Alopecia areata
Exam Tips
- OSCE classic: smooth, sharply demarcated, non-scarring patch with preserved follicular openings plus exclamation mark hairs at the edge strongly suggests alopecia areata.
- If there is scale, broken hairs of different lengths, pustules, or occipital nodes, actively exclude tinea capitis before giving steroids.
- State severity in exams (<25% mild, 25-50% moderate, >50% severe scalp involvement) because this changes referral urgency and treatment options.
- Nail pitting/ridging with ophiasis pattern is a high-yield marker of worse prognosis.
- Always include psychosocial assessment and safeguarding impact in children (school refusal, bullying risk) as part of holistic management.
Definition
Alopecia areata is a chronic, immune-mediated inflammatory disorder of hair follicles that causes sudden, non-scarring hair loss in discrete or diffuse patterns. It most often affects the scalp or beard but can involve any hair-bearing site (including eyebrows and eyelashes), with preserved follicular openings and potential relapse-remit episodes over time.
Pathophysiology
The core mechanism is loss of immune privilege at the anagen hair bulb, leading to a predominantly T-cell-mediated autoimmune attack on follicular structures. Cytotoxic and helper T-cell signalling (including interferon-driven and JAK-STAT pathways) promotes premature transition from anagen to catagen/telogen, producing dystrophic miniaturized hairs and characteristic "exclamation mark" hairs. Histology in active disease classically shows a peri-/intra-bulbar lymphocytic infiltrate ("swarm of bees") around anagen follicles, with reduced anagen: telogen ratio.
Risk Factors
- Personal or family history of alopecia areata (familial tendency; ~20% report affected relatives)
- Other autoimmune disease (for example autoimmune thyroid disease, vitiligo, pernicious anaemia, systemic lupus erythematosus)
- Atopic background
- Younger age at onset (including childhood onset for poorer long-term outcome)
- Psychological stress (possible trigger for onset or flare)
- Smoking (associated with increased risk in observational data)
- More severe initial pattern (ophiasis, extensive scalp involvement) as a marker of poorer prognosis
Clinical Features
Symptoms
- Sudden patchy hair loss, commonly scalp or beard
- Usually asymptomatic, but some report itch, tingling, burning, or tenderness before/with active loss
- Cosmetic distress, reduced self-esteem, social withdrawal, anxiety/depressive symptoms
Signs
- Well-circumscribed smooth round/oval non-scarring patches with preserved follicular ostia
- Exclamation mark hairs at lesion edge in active disease
- Black dots, broken hairs, yellow dots on trichoscopy
- Patterns: patchy focal loss, ophiasis (occipito-temporal band), sisaipho (inverse ophiasis), diffuse variant, alopecia totalis/universalis
- Nail involvement (pitting, longitudinal ridging, onycholysis, trachyonychia, leukonychia, red lunula, koilonychia)
Investigations
Management
Lifestyle Modifications
- Explain variable natural history (including spontaneous regrowth) and relapse risk; agree shared goals
- Assess psychosocial impact at each review; screen for anxiety/depression and offer mental health support
- Cosmetic support: wigs/hairpieces, eyebrow options, camouflage fibres; discuss UV/eye protection if eyebrow/eyelash loss
- Avoid traction hairstyles and harsh chemical/heat practices; encourage smoking cessation
- Safety-net for rapid progression, extensive disease, eyebrow/eyelash loss, or severe distress; refer dermatology early when indicated
- Image reference for pattern recognition: see DermNet and Primary Care Dermatology Society clinical image libraries (patchy, ophiasis, totalis/universalis, nail changes)
Pharmacological Treatment
Topical potent/very potent corticosteroids (first-line for localized scalp disease)
- Clobetasol propionate 0.05% scalp application once or twice daily for limited courses (for example 6-12 weeks, then review)
- Betamethasone valerate 0.1% scalp preparation once or twice daily
Common UK first-line approach for patchy disease. Avoid prolonged uninterrupted use due to skin atrophy, telangiectasia, and steroid adverse effects; use caution on face/flexures.
Intralesional corticosteroid (specialist practice, localized refractory patches)
- Triamcinolone acetonide intradermal injections (commonly 2.5-10 mg/mL every 4-6 weeks, concentration/site tailored by specialist)
Off-label in many settings; avoid injecting areas of active infection. Risks include local atrophy, dyspigmentation, pain, and rare systemic absorption.
Topical minoxidil (adjunct, not curative)
- Minoxidil 5% topical solution/foam to affected scalp once or twice daily
May support regrowth in some patients, usually as adjunct. Can cause irritant/contact dermatitis and hypertrichosis; avoid broken/inflamed skin.
JAK inhibitor for severe alopecia areata (specialist initiation)
- Baricitinib 4 mg orally once daily in adults with severe disease; may step down to 2 mg once adequate response
Specialist-only decision with baseline and ongoing monitoring (FBC, LFTs, lipids, infection risk). Important warnings: serious infection (including herpes zoster/TB risk), venous thromboembolism, major adverse cardiovascular events, malignancy risk; avoid in pregnancy and use caution in older patients or those with VTE/cardiovascular risk.
Systemic corticosteroids (selected rapidly progressive cases, specialist-led)
- Prednisolone oral short course (for example around 0.5 mg/kg/day, regimen individualized)
Not a durable long-term strategy due to relapse after withdrawal and systemic toxicity (hyperglycaemia, hypertension, mood change, infection risk, osteoporosis).
Complications
- Significant psychosocial morbidity (low self-esteem, social anxiety, depression, adjustment difficulties)
- Reduced quality of life and school/work participation problems
- Chronic relapsing disease burden with repeated treatment cycles
- Progression from patchy alopecia to alopecia totalis/universalis in a subset
Prognosis
Course is unpredictable and typically relapsing-remitting. Spontaneous regrowth within 1 year is common in limited recent-onset patchy disease (often quoted around one-third to one-half), but recurrence is frequent; approximately 15-25% of patchy cases may progress to totalis/universalis. Poorer outcomes are linked to childhood onset, extensive or longstanding disease, ophiasis pattern, nail involvement, family history, and coexisting atopy/autoimmune disease.
Sources & References
🏥BMJ Best Practice(1)
💊BNF Drug References(2)
- Baricitinib[management.pharmacological]
- Ritlecitinib[management.pharmacological]
✅NICE Guidelines(1)
- Alopecia areata[overview]
📖Textbook References(20)
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1684)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1685)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1685)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1623, 1624)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1626, 1627)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1684, 1685)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1627)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1683)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1652)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1651, 1652)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1683, 1684)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1824, 1825)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 82, 83)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 146)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 659, 660)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 146)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 81, 82)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 81, 82)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 90, 91)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 90, 91)[context]