Alopecia Areata

Alopecia areata is an autoimmune, non-scarring, localised hair loss. In normal conditions, hair follicles are immune-privileged sites. This immune privilege is disrupted in alopecia areata, thereby allowing autoreactive T-cells to target hair follicles. Inflammation disrupts normal hair cycling (hair follicles do not enter anagen), manifesting as patchy non-scarring hair loss

Hair loss in alopecia areata is not always complete. It is commonly caused by tinea capitis.

• Risk factors
  • HLA association (HLA-DQB1 and HLA-DRB1)
  • Family history of alopecia areata
  • Autoimmunity (associated with thyroiditis, vitiligo, SLE, and rheumatoid arthritis)
  • Environmental triggers, e.g. infection, stress, and vaccination
  • Hormonal changes, e.g., puberty, pregnancy, and menopause
  • Atopy
• Areas involved
  • Scalp
  • Beard area (In men, this is a more common presentation than on the scalp. Sometimes mistaken for an area of depigmentation)
  • Eyelashes
• Signs and symptoms
  • Patchy non-scarring hair loss
  • Exclamation mark hairs: usually seen at the edge of an area of alopecia. A sign of ongoing disease activity. The hair has started to grow, but this has set off inflammation around the follicle, and as the hair grows, the inflammation continues, and the hair becomes thinner and thinner until it falls out
  • Yellow dots (follicles without hairs) in the affected area
  • Nail pitting (much less obvious than those seen in psoriasis – not as deep, often from lines)
• Differentials
  • Tinea capitis
  • Androgenetic alopecia
  • Telogen effluvium
• Investigations
  • Dermatoscopy: yellow dots, black dots, broken hairs, and exclamation mark hairs
  • CBC, TFTs, ANA, ESR, and CRP to identify autoimmune conditions
  • Hair pull test: a positive pull test indicates active disease (if more than 10% hairs are pulled out easily)
  • Skin biopsy: peribulbar lymphocytic infiltrate (”swarm of bees”)
  • Patch testing: to exclude allergic contact dermatitis
• Treatment
  • Psychological support
  • Topical corticosteroids (first-line) if < 50% scalp involvement
  • Intralesional corticosteroids (if topical corticosteroids do not work)
  • Short-term systemic corticosteroids for > 50% scalp involvement or rapidly progressing disease.
  • Topical immunotherapy with DCP (diphenylcyclopropenone) is second-line
  • Minoxidil to stimulate hair growth
  • Phototherapy – PUVA
  • Laser