Alopecia areata

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Alopecia areata is an autoimmune attack on anagen hair follicles that interrupts growth without destroying the follicular unit. Classic disease produces one or more circular smooth patches; ophiasis follows the occipital and temporal margin, alopecia totalis removes all scalp hair and alopecia universalis extends across the body. Sudden diffuse alopecia areata can resemble telogen effluvium. Hair colour and scalp-to-hair contrast alter visibility, so examination must include touch, close inspection and dermoscopy rather than judging severity from a distant view.

Diagnosis is clinical when follicular openings persist and typical edge hairs, nail change or recurrence support it. The main safety task is not to miss tinea capitis, traction with evolving scar, trichotillomania or a primary cicatricial alopecia. Biopsy is reserved for uncertainty. Extent scores can support specialist treatment, but eyebrow, eyelash, beard and functional impact may be severe even when scalp percentage is modest.

Outcome varies. A first small patch of short duration has a meaningful chance of spontaneous regrowth, whereas childhood onset, ophiasis, nail disease, atopy and extensive longstanding loss predict a more difficult course. Treatment choice therefore ranges from observation and camouflage to topical or injected corticosteroid and specialist systemic therapy. A treatment that induces growth does not necessarily reset the underlying relapse tendency.

Key points

Alopecia areata causes sharply defined smooth patches of non-scarring hair loss; follicular openings remain visible and the scalp is usually neither markedly inflamed nor scaly.
Exclamation-mark hairs, black dots, broken hairs, yellow dots and short tapered regrowth support active disease but no single dermoscopic feature is mandatory.
Examine eyebrows, eyelashes, beard, body hair and nails; pitting or rough trachyonychia supports the diagnosis and extensive loss changes prognosis and treatment eligibility.
Tinea capitis produces scale, broken hairs or lymphadenopathy and needs fungal sampling and systemic antifungal care; a boggy kerion risks permanent scarring.
Thyroid and other autoimmune disease are associated, but blood testing should follow symptoms, personal history, family history or clinical indication rather than a universal broad panel.
Limited patches may regrow spontaneously. Potent topical corticosteroid or intralesional corticosteroid can be discussed, with site, age, pain and skin-atrophy risks considered.
NICE recommends baricitinib for severe alopecia areata in eligible adults and ritlecitinib for severe disease from age 12, delivered through specialist pathways with infection and reproductive safeguards.
Relapse can follow any treatment, and regrowing hair may initially be fine or white. Address camouflage, wigs, brows, lashes and psychological impact alongside biological therapy.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Autoimmune susceptibility

Genetic and immune factors permit lymphocytes to target anagen hair follicles, with associations including thyroid disease, atopy and other autoimmunity.

Unpredictable triggering

Illness, stress or life events may precede onset, but most episodes have no single provable trigger and are not the patient's fault.

Treatment-independent fluctuation

Spontaneous loss and regrowth complicate assessment, particularly in small recent patches, so photographs and adequate review intervals are essential.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Immune privilege collapses
The normally protected anagen bulb becomes visible to immune surveillance, allowing inflammatory cells to interrupt active hair production.
2
Anagen growth stops
Affected follicles prematurely leave productive growth, creating tapered, broken or shed hairs while their structural units remain present.
3
Follicles are preserved
Unlike cicatricial alopecia, inflammation does not routinely replace the follicle with fibrosis, preserving the biological possibility of future regrowth.
4
Nails share keratin biology
Immune disturbance can affect the nail matrix, causing regular pitting, ridging or trachyonychia alongside scalp and body-hair loss.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Smooth circumscribed patch

A round or oval area has normal-feeling skin, retained follicular openings and no substantial scale, pustulation or shiny scar.

Exclamation-mark edge hairs

Short broken hairs narrower near the scalp can mark active immune interruption at a patch margin, although they are not always present.

Ophiasis distribution

Band-like occipital and temporal loss is a recognised pattern associated with a more persistent course and need for specialist review.

Totalis and universalis

Complete scalp loss or loss across scalp, face and body indicates severe disease and substantially changes treatment and supportive needs.

Nail involvement

Fine regular pits, longitudinal ridging or sandpaper-like trachyonychia can accompany hair loss and supports broader immune follicular disease.

Follicular-destruction warningRed flag

Absent openings, perifollicular erythema or scale, pustules, pain and shiny atrophy point away from alopecia areata toward scarring disease.

Red flags requiring action

Loss of follicular openings, scalp pain, perifollicular scale, pustules, boggy inflammation, a rapidly enlarging mass or systemic illness is not uncomplicated alopecia areata and requires urgent infection, scarring-alopecia or tumour assessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Scalp, body-hair and nail examinationFirst step
Why
Confirm non-scarring loss and measure anatomic extent beyond the reported patch.
Interpretation and limitations
Retained openings and smooth skin support alopecia areata; document eyebrows, eyelashes, facial and body hair plus nail pitting because these alter impact and severity.
02
Trichoscopy
Why
Find active broken hairs and distinguish common non-scarring mimics.
Interpretation and limitations
Yellow dots, black dots, tapering hairs and short regrowth support alopecia areata but are interpreted as a pattern; comma hairs, marked scale or variable traumatic breakage suggest alternatives.
03
Hair pull at the margin
Why
Assess whether shedding is active around a patch or diffuse scalp.
Interpretation and limitations
Easily extracted dystrophic anagen hairs can support activity, but technique and recent shampooing affect the result and a negative test does not prove stability.
04
Fungal microscopy and culture
Why
Exclude tinea capitis when scale, inflammation, lymph nodes or epidemiology creates doubt.
Interpretation and limitations
Sample abnormal hairs and scale before treatment when possible; a convincing kerion needs prompt systemic management and should not wait for delayed culture.
05
Targeted blood tests
Why
Investigate thyroid, nutritional or systemic symptoms that may coexist or mimic diffuse loss.
Interpretation and limitations
Select TSH, full blood count, ferritin or other tests from history and examination; routine indiscriminate autoimmune serology does not confirm alopecia areata.
06
Scalp biopsy
Why
Resolve diffuse, inflamed or otherwise atypical hair loss after specialist assessment.
Interpretation and limitations
Sample an active representative site and state disease duration and treatment; a scarred centre cannot show the early follicular process reliably.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Tinea capitis

Scale, lymphadenopathy, black dots, comma hairs or boggy inflammation requires mycology and systemic antifungal treatment rather than immune suppression alone.

Trichotillomania

Irregular patches containing hairs broken at many lengths and an accessible distribution suggest repeated manipulation, which needs non-judgemental behavioural assessment.

Traction alopecia

Loss at sites of repeated tension, fringe signs and a hairstyle relationship support traction; longstanding disease can progress from reversible loss to scar.

Scarring alopecia

Absent follicular openings, perifollicular scale, erythema, pustules, pain or shiny atrophy signals follicular destruction and warrants expedited specialist assessment.

Telogen effluvium

Diffuse shedding several months after systemic stress retains scalp coverage pattern and lacks the classic circumscribed smooth patches of alopecia areata.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01New limited patchConfirm non-scarring disease and agree a goalFirst stepOne or a few smooth patches are present without infection or scarring features.

1Examine scalp, brows, lashes, body hair and nails, use trichoscopy where available and sample fungus only when scale or exposure supports it.
2Explain spontaneous regrowth, variable recurrence and prognostic factors, then offer observation, camouflage or a defined topical corticosteroid course according to age, site and preference.
3Photograph with consent and review after a hair-cycle interval, referring progression, diagnostic uncertainty or substantial distress rather than simply enlarging topical quantities.

02Local procedural treatmentUse injections selectivelyA small number of persistent adult patches merit stronger local treatment and the patient accepts injections.

1Dermatology confirms diagnosis and selects an intralesional triamcinolone concentration and volume appropriate to scalp, eyebrow or other site.
2Explain pain, temporary dents from dermal atrophy, telangiectasia and the need to avoid excessive dose near eyes, then inject at spaced points under aseptic technique.
3Review regrowth and adverse effects before repeating, stopping if progressive extensive disease makes repeated local injection disproportionate.

03Severe diseaseAssess systemic treatment eligibilityExtensive scalp loss, totalis, universalis or major functional burden meets a specialist severe-disease threshold.

1Refer to dermatology for severity scoring, previous-treatment review, vaccination history, infection risk, reproductive planning and shared discussion of expected benefit and relapse.
2For eligible adults consider NICE-recommended baricitinib, and from age 12 consider ritlecitinib, using the relevant commissioning and product-safety pathway.
3Screen and monitor tuberculosis, viral hepatitis, blood counts, liver function, lipids and other medicine-specific risks, withholding or stopping treatment for serious infection or significant toxicity.

04Supportive careTreat functional and psychological effectsHair loss affects identity, mood, eye protection, nasal symptoms, work or social participation.

1Offer information on NHS wig entitlement where applicable, camouflage fibres, brow products, false lashes and practical sun, cold, eye and nasal protection.
2Ask directly about bullying, anxiety, low mood and avoidance and refer to psychological or peer support when wanted.
3Record the person's priority outcome separately from scalp percentage, because brow or lash restoration and confidence may matter more than total hair count.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Reduces perifollicular immune inflammation and may accelerate regrowth in limited alopecia areata.

Potent topical corticosteroid for limited scalp disease

Apply the prescribed scalp formulation thinly once daily for a defined course, commonly reviewed after six to twelve weeks before any continuation or break.

Avoid prolonged uncontrolled use, especially on face or brows; monitor atrophy, telangiectasia and folliculitis, and account for total area, occlusion and concurrent corticosteroids.

A NICE-recommended Janus kinase inhibitor for severe alopecia areata in adults within specialist care.

Baricitinib

Eligible adults take the specialist-selected oral dose once daily, usually 4 mg or 2 mg when age, risk, interactions or tolerability favour the lower dose.

Screen for tuberculosis and viral hepatitis, update appropriate vaccination and monitor blood counts, liver tests and lipids. Review serious infection, herpes zoster, thrombosis, cardiovascular and malignancy risks, especially in older smokers; avoid pregnancy.

A NICE-recommended kinase inhibitor for severe alopecia areata from age 12 when commissioning criteria are met.

Ritlecitinib

People aged 12 years and over who meet the severe-disease pathway take 50 mg by mouth once daily under specialist supervision.

Assess infection, tuberculosis, hepatitis, immunisation and pregnancy before treatment; monitor blood indices and liver safety and follow current product advice for live vaccines, serious infection and interacting immunosuppression.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Extensive persistent loss

Patch disease can progress to ophiasis, totalis or universalis, reducing spontaneous recovery probability and increasing functional support needs.

Ocular and nasal symptoms

Absent lashes and nasal hair reduce particle protection and can contribute to eye irritation, dryness and upper-airway discomfort.

Psychological morbidity

Unpredictable visible loss can cause anxiety, depression, altered identity, bullying and withdrawal even when no other physical illness is present.

Treatment adverse effects

Skin atrophy from local corticosteroid and infection, laboratory, vascular or reproductive harm from systemic immunomodulation require structured surveillance.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Record scalp extent plus eyebrow, eyelash, facial, body-hair and nail involvement using reproducible photographs and a specialist severity method where relevant.
Review topical corticosteroid sites for atrophy, telangiectasia and folliculitis and stop automatic repeat prescribing without documented response.
For systemic kinase inhibition, follow the product-specific infection, tuberculosis, hepatitis, blood-count, liver and lipid schedule and maintain vaccination planning.
Ask about mood, social avoidance, school or work and wig or camouflage access at every major disease change.
After regrowth, explain that white or fine early hairs may thicken and repigment, while renewed shedding needs reassessment rather than immediate unsupervised drug escalation.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Follicles remain alive

Alopecia areata suppresses growth without replacing follicles by scar, which is why regrowth can occur even after extensive visible loss.

White regrowth can mature

Early returning hairs may lack pigment or calibre and later darken and thicken, so colour alone should not be judged as failed recovery.

Nails widen the phenotype

Pitting or trachyonychia supports follicular autoimmunity and can indicate a more extensive disease burden than scalp inspection shows.

Severity is more than area

Loss of brows or lashes affects eye protection and identity, while a small conspicuous patch can have greater personal impact than a larger hidden one.

Growth is not permanent tolerance

Local and systemic treatments can restore anagen activity without erasing autoimmune susceptibility, so relapse planning belongs in consent.

11Common pitfallsFrequent interpretation and management errors.

01
Treating a scaly broken-hair patch as alopecia areata without fungal sampling.
02
Missing loss of follicular openings and delaying treatment of irreversible scarring alopecia.
03
Ordering every autoimmune blood test without symptoms or a management consequence.
04
Using potent corticosteroid indefinitely without photographs, response review or skin examination.
05
Starting a kinase inhibitor without infection, vaccination, reproductive and vascular risk assessment.
06
Equating percentage scalp loss with the person's psychological or functional burden.