Overview
Recognise immune-mediated non-scarring hair loss, exclude infection and follicular destruction, grade extent and impact, and use topical or systemic treatment with realistic relapse and safety counselling.
Alopecia areata is an autoimmune attack on anagen hair follicles that interrupts growth without destroying the follicular unit. Classic disease produces one or more circular smooth patches; ophiasis follows the occipital and temporal margin, alopecia totalis removes all scalp hair and alopecia universalis extends across the body. Sudden diffuse alopecia areata can resemble telogen effluvium. Hair colour and scalp-to-hair contrast alter visibility, so examination must include touch, close inspection and dermoscopy rather than judging severity from a distant view.
Diagnosis is clinical when follicular openings persist and typical edge hairs, nail change or recurrence support it. The main safety task is not to miss tinea capitis, traction with evolving scar, trichotillomania or a primary cicatricial alopecia. Biopsy is reserved for uncertainty. Extent scores can support specialist treatment, but eyebrow, eyelash, beard and functional impact may be severe even when scalp percentage is modest.
Outcome varies. A first small patch of short duration has a meaningful chance of spontaneous regrowth, whereas childhood onset, ophiasis, nail disease, atopy and extensive longstanding loss predict a more difficult course. Treatment choice therefore ranges from observation and camouflage to topical or injected corticosteroid and specialist systemic therapy. A treatment that induces growth does not necessarily reset the underlying relapse tendency.