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Summary Table

Domain	Detail
Risk Factors	Personal or family history of autoimmune disease (Hashimoto thyroiditis, vitiligo, type 1 diabetes mellitus, celiac disease, rheumatoid arthritis); atopic dermatitis; Down syndrome; age of onset typically in childhood or young adulthood (most cases before age 30)
Etiology	Autoimmune, T-lymphocyte-mediated attack against the hair follicle bulb; collapse of the hair follicle immune privilege
Patient Presentation	Sudden onset of well-circumscribed, smooth, non-scarring patches of hair loss; usually painless and asymptomatic; patient may notice a "bald spot" found incidentally
Classic Physical Exam	Round or oval patches of complete hair loss with smooth, skin-colored scalp; exclamation point hairs (short, broken hairs that taper proximally) at the periphery of the patch; positive hair pull test at the active margins; nail pitting
Key Diagnostic Results	Clinical diagnosis in most cases; dermoscopy shows yellow dots, black dots, broken hairs, and exclamation point hairs; biopsy (rarely needed) shows peribulbar lymphocytic infiltrate ("swarm of bees" pattern)
Management	Limited disease: intralesional triamcinolone acetonide or topical corticosteroids. Extensive disease: topical immunotherapy (DPCP), JAK inhibitors (baricitinib, ritlecitinib). Children: topical corticosteroids first-line
Keywords	"Exclamation point hairs," "smooth round bald patch," "non-scarring," "peribulbar lymphocytic infiltrate," "swarm of bees," "nail pitting with hair loss," "autoimmune hair loss"

1. Pathophysiology

Alopecia areata is an organ-targeted autoimmune disorder directed against the hair follicle. Under normal conditions, the hair follicle bulb exists in a state of immune privilege, meaning it downregulates MHC class I and II expression and produces local immunosuppressive signals (such as TGF-beta and alpha-MSH) that prevent immune cells from recognizing follicular antigens. In alopecia areata, this immune privilege collapses.

Once immune privilege is lost, CD8+ NKG2D+ cytotoxic T-lymphocytes infiltrate the peribulbar region of the anagen (actively growing) hair follicle. These T-cells recognize melanocyte-associated antigens expressed in the hair bulb. The resulting inflammatory assault forces the follicle to prematurely shift from anagen into catagen (regression) and then telogen (resting), causing the hair shaft to detach and fall out. This is why the hair loss is sudden and well-demarcated.

A critical teaching point is that the follicle itself is not destroyed. The stem cell compartment in the bulge region of the follicle remains intact. This is the fundamental reason alopecia areata is classified as non-scarring (non-cicatricial) alopecia and why the condition is potentially reversible. If the autoimmune attack subsides, the follicle can re-enter anagen and regrow hair. This stands in contrast to scarring alopecias (such as lichen planopilaris or discoid lupus), where permanent follicular destruction occurs.

The exclamation point hairs seen at patch margins result from the inflammatory damage to the proximal hair shaft as it exits the attacked follicle. The proximal end is narrowed and hypopigmented while the distal end remains normal-caliber, creating a "!" silhouette. These hairs are a hallmark sign of active disease.

The association with other autoimmune conditions is driven by shared genetic susceptibility, particularly involving HLA class II alleles (HLA-DQB1, HLA-DRB1) and polymorphisms in genes encoding cytokines in the JAK-STAT signaling pathway (particularly IFN-gamma and IL-15). The JAK-STAT pathway is central to the pathogenesis because IFN-gamma signaling through JAK1/JAK2 upregulates MHC expression on the follicle, further amplifying the autoimmune loop. This molecular insight is directly relevant to treatment, as JAK inhibitors work by interrupting this cascade.

2. Classification and Clinical Manifestation

Subtype	Pattern of Hair Loss	Exam Relevance
Alopecia areata (patchy)	One or more well-circumscribed, round or oval patches on the scalp	Most common presentation; the "classic" vignette
Alopecia totalis	Complete loss of all scalp hair	Represents progression from patchy disease
Alopecia universalis	Complete loss of all body hair (scalp, eyebrows, eyelashes, axillary, pubic)	Most severe form; poor prognostic indicator
Ophiasis pattern	Band-like hair loss along the temporal and occipital hairline (wave-shaped)	Treatment-resistant pattern; important to recognize because it carries a worse prognosis
Sisaipho pattern (inverse ophiasis)	Hair loss sparing the temporal and occipital margins; affects the central and frontal scalp	Rare; better prognosis than ophiasis
Diffuse alopecia areata	Generalized thinning across the entire scalp without discrete patches	Easily confused with telogen effluvium or androgenetic alopecia; diagnosis confirmed by exclamation point hairs or biopsy

Nail involvement occurs in 10 to 50 percent of patients and may precede, accompany, or follow hair loss. The most common nail finding is geometric pitting (fine, regularly spaced pits described as "grid-like"), which differs from the coarser, irregular pitting of psoriasis. Other nail changes include trachyonychia (rough, sandpaper nails), longitudinal ridging, and rarely onychomadesis. Nail findings in a vignette paired with non-scarring hair loss should strongly point you toward alopecia areata.

3. Diagnostic Workup

Test	Role	Key Findings
Clinical examination	Best initial test; sufficient for diagnosis in most cases	Smooth, non-scarring patches; exclamation point hairs; positive pull test at active margins
Dermoscopy (trichoscopy)	Enhances clinical accuracy; best non-invasive confirmatory tool	Yellow dots (empty follicular ostia filled with keratinous material), black dots (broken hairs at scalp level), exclamation point hairs, short vellus hairs (sign of regrowth)
Hair pull test	Bedside assessment of disease activity	Positive (>10% of pulled hairs detach) at the periphery of active patches; negative in stable disease
Scalp biopsy	Gold standard / most accurate test (rarely performed)	Peribulbar lymphocytic infiltrate around anagen or catagen follicles ("swarm of bees" pattern); increased catagen/telogen follicle ratio; absence of scarring
Thyroid function (TSH)	Screening for associated autoimmune thyroiditis	Abnormal TSH prompts further thyroid workup
CBC, ferritin, vitamin D	Rule out contributing nutritional deficiencies	Not diagnostic for alopecia areata but relevant for management

Alopecia areata is predominantly a clinical diagnosis. The combination of a sudden-onset, well-circumscribed, smooth, non-scarring patch of hair loss with exclamation point hairs at the margin is virtually diagnostic, and no further testing is needed in a straightforward case.

Dermoscopy adds diagnostic confidence, particularly in ambiguous presentations such as diffuse alopecia areata. Yellow dots are the most frequently observed dermoscopic feature and represent distended follicular infundibula filled with sebaceous secretions and keratinous material in hair-less follicles. Black dots represent cadaverized hairs fractured at the scalp surface. Finding these features alongside exclamation point hairs on dermoscopy effectively confirms the diagnosis without biopsy.

Scalp biopsy is reserved for cases where the clinical picture is unclear, such as when the differential includes scarring alopecia or tinea capitis without obvious scale. The hallmark histopathologic finding is a dense peribulbar lymphocytic infiltrate surrounding anagen and early catagen follicles. The inflammatory cells cluster tightly around the hair bulb, which gives the classic description of a "swarm of bees." Importantly, there is no follicular destruction or fibrosis, which distinguishes it from cicatricial alopecias.

Because of the strong autoimmune association, it is reasonable to screen for thyroid disease (TSH at minimum) in all patients with new-onset alopecia areata. Further autoimmune workup (ANA, celiac panel) should be guided by symptoms rather than ordered reflexively.

4. Management and Treatment

Clinical Scenario	First-Line Therapy	Second-Line / Alternatives
Limited patchy disease (adults)	Intralesional triamcinolone acetonide (2.5 to 10 mg/mL, injected every 4 to 6 weeks)	High-potency topical corticosteroids (clobetasol propionate 0.05% applied daily); topical minoxidil 5% as adjunct
Limited patchy disease (children)	Topical corticosteroids (clobetasol 0.05% or betamethasone dipropionate); topical minoxidil	Intralesional injections avoided in young children due to pain
Extensive disease (>50% scalp involvement), alopecia totalis, alopecia universalis	JAK inhibitors: baricitinib (oral, 2 to 4 mg daily) or ritlecitinib (oral, 50 mg daily)	Topical immunotherapy with diphenylcyclopropenone (DPCP); systemic corticosteroids (pulse therapy) as bridge
Rapidly progressive disease	Oral corticosteroid pulse: prednisolone 200 mg once weekly or dexamethasone 5 mg on two consecutive days per week, for 3 to 6 months	Transition to steroid-sparing agent (JAK inhibitor) for long-term control
Adjunctive	Topical minoxidil 5% twice daily to promote regrowth alongside primary immunomodulatory therapy	Cosmetic options: wigs, scalp micropigmentation, support groups

Intralesional triamcinolone acetonide is the most commonly tested first-line treatment for limited alopecia areata in adults. The injection is delivered into the deep dermis or upper subcutis at the level of the hair bulb. A concentration of 2.5 to 5 mg/mL is typical for the scalp, and the injections are repeated every 4 to 6 weeks. The most common adverse effect is local skin atrophy, which is usually reversible. If no response is seen after 6 months, escalation is warranted.

Topical high-potency corticosteroids (clobetasol propionate 0.05%) are the preferred initial treatment in children and can be used in adults who decline injections. They are applied once or twice daily, often under occlusion, for cycles of 2 to 3 months with scheduled breaks to reduce the risk of cutaneous atrophy and telangiectasia.

For extensive or refractory disease, JAK inhibitors represent a major advance. Baricitinib (a JAK1/JAK2 inhibitor) was the first oral medication approved by the FDA for severe alopecia areata in adults. The mechanism directly targets the IFN-gamma/JAK-STAT axis that sustains the autoimmune attack. Ritlecitinib (a JAK3/TEC family kinase inhibitor) is also approved. Key counseling points include screening for tuberculosis and hepatitis B/C before initiation, monitoring for thromboembolic events, and the fact that hair loss typically recurs upon discontinuation, meaning these are long-term therapies.

Topical immunotherapy with DPCP works by inducing an allergic contact dermatitis on the scalp, which is thought to redirect the immune response away from the follicular antigens. It requires in-office sensitization followed by weekly application at increasing concentrations. This approach is effective in about 50 to 60 percent of patients but requires committed follow-up and causes local irritation by design.

Systemic corticosteroids are not recommended for long-term use due to predictable adverse effects (adrenal suppression, metabolic syndrome, osteoporosis) but can be used in pulse regimens as a bridge in rapidly progressive cases.

Topical minoxidil does not address the underlying autoimmune process but promotes follicular regrowth and is a useful adjunctive agent alongside primary immunomodulatory therapy.

5. Differential Diagnosis and Distractors

Differential	Why It Looks Similar	Key Discriminator
Tinea capitis	Patchy hair loss on the scalp in a child or young adult	Tinea capitis has scale, erythema, and broken hairs with black dots; KOH preparation is positive for fungal hyphae; may have posterior cervical lymphadenopathy. Alopecia areata patches are smooth and non-inflammatory
Trichotillomania	Patchy, irregular hair loss; often in children or adolescents	Patches are irregularly shaped (not round/oval), with hairs broken at varying lengths; no exclamation point hairs; biopsy shows trichomalacia and pigment casts; patient may have underlying anxiety or OCD
Telogen effluvium	Diffuse hair shedding that can mimic diffuse alopecia areata	Follows a precipitant 2 to 3 months prior (pregnancy, surgery, illness, medication); hair loss is diffuse without discrete patches; positive pull test is generalized rather than localized to patch margins
Androgenetic alopecia	Progressive hair thinning on the scalp	Gradual onset (not sudden); follows a patterned distribution (bitemporal recession and vertex thinning in men; diffuse thinning with preserved frontal hairline in women); no exclamation point hairs
Secondary syphilis	"Moth-eaten" patchy alopecia on the scalp	Patches are multiple, small, and irregular (moth-eaten appearance) rather than smooth and round; associated with systemic findings (diffuse rash including palms and soles, condylomata lata, lymphadenopathy); RPR/VDRL positive
Discoid lupus erythematosus (DLE)	Patchy hair loss on the scalp	DLE causes scarring alopecia with erythematous, scaly plaques, follicular plugging, and central atrophy; skin biopsy shows interface dermatitis at the dermoepidermal junction with follicular destruction
Traction alopecia	Hair loss in localized areas	Distribution follows areas of chronic tension (frontal hairline, temples); history of tight hairstyles; fringe sign (preserved fine hairs along the frontal hairline); early disease is non-scarring but becomes scarring over time

6. Traps and High-Yield Pearls

The most common trap with alopecia areata questions is confusing it with tinea capitis, especially in pediatric vignettes. Both present as patchy scalp hair loss in children. The discriminating detail the test-writer will embed is the surface quality of the patch: alopecia areata patches are smooth and non-inflammatory, while tinea capitis patches show scale, erythema, or pustules. If the vignette mentions KOH or Wood lamp, the answer is not alopecia areata.

A second frequent trap involves diffuse alopecia areata being mistaken for telogen effluvium. Both can present as generalized hair thinning with a positive pull test. The key is the timeline and trigger. Telogen effluvium has a clear precipitant (childbirth, febrile illness, crash diet) occurring 2 to 3 months before onset, while diffuse alopecia areata lacks such a trigger and will show exclamation point hairs or yellow dots on dermoscopy.

Students also get caught by secondary syphilis, which can produce patchy non-scarring alopecia. When a vignette describes "moth-eaten" hair loss, always look for systemic clues (palmar rash, genital lesions, constitutional symptoms) and a positive serologic test.

On the treatment side, the testable pearl is knowing that intralesional corticosteroid injection is first-line for limited adult disease, while topical corticosteroids are first-line for children. For the newer agents, know that JAK inhibitors (baricitinib, ritlecitinib) are indicated for severe or extensive disease and that their mechanism links directly to the IFN-gamma/JAK-STAT pathway discussed in pathophysiology. Expect questions that test whether you understand why these drugs work at the molecular level.

Finally, remember the nail finding: geometric nail pitting with non-scarring alopecia equals alopecia areata until proven otherwise. This is a classic "two-finding combo" that test-writers use to confirm the diagnosis in a vignette where the hair loss pattern alone might be ambiguous.

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