Alopecia areata !

Alopecia areata is an autoimmune disease causing round, smooth bald patches, mostly on the scalp. Hair often regrows, but loss can recur.

Updated 2026-11-01

Structures involved

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Why it happens

What it is

A chronic, non-scarring autoimmune hair loss in which the immune system attacks growing (anagen) hair follicles. It typically produces well-defined round bald patches on the scalp or beard, and may progress to loss of all scalp hair (totalis) or all body hair (universalis). The follicles are preserved, so regrowth is possible.

Who gets it

Lifetime risk is about 2%; it affects both sexes and all ethnic groups and often begins in childhood or before age 30–40. It is one of the most common causes of patchy hair loss seen in dermatology clinics in Colombia and Latin America.

Causes

Autoimmune attack by CD8+ T cells on anagen hair follicles after loss of their immune privilege
Genetic susceptibility (HLA and other immune genes); family history in about 1 in 5 patients
Possible triggers: emotional stress, infections, vaccination or illness, though often none is found

Risk factors

Family history of alopecia areata
Atopic diseases: atopic dermatitis, asthma, allergic rhinitis
Autoimmune thyroid disease, vitiligo, type 1 diabetes, systemic lupus erythematosus
Down syndrome

Pathophysiology

Normally anagen hair follicles are protected from the immune system ('immune privilege'). In alopecia areata this privilege collapses: follicles express more MHC molecules and interferon-gamma–driven signals, and CD8+ NKG2D+ T cells gather around the hair bulb ('swarm of bees' on histology). The attack pushes follicles abruptly into the resting phase, so hairs break off and fall. Signalling through the JAK-STAT pathway sustains this inflammation, which is why JAK inhibitors work. Because stem cells in the bulge are spared, there is no scarring.

Classification

Patchy alopecia areata (one or several patches; most common)
Alopecia totalis (loss of all scalp hair)
Alopecia universalis (loss of all scalp and body hair)
Ophiasis pattern (band-like loss along the back and sides of the scalp; harder to treat)
Diffuse alopecia areata (sudden diffuse thinning)

Symptoms and signs

Sudden round or oval smooth bald patches with normal-looking skin, no scale or scarring
'Exclamation-mark' hairs at the edge (short broken hairs thinner at the base)
Positive pull test at the edge of active patches
Loss of eyebrows, eyelashes or beard hair
Nail changes: fine pitting, ridging or rough nails (trachyonychia)
Regrowing hair may be white at first

Diagnosis

Clinical: Clinical diagnosis based on well-defined non-scarring patches, exclamation-mark hairs and a positive pull test at active edges. Trichoscopy shows yellow dots, black dots, broken hairs and exclamation-mark hairs.
Tests: Usually not needed. When the diagnosis is uncertain: KOH and fungal culture (tinea capitis), syphilis serology, and scalp biopsy (peribulbar lymphocytic infiltrate). TSH and thyroid antibodies may be checked because of the association with thyroid autoimmunity; ferritin or ANA if the history suggests.
Imaging: Not needed.

Differential diagnosis

Tinea capitis (scale, broken hairs, positive KOH, often in children)
Trichotillomania (irregular broken hairs of different lengths, often linked to anxiety or obsessive-compulsive traits)
Telogen effluvium (diffuse shedding 2–3 months after a trigger such as fever, childbirth or crash dieting)
Androgenetic alopecia (gradual thinning of the crown or frontotemporal area, no patches)
Scarring alopecias (discoid lupus, lichen planopilaris) and secondary syphilis

Goal of treatment

Encourage regrowth and limit spread, choose treatment by extent and age, and address the emotional impact; mild patchy disease may be watched because it often regrows by itself.

Treatment

Conservative: Watchful waiting is an option for a few small patches, which often regrow within a year.
Medical: Intralesional corticosteroid injections are first-line for limited patchy disease in adults; potent topical corticosteroids, especially in children. Oral JAK inhibitors (such as baricitinib or ritlecitinib) are approved for severe extensive disease; topical immunotherapy and minoxidil are other options.
Follow-up: With JAK inhibitors: screening for tuberculosis and hepatitis before starting, then blood counts, lipids and liver tests, and watching for infection and thrombosis.
Lifestyle: Wigs, hairpieces, eyebrow makeup and sun protection for the bald scalp; psychological support and patient groups.

Drugs for this condition

Baricitinib

Complications

Anxiety, depression and reduced quality of life
Sunburn of the bald scalp
Eye irritation from lost eyelashes
Relapse after regrowth; progression to totalis or universalis

Prognosis

Unpredictable. In limited patchy disease most patients regrow hair within a year, though relapses are common. Poorer outcome with extensive loss, ophiasis pattern, childhood onset, nail involvement, atopy and long duration; totalis and universalis seldom recover fully without treatment.

Test yourself

Think of the answer, then tap the question to see it.

What is the characteristic hair seen at the edge of an alopecia areata patch?

The exclamation-mark hair: a short broken hair that tapers towards the scalp.

Is alopecia areata scarring or non-scarring, and why does it matter?

Non-scarring: follicle stem cells are spared, so hair can regrow.

What is the first-line treatment for limited patchy disease in adults?

Intralesional corticosteroid injections.

Which pathway do the newer oral drugs for severe disease block?

The JAK-STAT pathway (JAK inhibitors).

Which nail change is associated with alopecia areata?

Fine nail pitting (also ridging or trachyonychia).

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Alopecia Areata (National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), 2026).

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Representative model, for educational purposes only.

Skin highlighted on the Durgical 3D model