Dermatology · Hair Disorders
The facts most likely to be tested
Alopecia areata is an autoimmune-mediated condition characterized by non-scarring hair loss resulting from T-cell attack on hair follicles.
Physical examination classically reveals well-demarcated, round or oval patches of hair loss with a smooth, non-inflamed scalp surface.
The pathognomonic finding on close inspection is the presence of exclamation point hairs, which are short, broken hairs that taper toward the proximal end.
Alopecia areata is frequently associated with other autoimmune disorders, most notably thyroid disease, vitiligo, and pernicious anemia.
The pull test is typically positive at the active margins of the lesion, indicating ongoing hair shedding.
First-line treatment for localized disease is intralesional corticosteroids (e.g., triamcinolone acetonide).
Severe or rapidly progressive cases may be managed with topical immunotherapy (e.g., squaric acid dibutyl ester) or JAK inhibitors (e.g., baricitinib) in refractory patients.
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A 24-year-old female presents to the clinic complaining of a bald spot on her scalp that appeared over the last three weeks. She denies any pain, itching, or burning in the area. Physical exam reveals a 3-cm well-demarcated, round patch of hair loss on the vertex of the scalp with a smooth, non-scarring surface. Close inspection shows several short, tapered hairs at the periphery of the lesion. Her medical history is significant for Hashimoto thyroiditis.
What is the most likely diagnosis?
Alopecia areata
The patient presents with the classic clinical features of alopecia areata, including a smooth, non-scarring patch and pathognomonic exclamation point hairs, occurring in the context of a known autoimmune condition.
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High yield triage
Etiology / Epidemiology
Autoimmune T-cell mediated attack on hair follicles; associated with atopy, thyroid disease, and vitiligo.
Clinical Manifestations
Sudden onset of smooth, round, non-scarring patches; exclamation point hairs are pathognomonic.
Diagnosis
Primarily clinical diagnosis; biopsy reserved for atypical cases showing peribulbar lymphocytic infiltrate.
Treatment
Intralesional corticosteroids are first-line; avoid systemic steroids due to high relapse rates.
Prognosis
Spontaneous remission common in limited disease; <50% scalp involvement predicts better recovery.
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Epidemiology & Etiology
Affects all ages, with a peak incidence in the second and third decades. It is an organ-specific autoimmune condition where hair follicles lose immune privilege. Strong genetic predisposition exists, often clustering with other autoimmune disorders.
Pertinent Anatomy
The process targets the anagen-phase hair follicle bulb. The inflammatory infiltrate is localized to the base of the follicle, sparing the stem cell-rich bulge area, which allows for potential hair regrowth.
Pathophysiology
CD8+ T-lymphocytes infiltrate the hair bulb, disrupting the normal hair cycle. This leads to premature transition from the growth phase to the telogen (resting) phase. The hair shaft becomes brittle and breaks at the skin surface.
Clinical Manifestations
Patients present with well-demarcated, circular patches of non-scarring alopecia. Look for exclamation point hairs—short, broken hairs that taper proximally—at the periphery of active lesions. Nail pitting or trachyonychia (sandpaper nails) may be present as a systemic marker.
Diagnosis
Diagnosis is clinical. A pull test is positive at the active margins, indicating ongoing hair loss. If the diagnosis is uncertain, a punch biopsy is the gold standard, revealing the classic swarm of bees pattern of lymphocytic infiltration.
Treatment
Intralesional triamcinolone is the first-line treatment for localized disease. For extensive cases, topical minoxidil or contact immunotherapy may be used. Systemic corticosteroids are generally avoided due to the high risk of rebound hair loss upon discontinuation.
Prognosis
Prognosis is variable; 30-50% of patients experience spontaneous resolution within one year. Poor prognostic factors include alopecia totalis (entire scalp) or alopecia universalis (entire body).
Differential Diagnosis
Tinea capitis: presence of scaling, crusting, and lymphadenopathy
Trichotillomania: hairs of varying lengths with broken shafts
Telogen effluvium: diffuse thinning rather than focal patches
Secondary syphilis: 'moth-eaten' alopecia pattern
Discoid lupus erythematosus: scarring alopecia with follicular plugging