and any hair-bearing area. The condition affects approximately 2% of the population at some point in their lifetime, With equal prevalence in males and females. The pathogenesis involves T-Cell Mediated Autoimmune Attack on the hair follicle, Causing disruption of the hair growth cycle during the anagen (Growth) phase. Key examination findings include "Exclamation Mark" Hairs (Short, broken hairs that taper at the base) at patch margins and Nail Changes (Pitting, Ridging) in 10-20% of patients. AA exists on a spectrum from Limited Patchy Disease to Alopecia Totalis (Complete Scalp Loss) and Alopecia Universalis (Complete Body Hair Loss). Spontaneous regrowth occurs in many patients with limited disease (30-50% within 1 year), But recurrence is common. Treatment options include Intralesional Corticosteroids (First-Line for Limited Disease), Topical Corticosteroids, Topical Immunotherapy (DPCP/SADBE), and the recently approved JAK Inhibitors (Baricitinib) for severe disease. Psychological impact is significant and should be addressed. [1,2,3]
Key Facts
| Fact | Value |
|---|---|
| Definition | Autoimmune, Non-scarring alopecia with patchy hair loss |
| Lifetime Prevalence | ~2% |
| Peak Age of Onset | less than 30 years (Can occur any age) |
| Sex | Equal |
| Characteristic Finding | "Exclamation mark" hairs |
| First-Line (Limited Disease) | Intralesional triamcinolone |
| New Treatment (Severe) | JAK inhibitors (Baricitinib) |
| Spontaneous Regrowth (Limited AA) | 30-50% within 1 year |
Clinical Pearls
"Exclamation Mark Hairs": Pathognomonic – Tapered, Broken hairs at patch margin.
"Non-Scarring": Follicles preserved. Regrowth potential maintained.
"Nail Pitting": Think alopecia areata (And psoriasis).
"Intralesional Steroids for Limited Disease": First-line. Monthly injections.
"JAK Inhibitors for Severe AA": Baricitinib is a game-changer.
Why This Matters Clinically
Alopecia areata is one of the most common causes of non-scarring alopecia presenting to dermatology and primary care. Its cosmetic and psychological impact is substantial, Often underestimated. Correct diagnosis (Distinguishing from scarring alopecias and other causes) determines management. The recent approval of JAK inhibitors has transformed treatment of severe disease. Understanding prognosis (Good for limited disease, Guarded for extensive) is essential for patient counselling. AA is frequently examined due to its classic clinical features, Autoimmune associations, And evolving treatment landscape.
Incidence & Prevalence
| Measure | Value | Notes |
|---|---|---|
| Lifetime Prevalence | ~2% | Common |
| Incidence | 20/100,000 per year | |
| Age of Onset | 66% less than 30 years | 20% less than 16 years |
| Peak Age | 15-29 years |
Demographics
| Factor | Details | Clinical Significance |
|---|---|---|
| Sex | Equal | |
| Ethnicity | All ethnicities | |
| Family History | 10-20% have first-degree relative | Genetic component |
Risk Factors and Associations
Genetic Factors:
- Family history (10-20%)
- HLA associations (HLA-DQB1, HLA-DRB1)
- Polygenic inheritance
Autoimmune Associations:
| Associated Condition | Prevalence in AA |
|---|---|
| Thyroid Disease | 8-28% |
| Vitiligo | 4-16% |
| Atopic Dermatitis | 10-30% |
| Autoimmune Polyendocrine Syndrome | Rare |
| Allergic Rhinitis/Asthma | Increased |
| Down Syndrome | 6-8% have AA |
Genetic Basis
Genome-Wide Association Studies (GWAS) Findings:
| Gene/Locus | Function | Significance |
|---|---|---|
| HLA-DQB1*03 | MHC Class II | Strongest association. Antigen presentation. |
| HLA-DRB1 | MHC Class II | Autoimmune susceptibility |
| CTLA4 | T-cell inhibition | Regulatory T-cell function |
| IL2RA | IL-2 receptor | T-cell activation |
| PTPN22 | Tyrosine phosphatase | T-cell signalling threshold |
| EOS (IKZF4) | Transcription factor | Regulatory T-cell development |
| NKG2D ligands (ULBP3/ULPB6) | NK cell activation | Cytotoxic attack on follicles |
Heritability:
- Twin studies show ~50% concordance in monozygotic twins
- First-degree relatives: 10-20% also affected
- Polygenic inheritance with environmental modifiers
Immunopathogenesis
Step 1: Loss of Hair Follicle Immune Privilege
The hair follicle bulb during anagen is normally an Immune-Privileged Site (Similar to eye, Testis, Brain). This is maintained by:
| Mechanism | Details |
|---|---|
| Low MHC Class I Expression | Reduces recognition by CD8+ T cells |
| MHC Class I Ib Expression | HLA-E, HLA-G – Inhibit NK cells |
| Local Immunosuppressants | TGF-β1, TGF-β2, α-MSH, IGF-1, ACTH |
| Fas Ligand Expression | Induces apoptosis of infiltrating T cells |
| Indoleamine 2,3-Dioxygenase (IDO) | Tryptophan depletion – Suppresses T cells |
In Alopecia Areata:
- IFN-γ upregulates MHC Class I and II on follicular keratinocytes
- Follicular antigens become visible to immune system
- "Immune privilege collapse" occurs
- Triggers autoimmune attack
Step 2: Autoimmune T-Cell Attack
| Cell Type | Role | Mechanism |
|---|---|---|
| CD8+ Cytotoxic T Cells | Primary effectors | Recognize follicular autoantigens via MHC Class I. Direct cytotoxicity (Perforin, Granzyme B). |
| CD4+ Helper T Cells | Support CD8+ attack | Th1 cytokine production (IFN-γ, IL-2). Activate macrophages. |
| NKG2D+ NK Cells | Cytotoxic | Recognize NKG2D ligands on stressed follicular cells. Contribute to killing. |
| Plasmacytoid Dendritic Cells | Antigen presentation | Type I interferon production. Located in peribulbar infiltrate. |
| Regulatory T Cells (Tregs) | Impaired in AA | Reduced suppression of autoreactive T cells |
Autoantigens (Targets):
| Autoantigen | Location |
|---|---|
| Trichohyalin | Inner root sheath |
| Tyrosinase | Melanocytes in hair bulb |
| Tyrosinase-Related Protein 1/2 | Melanocytes |
| MART-1/Melan-A | Melanocytes |
| Glycoprotein 100 | Melanocytes |
| Keratin 16/Keratin 6 | Hair cortex |
Note: Many autoantigens are melanocyte-associated, Which may explain why regrowth hairs are often white (Melanocyte destruction).
Step 3: JAK-STAT Pathway – Central Role
| Component | Role in AA |
|---|---|
| IFN-γ | Key cytokine driving pathology |
| IFN-γ Receptor | Binds IFN-γ on follicular cells |
| JAK1, JAK2 | Kinases downstream of IFN-γ receptor |
| STAT1 | Transcription factor activated by JAK phosphorylation |
| Downstream Effects | Upregulation of MHC Class I, II, Chemokines, Pro-inflammatory genes |
Why JAK Inhibitors Work:
- Block JAK1/JAK2 signalling
- Prevent IFN-γ effects
- Reduce MHC upregulation
- Allow restoration of immune privilege
- Stop T-cell attack
Step 4: Disruption of Hair Cycle
| Normal Cycle | In Alopecia Areata |
|---|---|
| Anagen (Growth): 2-7 years | Immune attack targets anagen follicles |
| Healthy matrix keratinocytes | Matrix cell apoptosis |
| Melanogenesis active | Melanocyte destruction |
| Hair shaft production | Dystrophic anagen, Premature catagen entry |
| "Exclamation mark" hairs: Narrowing at proximal end |
Step 5: Dystrophic Anagen and Telogen Shift
- Immune attack does NOT destroy follicular stem cells (Bulge region)
- Follicle enters "dystrophic anagen" – Abnormal, Non-productive
- Premature catagen initiation
- Shift to telogen (Resting phase)
- Empty follicles remain (Potential for regrowth preserved)
Step 6: Reversibility – Key Concept
| Feature | Implication |
|---|---|
| Hair follicle stem cells preserved | Follicles can regenerate |
| Non-scarring process | No permanent structural damage |
| Immune privilege can be restored | Treatment can reverse process |
| Spontaneous remissions occur | Immune attack may self-limit |
This reversibility distinguishes AA from scarring alopecias and is the basis for treatment optimism.
Histopathology
Acute/Active Alopecia Areata:
| Finding | Description |
|---|---|
| "Swarm of Bees" Sign | Dense peribulbar lymphocytic infiltrate around anagen follicles |
| Lymphocyte Composition | Predominantly CD4+ and CD8+ T cells |
| Location | Around hair bulb (Not in upper follicle) |
| Pigment Incontinence | Melanin in dermis from damaged melanocytes |
| Eosinophils | May be present in infiltrate |
| Increased Catagen/Telogen Follicles | Abnormal hair cycle |
| Miniaturised Hairs | Nanogen hairs |
Chronic/Stable Alopecia Areata:
| Finding | Description |
|---|---|
| Reduced Inflammation | Sparse or absent peribulbar infiltrate |
| Miniaturised Follicles | Predominant finding |
| Increased Telogen Count | Many resting follicles |
| "Streamers" | Fibrous tracts replacing follicles (But not true scarring) |
| Preserved Follicular Units | Distinguishes from scarring alopecia |
Comparison with Scarring Alopecia:
| Feature | Alopecia Areata | Scarring Alopecia |
|---|---|---|
| Follicular architecture | Preserved | Destroyed/Replaced by scar |
| Sebaceous glands | Present | Absent |
| Arrector pili | Present | Absent |
| Peribulbar inflammation | Yes | Perifollicular (Upper follicle) |
| Fibrosis | Minimal | Dense |
| Regrowth potential | Yes | No |
Triggering Factors
| Factor | Evidence | Mechanism |
|---|---|---|
| Psychological Stress | Epidemiological association | Stress hormones affect immune function |
| Viral Infections | CMV, EBV antibodies elevated in some studies | Molecular mimicry, Immune activation |
| Seasonal Variation | Some studies show autumn/Winter peaks | Vitamin D? Circulating immune changes? |
| Vaccinations | Rare case reports post-vaccination | Non-specific immune activation |
| Trauma | Koebner phenomenon reported | Local immune activation |
| Diet/Microbiome | Emerging area of research | Gut-immune axis |
Hair Cycle Summary
| Phase | Duration | Description | In AA |
|---|---|---|---|
| Anagen | 2-7 years | Active growth. Matrix cells rapidly dividing. Melanin production. | TARGET of immune attack |
| Catagen | ~2-3 weeks | Regression. Apoptosis of matrix. Follicle retracts. | Premature entry |
| Telogen | ~3 months | Resting. Club hair. Eventually sheds. | Increased proportion |
| Exogen | Active shedding | Hair releases from follicle | Shedding observed |
Pathophysiology Diagram
Classification by Extent
| Type | Description | Prevalence | Prognosis |
|---|---|---|---|
| Patchy Alopecia Areata | One or more well-circumscribed patches | 80-90% | Good (30-50% spontaneous regrowth) |
| Alopecia Totalis (AT) | Complete loss of all scalp hair | 5-10% | Guarded |
| Alopecia Universalis (AU) | Complete loss of all body hair | 5% | Poor for full regrowth |
Classification by Pattern
| Pattern | Description | Clinical Significance |
|---|---|---|
| Patchy | Round/oval patches, Random distribution | Most common presentation |
| Ophiasis | Band-like loss along temporal/occipital margins | Poor prognosis, Treatment-resistant |
| Sisaipho (Inverse Ophiasis) | Central scalp affected, Margins spared | Better prognosis than ophiasis |
| Diffuse Alopecia Areata | Generalised thinning without distinct patches | Difficult to diagnose, Mimics telogen effluvium |
| Alopecia Areata Incognita | Acute diffuse variant, Rapid onset | May progress to AT/AU |
Typical Presentation Features
| Feature | Description | Clinical Significance |
|---|---|---|
| Hair Loss Pattern | Well-demarcated, Round/Oval, Smooth patches | Characteristic appearance |
| Scalp Skin | Normal colour and texture, No scarring | Distinguishes from cicatricial |
| Scaling | Absent (Unless coexisting condition) | Distinguishes from tinea capitis |
| Erythema | Usually absent | Present in some early/active lesions |
| Speed of Onset | Sudden onset, Days to weeks | Often first noticed incidentally |
| Symptoms | Usually asymptomatic | Some report tingling, Burning before onset |
| Pull Test | Positive at patch margins if active | Indicates disease activity |
| Broken Hairs | At margins of expanding patches | Active disease |
| Exclamation Mark Hairs | Short (3-4mm), Tapers at base | PATHOGNOMONIC |
| Regrowth Pattern | Fine, Vellus, White initially | Later becomes pigmented terminal |
Site-Specific Presentations
Scalp (Most Common):
| Location | Pattern | Notes |
|---|---|---|
| Vertex | Common site | May be single or multiple |
| Occipital | Often part of ophiasis | More treatment-resistant |
| Temporal | May be symmetrical | Part of ophiasis pattern |
| Frontal Hairline | May mimic FFA | Check for scarring |
Beard (Alopecia Barbae):
| Feature | Details |
|---|---|
| Prevalence | Common in men with AA |
| Pattern | Single or multiple patches in beard |
| Treatment | Similar to scalp (ILC, Topical) |
| Impact | Cosmetically significant in men |
Eyebrows and Eyelashes (Madarosis):
| Feature | Details |
|---|---|
| Eyebrows | Partial or complete loss, May be only manifestation |
| Eyelashes | Upper and/or lower lids |
| Impact | Highly cosmetically and psychologically distressing |
| Treatment | Low-concentration ILC, Topical, Prostaglandins |
Body Hair:
| Site | Notes |
|---|---|
| Axillae | May be affected |
| Pubic Area | May be affected |
| Limbs | Patchy loss on arms/legs |
| Examination | Check all hair-bearing areas |
Nail Changes
Frequency: 10-20% of patients (Higher in extensive disease)
| Finding | Description | Frequency |
|---|---|---|
| Pitting | Fine, Shallow, Regular pits | Most common nail finding |
| Trachyonychia | Rough, Sandpapered surface ("20-nail dystrophy") | Associated with extensive AA |
| Longitudinal Ridging | Vertical lines | Common |
| Longitudinal Splitting | Onychorrhexis | |
| Brittle Nails | Easy breakage | |
| Red Lunulae | Erythematous nail matrix | Less common |
| Onycholysis | Nail plate separation | Rare |
| Koilonychia | Spoon-shaped nails | Rare |
Clinical Significance: Nail involvement correlates with disease severity and poorer prognosis.
Assessing Disease Activity
Active Disease Features:
Stable Disease Features:
Severity Assessment Tools
SALT Score (Severity of Alopecia Tool):
| SALT | Hair Loss | Interpretation |
|---|---|---|
| S0 | 0% | No loss / Complete regrowth |
| S1 | 1-25% | Mild |
| S2 | 26-50% | Moderate |
| S3 | 51-75% | Moderate-Severe |
| S4 | 76-99% | Severe |
| S5 | 100% | Alopecia Totalis |
Used in clinical trials as primary endpoint (e.g., SALT ≤20 = treatment success)
Psychological and Psychosocial Impact
| Impact Area | Details |
|---|---|
| Depression | Significantly elevated risk (Up to 40% in some studies) |
| Anxiety | Common, Especially social anxiety |
| Body Image | Profound impact on self-perception |
| Quality of Life | Comparable to chronic diseases (Psoriasis, Vitiligo) |
| Social Functioning | Avoidance, Withdrawal, Isolation |
| Occupational Impact | May affect work, Career choices |
| Relationships | Impact on intimacy, Self-esteem in dating |
| Children | Bullying risk, School difficulties, Self-esteem |
Screening Considerations:
Red Flags
[!CAUTION] Red Flags – Consider Alternative Diagnosis or Urgent Action:
- Scarring: Visible follicular loss, Atrophy, Smooth shiny skin → Urgent biopsy for cicatricial alopecia
- Erythema, Scale, Pustules: Tinea capitis? CCCA? → KOH, Culture, Biopsy
- Systemic Symptoms: Fever, Weight loss, Fatigue → Screen for systemic disease
- Rapid Total Loss in Adult: Consider telogen effluvium, Medication-induced
- Unusual Distribution or Texture Changes: May indicate different pathology
- Significant Psychological Distress: Suicidal ideation → Urgent psychiatric referral
Structured Approach
Scalp Examination:
| Finding | Interpretation |
|---|---|
| Well-Circumscribed Patches | Classic AA |
| Smooth Scalp Skin | Non-scarring |
| No Erythema/Scale | Not inflammatory/Infectious |
| Pull Test Positive Margin | Active disease |
| "Exclamation Mark" Hairs | Pathognomonic |
| Regrowth (Fine, White) | Recovering |
Hair Pull Test:
- Grasp ~60 hairs between thumb and fingers
- Gently pull from root to tip
- Positive if >10% hairs come out (>6 hairs)
- Perform at patch margin (Active disease)
Dermoscopy (Trichoscopy):
| Finding | Description |
|---|---|
| Yellow Dots | Empty follicles filled with keratinous debris |
| Black Dots | Cadaverised hairs |
| Exclamation Mark Hairs | Tapered, Broken |
| Short Vellus Hairs | Regrowth |
| Broken Hairs | Variable lengths |
Other Hair Sites:
- Eyebrows, Eyelashes (Madarosis)
- Beard
- Body hair
Nail Examination:
- Pitting, Ridging, Trachyonychia
General Examination:
- Signs of thyroid disease (Associated)
- Vitiligo patches (Associated)
- Atopic dermatitis features
Core Principle: Clinical Diagnosis
Alopecia areata is primarily a clinical diagnosis. In typical cases with classic features, investigations are NOT mandatory. The diagnosis is made on:
- Well-demarcated, round/oval patches of hair loss
- Smooth, non-scarred scalp skin
- Exclamation mark hairs at patch margins
- No scaling, erythema, or pustules
- Yellow dots and black dots on dermoscopy
Indications for Investigation
| Clinical Scenario | Recommended Investigations |
|---|---|
| Typical Patchy AA | No investigations required. Consider TFTs. |
| Atypical Presentation | Scalp biopsy, TFTs, ANA |
| Diffuse AA | Biopsy to distinguish from telogen effluvium |
| Suspected Scarring Alopecia | Urgent biopsy |
| Scaling Present | KOH/Fungal culture (Tinea capitis) |
| Systemic Symptoms | FBC, TFTs, ANA, ESR, VDRL |
| Before JAK Inhibitor Therapy | Full pre-treatment screening panel |
Laboratory Investigations
Thyroid Function Tests (TFTs):
| Test | Purpose | Expected in AA |
|---|---|---|
| TSH | Screen thyroid dysfunction | May be abnormal (8-28% have thyroid disease) |
| Free T4 | If TSH abnormal | Varies |
| Anti-TPO Antibodies | Autoimmune thyroiditis | Common positive in AA |
| Anti-Thyroglobulin Antibodies | Hashimoto's marker | May be positive |
Recommendation: Check TFTs at diagnosis and periodically (annually) due to high autoimmune thyroid association.
Full Blood Count (FBC):
| Parameter | Purpose |
|---|---|
| Haemoglobin | Exclude anaemia as differential |
| MCV | Iron/B12 deficiency |
| White Cells | Pre-JAK inhibitor baseline |
| Platelets | Pre-JAK inhibitor baseline |
Iron Studies:
| Test | Relevance |
|---|---|
| Serum Ferritin | Low ferritin associated with hair loss (though more telogen effluvium). Target greater than 70 for hair health. |
| Serum Iron | General iron status |
| Transferrin Saturation | Iron availability |
Other Investigations:
| Investigation | Indication | Notes |
|---|---|---|
| Vitamin D | If suspected deficiency | Associated with autoimmune conditions |
| ANA | If lupus suspected | Discoid lupus can cause scarring alopecia |
| VDRL/RPR | If secondary syphilis suspected | "Moth-eaten" alopecia pattern |
| ESR/CRP | If systemic disease suspected | Non-specific |
| Fasting Glucose/HbA1c | Pre-JAK inhibitor | Screen for diabetes |
Dermoscopy (Trichoscopy) – Key Diagnostic Tool
| Finding | Description | Significance |
|---|---|---|
| Yellow Dots | Empty follicular ostia filled with keratinous debris and sebum | Highly specific for AA. Also in trichotillomania. |
| Black Dots | Cadaverised (broken) hairs at follicular level | Active disease. Also in tinea. |
| Exclamation Mark Hairs | Short dystrophic hairs tapering at proximal end (3-4mm) | Pathognomonic. Indicates active disease. |
| Broken Hairs | Irregular lengths | Non-specific |
| Short Vellus Hairs | Fine, depigmented regrowing hairs | Indicates early regrowth |
| White Hairs | Depigmented terminal/vellus hairs | Regrowth phase |
| Coudability Hairs | Wavy/bent hairs | Regrowth |
| Tapered Hairs | Narrowed proximal ends | Active disease |
| Pigtail Hairs | Coiled regrowing hairs | Regrowth |
| Upright Regrowing Hairs | Short terminal hairs | Good prognosis sign |
Dermoscopy Differential:
| Condition | Dermoscopy Pattern |
|---|---|
| Alopecia Areata | Yellow dots, Black dots, Exclamation mark hairs |
| Tinea Capitis | Comma hairs, Corkscrew hairs, Black dots, Scale |
| Trichotillomania | Irregular broken hairs, Black dots, Flame hairs, Yellow dots |
| Androgenetic Alopecia | Hair diameter variability, Yellow dots, Vellus hairs |
Scalp Biopsy
Indications:
- Diagnostic uncertainty (Atypical pattern or features)
- Suspected scarring alopecia (Must distinguish urgently)
- Diffuse alopecia (Distinguish from telogen effluvium)
- Mixed patterns
- Non-response to treatment (Consider cicatricial component)
Technique:
- 4mm punch biopsy from active edge of patch
- Include normal-appearing adjacent scalp for comparison
- Request horizontal sectioning (Superior for follicular count)
- +/- Vertical for DIF if lupus suspected
Histopathology: Active Alopecia Areata:
| Feature | Description |
|---|---|
| "Swarm of Bees" Pattern | Dense peribulbar lymphocytic infiltrate around anagen follicles |
| Lymphocyte Types | Predominantly CD4+ and CD8+ T cells, Some NK cells |
| Target | Hair bulb matrix keratinocytes and melanocytes |
| Pigment Incontinence | Melanin granules in dermis (from destroyed melanocytes) |
| Increased Catagen/Telogen | Shifted follicle population |
| Eosinophils | May be present in infiltrate |
| Follicular Miniaturisation | Variable (More in chronic disease) |
| NO Scarring | Follicular architecture preserved |
| NO Fibrosis | Distinguishes from scarring alopecias |
Histopathology: Chronic/Stable Alopecia Areata:
| Feature | Description |
|---|---|
| Sparse Inflammation | Reduced peribulbar infiltrate |
| Miniaturised Follicles | Nanogen hairs predominate |
| Fibrous Streamers | Residual connective tissue tracts |
| Increased Telogen Ratio | High proportion resting follicles |
| Preservation of Follicular Units | Key distinguishing feature from scarring |
Differential Diagnosis – Comprehensive Table
| Condition | Key Features | How to Distinguish |
|---|---|---|
| Tinea Capitis | Scale, Broken hairs, Erythema, Lymphadenopathy | KOH positive. Dermoscopy: Comma/Corkscrew hairs |
| Trichotillomania | Irregular patches, Geometric borders, Variable hair lengths | History (Often denied). Dermoscopy: Flame hairs. Biopsy: Trichomalacia |
| Traction Alopecia | Marginal distribution, History of tight hairstyles | Frayed hairs. Folliculitis at margins |
| Telogen Effluvium | Diffuse thinning, Positive pull test, Trigger 2-4 months prior | Hair count normal. Biopsy: Increased telogen without inflammation |
| Androgenetic Alopecia | Male pattern (Vertex, Frontotemporal). Female pattern (Crown thinning) | Miniaturisation on dermoscopy. Preserved density initially |
| Cicatricial (Scarring) Alopecias | Loss of follicular openings, Atrophy, Erythema | Biopsy shows fibrosis, Destroyed follicles. Irreversible |
| Lichen Planopilaris | Perifollicular erythema, Scale, Pruritus | Biopsy: Interface dermatitis. DIF positive |
| Frontal Fibrosing Alopecia | Progressive frontal hairline recession, Eyebrow loss | Band-like. Histology similar to LPP |
| Discoid Lupus | Erythematous plaques, Follicular plugging, Scarring | DIF positive (Lupus band). Photosensitive |
| Secondary Syphilis | "Moth-eaten" pattern, Systemic symptoms, Rash | VDRL/RPR positive. Spirochetes on darkfield |
| Alopecia Syphilitica | Patchy non-scarring alopecia | Serology positive. Resolves with treatment |
| Loose Anagen Syndrome | Easily extractable hairs, Children | Pull test: Anagen hairs with ruffled cuticle |
| Pressure Alopecia | History of prolonged pressure (Surgery, ICU) | Resolves spontaneously |
JAK Inhibitor Pre-Treatment Screening Panel
| Test | Purpose | Action if Abnormal |
|---|---|---|
| FBC | Baseline cytopenias | Do not start if significant cytopenias |
| LFTs | Hepatic function | Avoid or reduce dose in hepatic impairment |
| Renal Function (eGFR) | Dose adjustment | Reduce dose if impaired |
| Lipid Profile | JAK inhibitors increase lipids | Manage with statins if needed |
| TB Screening | QuantiFERON or Mantoux | Treat latent TB before starting |
| Hepatitis B/C Serology | Reactivation risk | If positive, Consider prophylaxis |
| Varicella Status | Zoster risk | Vaccinate before starting if seronegative |
| Chest X-Ray | TB screening | If TB suspected |
| HIV Serology | If risk factors | Manage appropriately |
| Pregnancy Test | Contraindicated in pregnancy | Ensure contraception |
Management Algorithm
General Principles
| Principle | Details |
|---|---|
| Reassurance | Benign condition. Regrowth possible. Non-contagious. |
| Prognosis Discussion | Limited AA often regrows spontaneously. Extensive has guarded prognosis. Honest communication. |
| Psychological Support | Cosmetic impact significant. Screen for depression/Anxiety. Refer to psychology if needed. |
| Patient Education | Explain autoimmune nature, Treatment options, Realistic expectations. |
| Wig/Camouflage | Discuss options. Prescribable on NHS in UK. Various options available. |
| Support Groups | Alopecia UK, NAAF (National Alopecia Areata Foundation), Online communities. |
| Shared Decision-Making | Treatment choice depends on patient preferences, Extent, And goals. |
Treatment Algorithm by Extent
Step 1: Assess Extent of Disease
| Classification | Definition | Management Approach |
|---|---|---|
| Limited Patchy AA | less than 50% scalp involvement | Intralesional steroids ± Topical |
| Moderate AA | 50-75% scalp | Topical immunotherapy OR JAK inhibitor |
| Severe AA (AT/AU) | >75% scalp or Totalis/Universalis | JAK inhibitor (First-line) OR Topical immunotherapy |
Treatment Details by Modality
1. Intralesional Corticosteroids (First-Line for Limited Disease)
Technique:
| Parameter | Detail |
|---|---|
| Drug | Triamcinolone acetonide suspension |
| Concentration (Scalp) | 5-10 mg/mL (Most commonly 5 mg/mL) |
| Concentration (Eyebrows) | 2.5-5 mg/mL (Lower to avoid atrophy) |
| Concentration (Beard) | 5 mg/mL |
| Needle | 30-gauge, 0.5 inch |
| Volume per Injection Site | 0.05-0.1 mL |
| Depth | Intradermal (Superficial dermis) |
| Spacing | Injections 0.5-1 cm apart across patch |
| Maximum per Session | 20-40 mg total (To avoid systemic effects) |
| Interval | Every 4-6 weeks |
| Number of Sessions | 4-6 initially, Then assess response |
Response:
- Regrowth typically seen at injection sites by 4-8 weeks
- Hairs may initially be white, Then pigmented
- Works better for smaller, Fewer patches
Side Effects:
| Side Effect | Prevention/Management |
|---|---|
| Skin Atrophy | Use lower concentration, Avoid repeat injections in same spot |
| Hypopigmentation | More common in darker skin types |
| Pain | Topical anaesthetic cream (EMLA) beforehand. Vibration device. |
| Telangiectasia | Usually reversible |
| Systemic Absorption | Limit total dose per session |
When to Stop:
- No response after 6 months
- Disease progression despite treatment
- Unacceptable side effects
2. Topical Corticosteroids
Options:
| Steroid | Strength | Formulation | Application |
|---|---|---|---|
| Clobetasol Propionate 0.05% | Superpotent | Foam, Lotion, Ointment | Once-twice daily |
| Betamethasone Dipropionate 0.05% | Potent | Lotion, Ointment | Once-twice daily |
| Fluocinolone Acetonide 0.025% | Moderate | Solution, Ointment | Once-twice daily |
| Mometasone Furoate 0.1% | Potent | Lotion | Once daily |
Protocol:
- Apply to affected areas once or twice daily
- Can use under occlusion for enhanced penetration
- Duration: 3-6 months trial
- Taper if successful, Monitor for recurrence
Side Effects:
- Folliculitis (Common)
- Skin atrophy (Prolonged use)
- Telangiectasia
- Striae (Rare on scalp)
Evidence: Moderate – Less effective than intralesional but useful adjunct.
3. Topical Minoxidil
| Parameter | Details |
|---|---|
| Concentration | 5% (Men and Women) |
| Formulation | Solution or Foam |
| Application | Twice daily to affected areas |
| Mechanism | Vasodilation, Prolongs anagen, Increases hair diameter |
| Use in AA | Adjunctive therapy. Not effective alone. |
| Response | May enhance cosmetic density of regrowth |
| Side Effects | Hypertrichosis (Facial hair), Scalp irritation, Initial shedding |
4. Topical Immunotherapy (DPCP/SADBE)
Agents:
| Agent | Full Name |
|---|---|
| DPCP | Diphencyprone (Diphenylcyclopropenone) – Most commonly used |
| SADBE | Squaric Acid Dibutylester |
| DNCB | Dinitrochlorobenzene (Less used – Mutagenic concerns) |
Mechanism:
- Induce allergic contact dermatitis
- Shifts immune response away from follicle destruction
- Antigenic competition hypothesis
- Alters local cytokine milieu
Protocol (DPCP):
| Step | Details |
|---|---|
| Sensitisation | Apply 2% DPCP to small scalp area. Creates contact allergy. |
| Wait Period | 2 weeks for sensitisation to develop |
| Initial Treatment | Apply very low concentration (0.001%) to affected areas |
| Titration | Gradually increase concentration to achieve mild eczematous reaction |
| Target Reaction | Mild erythema, Pruritus, Vesiculation tolerated |
| Frequency | Weekly applications in clinic |
| Duration | 6-12 months to assess response |
| Response Rate | 30-50% achieve significant regrowth (Higher in limited disease) |
Side Effects:
| Side Effect | Frequency | Management |
|---|---|---|
| Severe Contact Dermatitis | Common | Reduce concentration, Extend interval |
| Blistering | Occasional | Topical steroids, Reduce concentration |
| Lymphadenopathy | Occasional | Usually resolves |
| Dyspigmentation | Occasional | May be permanent |
| Vitiligo (Paradoxical) | Rare | Stop treatment |
| Flu-like Symptoms | Rare | Symptomatic |
Contraindications:
- Pregnancy (Teratogenic potential)
- Unable to attend weekly appointments
- Previous severe reaction
5. JAK Inhibitors (New Era of Treatment)
Approved Agents:
| Drug | Selectivity | Approval | Indication |
|---|---|---|---|
| Baricitinib (Olumiant) | JAK1/JAK2 | FDA/NICE 2022 | Adults ≥50% scalp hair loss |
| Ritlecitinib (Litfulo) | JAK3/TEC | FDA 2023 | Adults and adolescents ≥12 yrs |
Baricitinib (Olumiant):
| Parameter | Details |
|---|---|
| Dose | 2 mg or 4 mg once daily (4 mg more effective) |
| Efficacy (BRAVE Trials) | 35-39% achieve SALT ≤20 (≥80% coverage) at 36 weeks |
| Time to Response | Some response by 12 weeks, Maximum benefit 36-52 weeks |
| Maintenance | Continued treatment required. Relapse off treatment. |
Ritlecitinib (Litfulo):
| Parameter | Details |
|---|---|
| Dose | 50 mg once daily |
| Age | ≥12 years |
| Efficacy (ALLEGRO Trials) | ~25-30% achieve SALT ≤20 at 24 weeks |
| Uniqueness | JAK3/TEC selectivity (Different from JAK1/2) |
Off-Label JAK Inhibitors:
| Drug | Notes |
|---|---|
| Tofacitinib | JAK1/3. Used off-label. Evidence from case series. 5-10 mg twice daily. |
| Ruxolitinib (Topical) | JAK1/2. Topical cream 1.5%. Under investigation. Avoids systemic effects. |
Pre-Treatment Screening (All JAK Inhibitors):
| Test | Purpose |
|---|---|
| FBC | Baseline cytopenias screening |
| LFTs | Hepatic function |
| Renal Function | Dose adjustment if impaired |
| Lipid Profile | JAK inhibitors increase lipids |
| TB Screening (QuantiFERON/Mantoux) | Risk of TB reactivation |
| Hepatitis B/C Serology | Risk of reactivation |
| Varicella Status | Herpes zoster risk |
| Age-Appropriate Cancer Screening | Baseline |
| Cardiovascular Risk Assessment | FDA box warning for CV events |
Monitoring on Treatment:
| Test | Frequency |
|---|---|
| FBC | 4-8 weeks, Then 3-monthly |
| LFTs | 3-monthly |
| Lipids | 12 weeks, Then annually |
| Clinical Assessment | 3-6 monthly |
Side Effects:
| Side Effect | Frequency | Notes |
|---|---|---|
| Upper Respiratory Infections | Common | Self-limiting |
| Headache | Common | Usually mild |
| Acne | Common | May need treatment |
| Herpes Zoster | Increased | Consider vaccination pre-treatment |
| Cytopenias | Uncommon | Monitor FBC |
| Lipid Elevations | Common | May need statin |
| VTE | Rare (FDA Warning) | Risk assessment |
| Malignancy | Rare (FDA Warning) | Surveillance |
| MACE | Rare (FDA Warning) | CV risk assessment |
Contraindications:
- Active serious infection
- Pregnancy/Breastfeeding
- Severe hepatic impairment
- Uncontrolled cytopenias
- Recent VTE (Relative)
6. Systemic Corticosteroids
| Regimen | Details |
|---|---|
| Oral Prednisolone Pulse | 5 mg/kg on 2 consecutive days monthly for 3-6 months |
| Mini-Pulse Oral Dexamethasone | 5 mg on 2 consecutive days weekly |
| IV Methylprednisolone Pulse | 500 mg-1g for 3 days (Inpatient) |
Indications:
- Rapidly progressive disease
- Bridge while awaiting other treatment
- AT/AU (Limited evidence)
Side Effects:
- Multiple with prolonged use (Osteoporosis, Cushingoid, DM, HTN, Adrenal suppression)
- Not sustainable long-term
7. Other Systemic Agents (Off-Label/Limited Evidence)
| Agent | Dose | Notes |
|---|---|---|
| Methotrexate | 15-25 mg weekly | Steroid-sparing. Case series. |
| Azathioprine | 1-2 mg/kg daily | Case reports. |
| Ciclosporin | 3-5 mg/kg daily | Effective but high relapse. Nephrotoxic. |
| Sulfasalazine | 500 mg TDS | Limited evidence. |
Emerging and Experimental Therapies
| Therapy | Mechanism | Status |
|---|---|---|
| Topical Ruxolitinib | Topical JAK1/2 inhibitor | Phase 3 trials, Promising |
| Deuruxolitinib (CTP-543) | Oral JAK1/2 inhibitor | Phase 3 trials |
| Brepocitinib | TYK2/JAK1 inhibitor | Phase 2 |
| PRP (Platelet-Rich Plasma) | Growth factors | Case series. Variable results. |
| Low-Level Laser Therapy | Photobiomodulation | Limited evidence |
| Excimer Laser 308nm | Targeted UV | Some evidence for localised |
| Stem Cell Transplant | Immune reset | Anecdotal. Experimental. |
| Faecal Microbiota Transplant | Microbiome modulation | Case reports. Research. |
Special Populations
Children:
| Consideration | Details |
|---|---|
| Baseline | Higher rate of spontaneous remission. Watch and wait often appropriate. |
| Topical Steroids | First-line for children. |
| Intralesional Steroids | From age ~10 (Depending on cooperation). |
| Topical Immunotherapy | From age ~8. Requires parental commitment. |
| JAK Inhibitors | Ritlecitinib approved ≥12 years. |
| Psychological Support | Especially important (Bullying, Self-esteem). |
Eyebrow/Eyelash Alopecia:
| Treatment | Details |
|---|---|
| Intralesional Triamcinolone | Very low concentration (2.5-5 mg/mL). Careful technique. Risk of atrophy. |
| Topical Steroids | Mild-moderate potency. Avoid eyes. |
| Bimatoprost 0.03% | Off-label. Prostaglandin analogue. May stimulate lash growth. |
| Cosmetic Options | Eyebrow pencil, Microblading (Permanent makeup), False lashes. |
Beard (Alopecia Barbae):
| Treatment | Details |
|---|---|
| Intralesional Steroids | Similar to scalp. 5 mg/mL. |
| Topical Steroids | Effective for limited patches. |
| JAK Inhibitors | Effective for extensive. |
Cosmetic and Supportive Options
| Option | Details |
|---|---|
| Wigs | Synthetic or human hair. Prescribable on NHS (UK). Custom-made options. |
| Hairpieces/Toupees | For partial loss. |
| Scarves/Head Coverings | Fashion options. |
| Scalp Micropigmentation | Tattoo technique to simulate hair follicles. |
| Eyebrow Microblading | Semi-permanent makeup for eyebrows. |
| False Eyelashes | Magnetic or glue-on. |
| Theatrical/Medical Adhesive Wigs | For active lifestyles. |
Psychological Support
| Intervention | Details |
|---|---|
| Screening | Screen for anxiety, Depression (PHQ-9, GAD-7). |
| Counselling | CBT effective for body image issues. |
| Support Groups | Alopecia UK, NAAF, Online forums. |
| Children | School liaison, Anti-bullying strategies. |
| Dermatology-Psychology Liaison | Psychodermatology clinics. |
Treatment Algorithm Summary
Alopecia Areata Diagnosis
│
▼
┌────────────────────────────────────────────┐
│ ASSESS EXTENT OF DISEASE │
└────────────────────────────────────────────┘
│
┌────┴────┐────────────────┐
▼ ▼ ▼
less than 50% 50-75% >75%/AT/AU
│ │ │
▼ ▼ ▼
┌────────┐ ┌────────────┐ ┌─────────────┐
│ ILC + │ │ Topical │ │ JAK │
│ Topical│ │ Immuno- │ │ Inhibitor │
│ ± Minox│ │ therapy OR │ │ (Baricitinib│
│ │ │ JAK inh │ │ Ritlecitinib│
└────────┘ └────────────┘ └─────────────┘
│
▼
┌────────────────────────────────────────────┐
│ ALL: Psychological Support, Cosmetic │
│ Options, Patient Education │
└────────────────────────────────────────────┘
Disease Complications
| Complication | Notes |
|---|---|
| Progression to AT/AU | ~5-10% of patchy AA |
| Psychological Impact | Anxiety, Depression, Low self-esteem |
| Social Stigma | Especially eyebrow/Eyelash loss |
| Recurrence | Common (>50%) |
Treatment Complications
| Treatment | Complications |
|---|---|
| Intralesional Steroids | Skin atrophy, Pain, Hypopigmentation |
| Topical Steroids (Prolonged) | Atrophy, Telangiectasia |
| Topical Immunotherapy | Severe eczema, Lymphadenopathy, Vitiligo |
| JAK Inhibitors | Infections (Herpes zoster), VTE, Cytopenias, Lipid changes |
Natural History
| Factor | Prognosis |
|---|---|
| Limited Patchy AA | Good. 30-50% spontaneous regrowth within 1 year. |
| Extensive AA/AT/AU | Guarded. less than 10% long-term full regrowth. |
| Recurrence | Common. >50% will have further episodes. |
Prognostic Factors
Good Prognosis:
- Limited number of patches
- Small patches
- Later age of onset (Adult)
- Short duration
- No nail involvement
Poor Prognosis:
- Extensive disease (AT, AU)
- Early childhood onset
- Ophiasis pattern
- Long duration (>1 year)
- Nail changes
- Atopy
- Family history
- Associated autoimmune disease
Key Guidelines
| Guideline | Organisation | Year | Key Recommendations |
|---|---|---|---|
| BAD Guidelines for Alopecia Areata | British Association of Dermatologists | 2012 | ILC first-line for limited; Topical immunotherapy for extensive |
| AAD Clinical Guidelines | American Academy of Dermatology | 2023 | JAK inhibitors for severe AA; Stepped care approach |
| NICE TA875 | NICE | 2022 | Baricitinib recommended for severe AA (≥50% scalp) |
| European Dermatology Forum | EDF | 2020 | Consensus on treatment algorithms |
| Japanese Dermatological Association | JDA | 2017 | Emphasis on topical immunotherapy |
Landmark Trials
BRAVE-AA1 and BRAVE-AA2 Trials (2022) – Baricitinib:
- Phase 3 RCTs, n=1200 combined
- Baricitinib 2mg vs 4mg vs Placebo for severe AA
- Primary Endpoint: SALT ≤20 (≥80% hair coverage) at 36 weeks
- Result: 35-39% on 4mg achieved SALT ≤20 vs 6% placebo
- Established efficacy of oral JAK inhibition
- Led to FDA/NICE approval
- PMID: 35333422
BRAVE-AA Extension (2023):
- Long-term data to 52 weeks
- Sustained response with continued treatment
- Relapse common on discontinuation
- Safety profile maintained
ALLEGRO Phase 2b/3 Trials (2023) – Ritlecitinib:
- Phase 2b/3 RCT in severe AA
- Ritlecitinib (JAK3/TEC inhibitor) 50mg daily
- Result: ~25-30% achieved SALT ≤20 at 24 weeks
- First adolescent approval (≥12 years)
- PMID: 37315636
CTP-543 (Deuruxolitinib) Phase 2:
- Oral JAK1/2 inhibitor
- Phase 2 results promising
- Phase 3 ongoing
Topical Immunotherapy Meta-Analysis (Cochrane 2008):
- Reviewed DPCP/SADBE trials
- Overall response rate 30-50%
- Higher in limited vs extensive disease
- Quality of evidence moderate
Evidence Strength Summary
| Intervention | Evidence Level | Recommendation |
|---|---|---|
| Intralesional Corticosteroids | 2b (Cohort studies) | First-line for limited AA |
| Topical Corticosteroids | 2b | Adjunctive |
| Topical Immunotherapy (DPCP) | 2a (Systematic reviews) | Moderate-severe AA |
| Baricitinib | 1a (Phase 3 RCTs) | Severe AA |
| Ritlecitinib | 1b (Phase 3 RCT) | Severe AA (Including adolescents) |
| Oral Corticosteroid Pulse | 2b | Rapidly progressive |
| Minoxidil | 3 (Case series) | Adjunctive only |
SALT Score (Severity of Alopecia Tool)
| SALT Score | Description | Clinical Meaning |
|---|---|---|
| 0 | No hair loss | Complete regrowth |
| ≤20 | ≤20% hair loss | ≥80% coverage – Treatment success endpoint |
| 21-49 | 21-49% hair loss | Moderate |
| 50-99 | 50-99% hair loss | Severe |
| 100 | Complete hair loss | Alopecia totalis |
What is Alopecia Areata?
Alopecia areata is a condition where your immune system attacks your hair follicles, Causing hair to fall out in round, Smooth patches. It is NOT contagious and you cannot "catch" it from someone else.
Why does it happen?
It's an autoimmune condition – Your immune system 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 autoimmune conditions (Like thyroid disease or vitiligo).
Possible triggers (in some people) include:
- Stress or emotional trauma
- Viral infections
- Family history
Who gets alopecia areata?
- It affects about 2% of people at some point in their life
- It can happen at any age, But often starts before age 30
- Men and women are affected equally
- It runs in families in about 10-20% of cases
Will my hair grow back?
For Patchy Alopecia Areata (Small Patches):
- Good news – 30-50% of people see regrowth within a year, Even without treatment
- Hair may grow back white initially, Then returns to normal colour
- Recurrence is common – Hair may fall out again later
For Extensive Hair Loss (Totalis/Universalis):
- More difficult, And full regrowth is less common
- New treatments like JAK inhibitors are helping more people
- Some people achieve significant regrowth with these new medicines
What treatments are available?
For Small Patches (Less Than Half the Scalp):
| Treatment | How It Works | What to Expect |
|---|---|---|
| Steroid Injections | Injected into the patches monthly | Most common treatment. Regrowth often seen in 4-8 weeks at injection sites. |
| Steroid Creams/Foams | Applied daily to patches | Less effective than injections. Useful for children or needle-phobic. |
| Minoxidil (Regaine) | Applied twice daily | May enhance regrowth. Used alongside other treatments. |
For Extensive Hair Loss (More Than Half the Scalp):
| Treatment | How It Works | What to Expect |
|---|---|---|
| Immunotherapy Creams (DPCP) | Applied weekly in clinic. Creates mild allergic reaction. | Specialist treatment. Takes 6-12 months to assess. 30-50% response. |
| JAK Inhibitor Tablets (Baricitinib) | Daily tablet. Blocks inflammation. | New treatment (2022). About 35-40% achieve good regrowth. |
Important: Treatments need to be continued. Hair often falls out again when treatment stops.
What about wigs and hairpieces?
Wig Options:
| Type | Details |
|---|---|
| Synthetic Wigs | Affordable. Pre-styled. Less natural. |
| Human Hair Wigs | More natural look and feel. More expensive. Can be styled. |
| Partial Hairpieces | For patchy loss. Clip-on or adhesive. |
| Scalp Micropigmentation | Tattoo technique to simulate hair follicles. Permanent. |
NHS Prescriptions: In the UK, Wigs can be prescribed on the NHS for medical hair loss. Ask your GP or dermatologist.
Where to Get Help:
- Alopecia UK (www.alopecia.org.uk) – Charity with advice and support groups
- NAAF (National Alopecia Areata Foundation) – US-based but excellent resources
- Hospital wig fitting services
Eyebrows and Eyelashes
If you've lost eyebrows or eyelashes:
- Eyebrow pencils and makeup can help with daily camouflage
- Microblading is a semi-permanent tattoo option for eyebrows
- False eyelashes (Magnetic or glue-on) are available
- Some treatments may help – Ask your dermatologist
Psychological Support
Losing hair can be very distressing, Even though it is not medically dangerous. Your feelings are valid.
Where to Get Help:
| Resource | Details |
|---|---|
| Your GP | Can refer for counselling. Can prescribe medication for anxiety/depression if needed. |
| Alopecia UK | Support groups (Online and in-person). Peer support. |
| Therapy | CBT (Cognitive Behavioural Therapy) is effective for body image concerns. |
| Online Communities | Facebook groups, Instagram communities for people with alopecia. |
Children with Alopecia:
- Schools should be informed to prevent bullying
- Child psychology services can help
- Look for age-appropriate support resources
Frequently Asked Questions
Q: Is alopecia areata contagious? A: No, You cannot catch it from someone else or pass it to others.
Q: Will I lose all my hair? A: Most people with patchy alopecia areata do NOT progress to total hair loss (Only 5-10%).
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.
Q: Are the new JAK inhibitor treatments available on the NHS? A: Baricitinib was approved by NICE in 2022 for severe alopecia areata. Ask your dermatologist if you qualify.
Q: Can I colour my hair? A: Yes, If you have regrowth, You can use hair dye. It will not affect alopecia areata.
Primary Guidelines
-
Messenger AG, et al. British Association of Dermatologists Guidelines for Alopecia Areata. Br J Dermatol. 2012;166(5):916-926. PMID: 22524397
-
NICE Technology Appraisal TA875. Baricitinib for treating severe alopecia areata. NICE. 2022.
-
Strazzulla LC, et al. JAK inhibitors and alopecia areata. J Am Acad Dermatol. 2018;78(6):1223-1226. PMID: 29291815
Landmark Trials
- King B, et al. Two randomized, Controlled trials of baricitinib for alopecia areata (BRAVE-AA). N Engl J Med. 2022;386(18):1687-1699. PMID: 35333422
Pathophysiology and Evidence
-
Gilhar A, et al. Alopecia areata. N Engl J Med. 2012;366(16):1515-1525. PMID: 22512484
-
Pratt CH, et al. Alopecia areata. Nat Rev Dis Primers. 2017;3:17011. PMID: 28300084
-
Xing L, et al. Alopecia areata is driven by cytotoxic T lymphocytes via JAK3. Nat Med. 2014;20(9):1043-1049. PMID: 25129481
Additional References
-
Alkhalifah A, et al. Alopecia areata update. J Am Acad Dermatol. 2010;62(2):177-190. PMID: 20115946
-
Cranwell W, Sinclair R. Common causes of hair loss. Aust Fam Physician. 2016;45(3):111-114. PMID: 27695716
-
Tosti A, et al. Dermoscopy of hair. J Am Acad Dermatol. 2006;54(4):574-578.
-
Safavi K. Prevalence of alopecia areata in Rochester, Minnesota. Mayo Clin Proc. 1995;70(7):628-633. PMID: 7791384
-
Paus R, et al. Collapse of hair follicle immune privilege in alopecia areata. J Investig Dermatol Symp Proc. 2013;16(1):S25-27.
-
Shapiro J. Current treatment of alopecia areata. J Investig Dermatol Symp Proc. 2013;16(1):S42-44.
-
Jabbari A, et al. Therapeutic approaches in alopecia areata. Dermatol Clin. 2019;37(4):407-418. PMID: 31466584
-
Darwin E, et al. Alopecia areata: Review of epidemiology, Clinical features, Pathogenesis, And new treatment options. Int J Trichology. 2018;10(2):51-60. PMID: 29769777
Common Exam Questions
-
Diagnosis Question: "A 28-year-old man presents with a well-circumscribed, Smooth, Round patch of hair loss on the scalp. What is the most likely diagnosis?"
- Answer: Alopecia areata.
-
Clinical Finding: "What is the pathognomonic dermoscopic finding in alopecia areata?"
- Answer: "Exclamation mark" hairs – Short, Broken hairs that taper towards the scalp.
-
Treatment Question: "What is the first-line treatment for limited patchy alopecia areata?"
- Answer: Intralesional triamcinolone acetonide (5-10 mg/mL, Monthly).
-
New Treatment: "What class of medication has recently been approved for severe alopecia areata?"
- Answer: JAK inhibitors (Baricitinib).
-
Associations: "What autoimmune conditions are associated with alopecia areata?"
- Answer: Thyroid disease, Vitiligo, Atopic conditions.
Viva Points
Opening Statement:
"Alopecia areata is a common autoimmune, Non-scarring alopecia characterised by patchy hair loss with well-demarcated smooth patches. The pathognomonic finding is 'exclamation mark' hairs. It affects approximately 2% of the population and is associated with other autoimmune conditions, Particularly thyroid disease."
Key Facts:
- T-cell mediated attack on anagen follicles
- JAK-STAT pathway activation (Target of JAK inhibitors)
- Non-scarring – Follicle preserved – Regrowth potential
- Intralesional steroids first-line for limited
- Baricitinib (JAK inhibitor) for severe (BRAVE trials)
- Nail pitting in 10-20%
Evidence to Cite:
- "BRAVE-AA1 and BRAVE-AA2 Phase 3 trials showed baricitinib achieved ≥80% hair coverage in 35-39% of patients with severe AA"
Common Mistakes
What fails candidates:
- ❌ Confusing with scarring alopecias
- ❌ Not knowing "exclamation mark" hairs
- ❌ Not mentioning JAK inhibitors as new treatment
- ❌ Forgetting thyroid screening
- ❌ Overlooking psychological impact
Dangerous Errors:
- ⚠️ Missing tinea capitis (Needs KOH if scale present)
- ⚠️ Missing lupus (If scarring features)
Last Reviewed: 2025-12-25 | 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 and current guidelines.