Three distinct patterns of hair loss with different pathophysiology and management.
Also known as: alopecia areata, androgenetic alopecia, telogen effluvium, hair loss, male pattern baldness, female pattern hair loss
Overview
Alopecia is hair loss from any cause. Three high-yield non-scarring patterns dominate clinical practice: alopecia areata (autoimmune, patchy), androgenetic alopecia (hormonally and genetically mediated patterned thinning), and telogen effluvium (diffuse shedding after a physiologic or psychologic stressor).
Epidemiology
Androgenetic alopecia affects roughly 50% of men by age 50 and 40% of women by 70. Alopecia areata has a lifetime prevalence of about 2%, with peak onset in childhood and young adulthood; strong association with other autoimmune disease (thyroid, vitiligo, atopy). Telogen effluvium is extremely common, particularly postpartum and after surgery, severe illness, or weight loss.
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Question 1DermatologyMedium
A 35-year-old male presents with a 6-month history of multiple well-demarcated patches of complete hair loss measuring 2-3 cm, without scaling or scarring. Pull test is positive at the advancing margins. He has a history of autoimmune thyroid disease. Dermatoscopy shows exclamation mark hairs and yellow dots at follicular ostia. Which of the following is the most likely diagnosis?
ATrichotillomania
BTinea capitis
CAndrogenetic alopecia
DAlopecia areata
Reveal answer & full explanation
Correct answer: D — Alopecia areata
ATrichotillomania
BTinea capitis
CAndrogenetic alopecia
DAlopecia areata✓
Why Alopecia areata is correct
Alopecia areata is an autoimmune T-cell-mediated attack on hair follicle bulge cells; it is non-scarring with regrowth potential
Associations include thyroid disease (15-20%), vitiligo, and atopic dermatitis — this patient has autoimmune thyroid disease
Dermatoscopy hallmarks: exclamation mark hairs (tapered proximal shaft), yellow dots (dilated follicular ostia), and black dots (cadaverized hair shafts) — all present here
Positive pull test at advancing margins is consistent with active alopecia areata
Why the others are wrong
Trichotillomania — caused by hair-pulling behavior; patches are irregular and geometric, without exclamation mark hairs or autoimmune associations (confused-with traction)
Tinea capitis — fungal infection presenting with scaling, broken hairs, and possible kerion; no scaling is present here (right-concept-wrong-cause)
Androgenetic alopecia — gradual diffuse thinning in a patterned distribution; no exclamation mark hairs, yellow dots, or autoimmune associations (anchoring on hair loss)
Extensive disease (>50% scalp, totalis, universalis): JAK inhibitors (baricitinib, ritlecitinib) and topical immunotherapy (DPCP)
Spontaneous remission occurs in ~50% of limited cases
Question 2DermatologyEasy
A 28-year-old female has a 3-year history of diffuse patchy hair loss on the vertex and crown with preserved hairline. Scalp biopsy shows miniaturized follicles with increased telogen/vellus follicles. Her mother and grandmother have similar patterns. Which of the following is the most likely diagnosis?
AAlopecia areata totalis
BAcute telogen effluvium
CFemale pattern hair loss
DInflammatory tinea capitis
Reveal answer & full explanation
Correct answer: C — Female pattern hair loss
AAlopecia areata totalis
BAcute telogen effluvium
CFemale pattern hair loss✓
DInflammatory tinea capitis
Why Female pattern hair loss is correct
Female pattern hair loss (androgenetic alopecia) is the most common alopecia in women, caused by androgen-mediated follicular miniaturization
Ludwig distribution: vertex and crown thinning with a preserved frontal hairline
Scalp biopsy shows miniaturized follicles with increased telogen/vellus follicles
Positive family history (mother and grandmother) supports hereditary androgenetic alopecia
Why the others are wrong
Alopecia areata totalis — autoimmune; presents with discrete circular bald patches (or complete scalp loss in the totalis form), exclamation-point hairs, and nail pitting, with a peribulbar lymphocytic infiltrate on biopsy (confused-with patchy loss)
Acute telogen effluvium — diffuse shedding triggered by a physiologic stressor (illness, surgery, postpartum); reversible and not associated with miniaturized follicles (confused-with diffuse thinning)
Inflammatory tinea capitis — fungal scalp infection with scaly pruritic patches, broken-off hairs, and lymphadenopathy; uncommon in adults (anchoring on scalp findings)
Additional high-yield points
Topical minoxidil 5% foam (FDA-approved for women) once daily; oral minoxidil 0.25-2.5 mg daily is highly effective with dose-dependent hypertrichosis
Spironolactone 100-200 mg daily provides an anti-androgenic effect; finasteride 2.5-5 mg daily is off-label and contraindicated in pregnancy
Platelet-rich plasma and low-level laser therapy are adjuncts
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Alopecia areata: family history of AA, atopy, autoimmune thyroid disease, vitiligo, type 1 DM, Down syndrome
Androgenetic alopecia: family history, age, androgen exposure (genetic susceptibility of follicles to dihydrotestosterone)
Telogen effluvium: childbirth (typically 2-4 months postpartum), major surgery, severe febrile illness, crash dieting, iron deficiency, thyroid disease, drugs (heparin, lithium, retinoids, valproate, ACE inhibitors, beta-blockers, antithyroid drugs)
Pathophysiology
Alopecia areata: T-cell mediated attack on the anagen hair follicle bulb; collapse of follicular immune privilege; reversible because the stem cell compartment is preserved. Androgenetic alopecia: progressive miniaturization of genetically susceptible follicles under 5α-reductase-driven conversion of testosterone to dihydrotestosterone, shortening the anagen phase. Telogen effluvium: a synchronizing insult abruptly shifts a large fraction of anagen follicles into telogen, with shedding manifesting 2-4 months later.
Clinical presentation
Symptoms
Alopecia areata: sudden well-circumscribed round or oval bald patches, asymptomatic; nail pitting common; rarely progresses to alopecia totalis (entire scalp) or universalis (all body hair)
Androgenetic alopecia (males, Hamilton-Norwood pattern): bitemporal recession and vertex thinning; (females, Ludwig pattern): diffuse central thinning with preserved frontal hairline
Telogen effluvium: diffuse, often dramatic shedding (hair-on-pillow, sink-full); appears 2-4 months after the inciting event; rarely causes total loss of more than 50% density
Signs / physical exam
Alopecia areata: smooth bald patches with 'exclamation point' hairs at the margins (tapered proximally), no scaling, no scarring; nail pitting or trachyonychia
Telogen effluvium: positive 'pull test' (>3-6 telogen hairs with each gentle pull from several scalp sites); no patchy loss
Classic findings
Coin-shaped smooth patch with exclamation-point hairs (AA); patterned bitemporal/vertex recession (AGA); diffuse postpartum or post-illness shedding (TE).
Differential diagnosis
Tinea capitis — Children > adults; scaly patches with broken hairs ('black dot'), occipital lymphadenopathy; KOH and fungal culture positive
Trichotillomania — Irregular patches of broken hairs of varying length, often on accessible scalp; behavioral context
Scarring (cicatricial) alopecia (lichen planopilaris, frontal fibrosing alopecia, discoid lupus, CCCA, folliculitis decalvans) — Loss of follicular ostia, perifollicular erythema or scale, scarring permanent; biopsy required
Secondary syphilis — 'Moth-eaten' patchy alopecia with other features of secondary syphilis; RPR positive
Anagen effluvium — Acute diffuse loss days after chemotherapy or severe toxic exposure; follicles arrested mid-anagen; usually reversible
Loose anagen syndrome (children) — Easily extractable hair without pain; usually self-limited
Diagnostic workup
Diagnostic criteria
Diagnoses are clinical: AA — smooth, round, non-scarring patches with exclamation-point hairs; AGA — patterned miniaturization following Hamilton-Norwood (men) or Ludwig/Olsen (women) classifications; TE — diffuse shedding >100 hairs/day with a clear preceding trigger 2-4 months earlier and reversible course over 3-6 months.
Labs
Generally clinical diagnosis; consider lab workup if diffuse loss or atypical features
TSH, ferritin (target >40-70 ng/mL for hair regrowth), CBC
Vitamin D, zinc if dietary inadequacy suspected
ANA if scarring or systemic features suggest lupus
RPR if secondary syphilis is on the differential
Androgen panel (total/free testosterone, DHEAS, prolactin) in women with rapid virilization or signs of PCOS
Imaging
No routine imaging
Dermoscopy (trichoscopy) is invaluable: exclamation-point and yellow dots in AA; miniaturized hairs and hair-shaft diameter diversity >20% in AGA; uniform pull-test telogen bulbs in TE
Scalp biopsy (4 mm punch, horizontal sectioning) when scarring alopecia or atypical pattern suspected
Diagnostic algorithm
Feature
Alopecia Areata
Androgenetic Alopecia
Telogen Effluvium
Pattern
Discrete round patches
Bitemporal/vertex (M); central diffuse (F)
Diffuse, no patches
Onset
Sudden over weeks
Gradual over years
Acute 2-4 months after trigger
Scalp exam
Smooth, exclamation-point hairs
Miniaturized hairs in pattern
Positive pull test, no patches
Nail findings
Pitting, trachyonychia
None
None
Pathophysiology
Autoimmune T-cell attack on bulb
DHT-driven follicle miniaturization
Synchronous anagen-to-telogen shift
First-line therapy
Intralesional steroids; JAKi if severe
Minoxidil ± finasteride
Correct trigger; reassure
Reversible?
Often (relapsing-remitting)
Slowly progressive
Yes, within 3-6 months
Three high-yield non-scarring alopecias: distinguishing features and first-line therapy.
Treatment
First-line
Alopecia areata, limited (<50% scalp): intralesional triamcinolone 2.5-10 mg/mL every 4-6 weeks; topical clobetasol 0.05% or other potent steroid; topical minoxidil 5% adjunct
Alopecia areata, extensive/severe (>50%): topical/oral immunotherapy with squaric acid dibutyl ester or diphencyprone; oral JAK inhibitors — baricitinib (FDA-approved 2022 BRAVE-AA1/AA2 trials), ritlecitinib (FDA-approved 2023 ALLEGRO trial)
Androgenetic alopecia: topical minoxidil 2% or 5% solution/foam BID for both sexes; oral finasteride 1 mg/day for men (5α-reductase inhibitor); low-level laser therapy as adjunct
Telogen effluvium: identify and correct the trigger (treat thyroid disease, repair iron deficiency with ferrous sulfate, address weight loss/medications); reassure that regrowth begins within 3-6 months
Second-line / adjunct
Alopecia areata: methotrexate, cyclosporine, systemic corticosteroids (pulse) for rapidly progressive disease — high relapse off therapy; consider wigs and cranial prostheses
Androgenetic alopecia: oral dutasteride (off-label, more potent 5α-reductase inhibition); spironolactone or oral contraceptives for women with hyperandrogenism; platelet-rich plasma scalp injections; hair transplantation for established patterned loss
Telogen effluvium: ensure ferritin >40-70 ng/mL; consider topical minoxidil to accelerate regrowth in chronic telogen effluvium
Complications
Psychosocial distress, depression, anxiety — significant in all forms
Alopecia areata: progression to totalis/universalis, irreversibly long-standing disease in 10-15%
Finasteride: sexual side effects (decreased libido, erectile dysfunction in <5%); rare 'post-finasteride syndrome' debated
Minoxidil: hypertrichosis at unintended sites, transient telogen shedding when starting, reflex tachycardia and pedal edema with oral low-dose minoxidil
Exclamation-point hairs and nail pitting strongly support alopecia areata.
Pull test (>6 telogen hairs in 60 grasp) is essentially diagnostic of active telogen effluvium when paired with appropriate timeline.
Always rule out iron deficiency and thyroid disease in diffuse hair loss, especially in women.
Topical minoxidil works for both AGA and helps AA — counsel about transient initial shedding.
Finasteride takes 6-12 months for visible improvement; preserves hair more than it regrows.
JAK inhibitors (baricitinib, ritlecitinib) have transformed severe alopecia areata but require infection and lipid monitoring.
Differentiate non-scarring from scarring alopecia at the bedside — loss of follicular ostia is the key sign and a reason to biopsy and treat aggressively.
References
AAD 2020 — Strazzulla LC et al. Alopecia areata: disease characteristics, clinical evaluation, and new perspectives on pathogenesis (JAAD 2018)
BRAVE-AA1 and BRAVE-AA2 — King B et al. Two Phase 3 Trials of Baricitinib for Alopecia Areata (NEJM 2022)
ALLEGRO trial — King B et al. Efficacy and safety of ritlecitinib in adults and adolescents with alopecia areata (Lancet 2023)
AAD AGA Guideline — Olsen EA. Current and novel methods for assessing efficacy of hair growth promoters in pattern hair loss (JAAD 2003)
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