Chapter 8 — Alopecia Areata | Trichology for GP

GP-Level Analogy

"Alopecia areata is a case of mistaken identity in the body's security system. The immune system — normally expert at identifying foreign invaders — misidentifies its own hair follicles as enemies and launches a targeted strike. The follicles are not destroyed, just locked out of the factory. Given the right signal — resolution of the immune attack — most will restart. The newer JAK inhibitor treatments work by deactivating the alarm system entirely."

Alopecia areata (AA) is an organ-specific autoimmune, non-scarring alopecia affecting the hair follicle. It is the third most common cause of hair loss presenting to dermatology globally, affecting approximately 2% of the world population at some point in their lifetime. It affects all races, both sexes, and all ages — though peak incidence is in the second and third decades.

AA has a profound psychological impact disproportionate to its physical severity. It can develop within days, affect children visibly, and fluctuate unpredictably. The GP's role includes accurate diagnosis, early autoimmune screening, realistic prognostic counselling, and timely referral for moderate-to-severe disease.

At-a-glance key facts

Type

Non-scarring autoimmune

Follicular stem cells (bulge) are spared — regrowth is always biologically possible. The immune attack targets the bulb, not the bulge.

Pattern

Patches to total loss

From one small smooth patch to loss of all scalp hair (alopecia totalis) or all body hair (alopecia universalis). Same immune mechanism, different extent.

Prognosis

Highly variable

Patchy AA: 50–80% spontaneous regrowth within 12 months. Alopecia totalis/universalis: poor spontaneous prognosis; requires systemic treatment.

The critical GP insight

AA is never a scarring alopecia. The bulge (stem cell niche) is immunologically privileged and spared even in longstanding disease. Regrowth is always biologically possible — even after years of total scalp hair loss. Communicate this hope accurately to patients.

Immunopathology

AA occurs when the hair follicle's normal immune privilege is breached. Understanding this mechanism is important because it explains why JAK inhibitors — the most significant therapeutic advance in decades — work so effectively.

Fig 8.1 — Immune privilege collapse and the AA immunological cascade

Fig 8.1: The immunopathological cascade in AA. Normal follicular immune privilege is disrupted by a trigger. CD8+ T cells accumulate around the bulb (the "swarm of bees" on histology), driven by IFN-γ/IL-15 through JAK1/JAK2. JAK inhibitors interrupt this cascade. Critically, the bulge retains its immune privilege and is spared, preserving the potential for regrowth.

Why the bulge is spared

The hair follicle bulge maintains its immune privilege even in active AA. This is mediated by CD200, TGF-β, and other local immunosuppressants expressed by bulge cells. Because the follicular stem cells survive, regrowth remains biologically possible even after years of total hair loss — the single most important fact to communicate to patients.

Genetic and associated conditions

Association	Detail	Prevalence in AA
Thyroid disease	Hashimoto thyroiditis (most common); Graves disease	8–28% — always screen TFTs
Atopic disease	Atopic eczema, asthma, allergic rhinitis	Up to 40%
Other autoimmune	Vitiligo, type 1 diabetes, RA, pernicious anaemia	10–25%
Family history of AA	First-degree relative with AA	10–25% — polygenic inheritance
Down syndrome	Strong association	6–8× increased risk
Nail changes	Pitting, trachyonychia, Beau's lines	10–66%; correlates with severity

Clinical spectrum of alopecia areata

Fig 8.2 — Severity spectrum from patchy AA to alopecia universalis

Fig 8.2: Clinical spectrum of AA from patchy (best prognosis) through multifocal, ophiasis (worst non-totalis prognosis), to alopecia totalis and universalis. The ophiasis pattern targets the normally androgen-resistant fringe — explaining its treatment resistance.

Patchy AA

1–2 discrete patches, <50% scalp

Best prognosis

Multifocal AA

Multiple patches, 50–95% scalp

Moderate

Ophiasis

Band at temporal/occipital margin

Poor — resist.

Alopecia totalis

All scalp hair lost

<10% spontaneous

Alopecia universalis

All body hair lost

JAK inhibitors

Clinical features

AA typically presents with sudden, rapid onset of well-defined, smooth, asymptomatic patches of hair loss. Most patients notice an area of hair loss within days. A minority describe a preceding tingling or pruritus at the affected site.

Fig 8.3 — Key examination findings in alopecia areata

Fig 8.3: Key examination findings in AA. The smooth, well-defined oval patch with exclamation mark hairs at the margin and yellow dots inside is the classic appearance. The normal scalp surface with visible follicular ostia confirms non-scarring disease.

Nail changes in AA

Nail finding	Description	Frequency
Geometric nail pitting	Regular shallow pits across nail plate	Most common (20–40%)
Trachyonychia	Rough, sandpaper-like texture — all 20 nails	Severe AA indicator
Beau's lines	Transverse ridges — temporary matrix arrest	Acute/active disease
Onychorrhexis	Longitudinal ridging and brittleness	Moderate AA
Leukonychia	White discolouration	Variable

Prognostic factors

Poor prognosis (OCEAN)

Ophiasis pattern · Childhood onset (pre-pubertal) · Extensive nail involvement · Atopy association · No response to first treatments

Also: AT/AU extent, family history of AA, Down syndrome

Good prognosis indicators

Single small patch, first episode · Short duration (<1 year) · No nail involvement · No family history of AA · No atopy · Age of onset >40 · Absence of ophiasis pattern

Trichoscopy in alopecia areata

Trichoscopy is the most useful diagnostic tool in AA at the GP level. Characteristic findings allow confident diagnosis, activity assessment, and monitoring of treatment response — often without biopsy.

Fig 8.4 — Trichoscopy activity atlas for alopecia areata

Fig 8.4: Trichoscopy atlas for AA activity states. Top row (yellow dots, black dots + exclamation hairs, tapered dystrophic hairs) = active disease. Bottom row (quiescent, vellus regrowth, terminal regrowth) = recovery. Serial trichoscopy is the non-invasive activity index for AA.

Trichoscopy activity scoring

Trichoscopy finding	Activity state	GP action
Numerous yellow + black dots + exclamation hairs	Active, progressive	Treat urgently — risk of extension
Yellow dots, few exclamation hairs	Active but slowing	Treat — monitor for progression
Yellow dots only, no exclamation hairs	Stable / quiescent	Watchful waiting acceptable
Vellus hairs appearing, decreasing yellow dots	Early remission	Continue treatment; reassure patient
Terminal hairs appearing, no yellow/black dots	Remission	Consider treatment step-down

Diagnosis and investigation

AA is primarily a clinical diagnosis. The smooth oval patch with exclamation mark hairs at the margin is usually pathognomonic. Trichoscopy confirms and assesses activity. Investigations screen for associated autoimmune conditions — not to diagnose AA itself.

Sufficient for diagnosis

Classic presentation

Well-defined smooth oval patch + exclamation mark hairs + trichoscopy showing yellow/black dots = diagnose clinically. Biopsy not required.

Biopsy when uncertain

Atypical presentations

Diffuse AA mimicking TE, ophiasis mimicking scarring alopecia, or co-existing conditions. Histology: peribulbar lymphocytic infiltrate ("swarm of bees").

Mandatory investigations in all AA patients

Investigation	Rationale	Action if abnormal
TSH + free T4	Hashimoto in 8–28%; Graves disease	Treat thyroid; do not assume AA will improve automatically
Anti-TPO antibodies	Subclinical thyroid autoimmunity	Annual TFT monitoring if positive with normal TSH
FBC	Anaemia, pernicious anaemia	B12/folate if macrocytic anaemia
Ferritin	Iron deficiency compounds AA-related shedding	Supplement to >70 mcg/L
ANA	Screen for SLE, mixed CTD	Rheumatology if high titre + clinical features
Fasting glucose / HbA1c	Association with type 1 diabetes	Refer endocrinology if abnormal

Differential diagnosis

Condition	Distinguishing features	Key test
Tinea capitis	Children; scaling; broken hairs; posterior cervical LN	Mycology swab; Wood's lamp
Trichotillomania	Irregular patch; varied lengths; no yellow dots	Trichoscopy: flame/tulip hairs
Telogen effluvium (diffuse)	Diffuse; uniform calibre; pull test all zones; no yellow/black dots	Trichoscopy: no miniaturisation
Secondary syphilis	Moth-eaten patchy loss; lymphadenopathy; rash	VDRL / TPHA
LPP (vs ophiasis)	Perifollicular erythema and scale; absent ostia	Trichoscopy: white dots; biopsy
Androgenetic alopecia	Gradual; calibre diversity; no yellow dots in patches	Trichoscopy: miniaturisation ratio

Treatment of alopecia areata

Treatment selection is guided by extent of hair loss, patient age, rate of progression, and quality of life impact. The introduction of JAK inhibitors (baricitinib 2022) represents the most significant therapeutic advance in the history of AA.

GP Analogy — Treatment Philosophy

"Treatment of AA is about silencing a false alarm. Topical corticosteroids dampen the alarm locally; systemic corticosteroids turn it off temporarily then it rings again louder; JAK inhibitors cut the wiring to the alarm panel entirely — the most effective approach we have ever found."

Fig 8.5 — Treatment algorithm by disease extent

Fig 8.5: Treatment algorithm by disease extent. GP-level treatments cover mild/patchy disease. Moderate disease requires specialist management. Severe disease (AT/AU) is the primary indication for oral JAK inhibitors — the first truly disease-modifying therapy for AA.

JAK inhibitors — the landmark advance

Drug	Type	Evidence	Key side effects
Baricitinib (Olumiant)	Oral JAK1/JAK2	BRAVE-AA1 and AA2 RCTs: 35–40% achieve >80% scalp coverage at 36 weeks. FDA/EMA approved for severe AA (≥50% loss)	URTI, acne, elevated lipids, VTE risk, herpes zoster
Ruxolitinib (Opzelura)	Topical JAK1/JAK2	TRuE-AA1 and AA2: ~50% achieve ≥90% scalp coverage at 24 weeks in moderate-severe AA	Application site reactions; minimal systemic absorption
Deuruxolitinib	Oral JAK1/TYK2	Phase 3: 42% achieve SALT ≤10 at 24 weeks — among highest response rates reported	Similar to baricitinib class

Intralesional triamcinolone — GP procedure

Aspect	Detail
Concentration	10 mg/mL (standard); dilute to 5 mg/mL for temporal or eyebrow areas
Volume / technique	0.1 mL per injection site; intradermal (NOT subcutaneous — avoids fat atrophy); sites 1 cm apart
Interval	Every 4–6 weeks; assess response at 3 months
Response rate	60–70% show regrowth at treated site within 4–8 weeks
Limitation	Does not prevent new patches; does not treat diffuse/total disease
Side effects	Skin atrophy (temporary), hypopigmentation, post-injection pain

JAK inhibitors: key prescribing points

JAK inhibitors must be continued indefinitely — stopping causes relapse in 70–80% within months. Pre-treatment: document VZV serostatus, TB screen (IGRA), baseline FBC/lipids, ensure vaccinations up-to-date. Herpes zoster vaccination (Shingrix) recommended before initiation. Not licensed under 18 in most countries.

Quick Recall

Pathology: JAIL

J·A·I·L

JAK pathway — the immune cascade driver
Anagen arrest — follicle locked out
Immune privilege collapse — MHC-I exposed
Lymphocytes (CD8+) — peribulbar "swarm of bees"

Trichoscopy: YBET

Y·B·E·T

Yellow dots — empty follicles, active
Black dots — broken hairs, active
Exclamation mark hairs — pathognomonic
Terminal regrowing hairs — remission

Poor prognosis: OCEAN

O·C·E·A·N

Ophiasis pattern
Childhood onset (pre-pubertal)
Extensive nail involvement
Atopy association
No response to first treatments

Associations: AVATAR

A·V·A·T·A·R

Atopic disease (eczema, asthma)
Vitiligo
Autoimmune thyroid (Hashimoto's)
Type 1 diabetes
ANA-positive CTD
Rheumatoid arthritis

GP Quick-Reference Action Card

Presentation	Diagnosis	Investigation	Treatment	Refer?
Single smooth oval patch, adult, exclamation hairs	Patchy AA	TFTs, anti-TPO, FBC, ferritin	ILT 10 mg/mL ± potent topical CS	Not urgent unless progressive
Multiple patches, child, rapid spread	Multifocal AA	TFTs, ANA, FBC, glucose	Topical CS; refer dermatology	Refer — specialist management
Band of loss at scalp margin	Ophiasis AA	Full autoimmune screen	DPCP or JAK inhibitor	Urgent — poor prognosis
Total scalp hair loss	Alopecia totalis	Full screen + psychological assessment	Baricitinib (specialist)	Urgent specialist referral
Patchy loss + broken hairs, child, no yellow dots	Exclude trichotillomania/tinea	Trichoscopy; mycology; psychology	Per diagnosis	Psychology if TTM; paed derm if tinea

🎓 Trichology for GP — Complete

You have completed all 8 chapters. This book covers the core trichology knowledge required for confident GP-level diagnosis and management of the most common hair and scalp disorders. Key mnemonics across the series: HET · SCALP · DICS · YBWR · DART · DOTGP · CHIPS · FTBVZ · YBET · OCEAN · AVATAR · JAK

Anki Flashcard Deck — Chapter 8

24 cards — the complete AA deck covering immunopathology, spectrum, clinical features, trichoscopy, diagnosis, and treatment. Tap to flip.

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References

APA 7th edition format.

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