Alopecia (Areata, Androgenetic, Telogen Effluvium)

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

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 algorithm

Treatment

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)