Alopecia areata — patchy hair loss

h2>What is Alopecia Areata?

Alopecia areata (AA) is an autoimmune disease in which the body's immune system attacks hair follicles. It is characterized by sharply defined bald patches — usually round or oval — that appear within a few weeks. The follicles are not destroyed but put into a resting phase; in many cases, the hair can spontaneously regrow.

Prevalence: about 2% of the population experience at least one episode in their lifetime. Often first occurring between 15 and 30 years of age, but can appear at any age.

How does AA differ from common hair loss?

Androgenetic Alopecia

• Gradual thinning over years
• Typical patterns (receding hairline, bald spot at the crown in men; part thinning in women)
• Follicle miniaturization
• Hormonally mediated

Alopecia Areata

• Sudden, sharply defined bald patches
• Smooth skin with no visible inflammation
• Often on the scalp, but can affect beard, eyebrows, eyelashes, or body
• Autoimmune — no miniaturization
• Spontaneous remission possible

Telogen Effluvium

• Diffuse loss over the entire head, no sharp areas
• Triggering stress (stress, illness, hormonal changes) 2–3 months prior
• Mostly reversible — see Telogen Effluvium article

Forms of Alopecia Areata

• Alopecia areata circumscripta — one or more sharply defined bald patches, most common form
• Alopecia areata totalis (AT) — loss of all scalp hair
• Alopecia areata universalis (AU) — loss of all body hair, including eyebrows and eyelashes
• Alopecia areata diffusa — diffuse form, difficult to distinguish from telogen effluvium
• Ophiasis type — band-like loss at the back of the head and temples, prognostically unfavorable
• Sisaipho type — inverse, bald patches only on the top of the head, marginal areas remain hairy

Diagnosis

An experienced dermatology practice usually recognizes alopecia areata clinically — complementary trichoscopy is crucial.

Typical Trichoscopic Findings

• Exclamation mark hairs — thin towards the base, characteristic of active AA
• Cadaverized hairs — broken hairs at skin level
• Yellow dots — follicular openings filled with sebum
• Black dots — hair remnants in the follicular openings
• Vellus hairs — fine anagen hairs as a sign of incipient regeneration

Further Diagnostics

• Anamnesis: family history, other autoimmune diseases, stressors
• Pull test at the edge of bald patches — positive in active AA
• In case of suspected autoimmune comorbidity: thyroid antibodies, ANA
• In diffuse form: biopsy for differentiation

Course and Prognosis

• Spontaneous remission in 30–50% of cases within 12 months
• Relapses are common — throughout life
• Unfavorable prognosis in: young onset, ophiasis type, long disease duration, family history, pronounced comorbidity (atopy, thyroid dysfunction)
• Complete recovery is rarer in AT and AU — current therapies can help here

Treatment Options

Treatment depends on severity, extent, and course dynamics. Since AA is an autoimmune disease, therapies aim to modulate the immune response at the follicle.

Local Therapies (for smaller areas)

• Local corticosteroid injections (intralesional triamcinolone) — standard for circumscribed lesions, 4–6 week interval
• Topical corticosteroids (Class III–IV)
• Topical contact sensitization with diphencyprone (DPCP) for extensive forms
• Topical calcineurin inhibitors off-label

Systemic Therapies (for extensive involvement)

• Systemic corticosteroids — short-term, only in exceptional cases due to side effects
• JAK inhibitors (e.g., Baricitinib, Ritlecitinib) — new approved therapy for severe AA, often impressive success even in AT/AU
• Methotrexate off-label
• Cyclosporin A off-label, rare

Complementary Measures

• PRP treatments — studies show efficacy, especially in combination with corticosteroids
• Mesotherapy with immunomodulatory agents
• Stress management, psychological support — stress can trigger flares
• Micronutrient optimization (Vitamin D, zinc, iron)

Why a hair transplant is usually NOT the answer

In active alopecia areata, a transplant is contraindicated. Reasons:

• The immune system would attack the transplanted follicles just as it does the original ones
• The area can become active again at any time
• The transplanted grafts are highly likely to be lost again

Exceptions: stably burned-out form — if an area has been stably bald for several years and shows no new activity, a transplant may be considered in rare cases. However, the indication must be carefully determined by a dermatology practice, ideally in interdisciplinary consultation.

Psychological Burden

Alopecia areata can be a massive burden — especially for young patients, with visible areas, or with total hair loss. The psychological component should be taken seriously and, if necessary, supported. Self-help groups and specialized psychotherapy can help.

When to see a specialist?

• First bald spot that appears suddenly
• Multiple areas simultaneously
• Involvement of eyebrows, eyelashes, beard, or body hair
• Rapid progression within weeks
• Family history of autoimmune diseases
• Psychological burden due to hair loss

Frequently Asked Questions

Is alopecia areata contagious?

No. It is an autoimmune reaction, not an infection — no transmission to other people is possible.

Will my hair grow back?

In circumscribed AA, spontaneously in 30–50% of cases within 12 months. Significantly more often with rapid therapy after initial diagnosis. In AT and AU, the chances of spontaneous recovery are lower — new JAK inhibitor therapies have significantly improved the prognosis here.

What triggers a flare?

Common triggers: severe emotional stress, infections, hormonal changes (pregnancy, menopause), trauma or surgery, sometimes vaccinations or new medications. Genetic predisposition is the basis — triggers are planted on this ground.

Do I need a blood test?

Yes, upon initial diagnosis — especially to rule out accompanying autoimmune diseases such as Hashimoto's thyroiditis. Repeated checks are useful for recurrent AA.

Can I treat AA myself?

No. AA belongs in the hands of a doctor — the diagnosis is not trivial (confusion with tinea, scarring alopecia, trichotillomania), and therapy requires clear indication. Self-experiments with non-evidence-based remedies often delay treatment.

Does stress reduction help?

Stress alone does not cure AA — but it is a common trigger for flares. Stress management, sufficient sleep, and psychological support should be part of a comprehensive treatment concept.