Alopecia (Areata, Androgenetic, Telogen Effluvium)
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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Risk factors
- 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
- Androgenetic alopecia: miniaturized vellus-like hairs in affected zones; preserved follicular ostia
- 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 |
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
- JAK inhibitors: infections (HSV, VZV, TB reactivation), thromboembolism, lipid changes, lymphopenia
PANCE pearls
- 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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