Alopecia Areata

Please take a history and examine this 30 year old lady with hair loss.

HISTORY (3mins)

  • Timing Questions: since when did the hair loss start, is it getting worse, did it happen suddenly or gradually, when does hair loss happen. Does anything make the hair loss better or worse
  • Patchy/widespread hair loss
  • Scarring?
  • Red/scaly
  • Scalp/beard/body/eyebrows/eyelashes affected
  • Does it regrow white?
  • Nails
  • PMH: autoimmune eg DM, PA, vitiligo,coeliac, thyroid and screen for these conditions- ask about tiredness
  • Fx of hair loss
  • Dx- chemo, heparin, warfarin, OCP
  • Sx- diet, stress, illness, trauma, surgery

EXAMINE (3mins)

  • Hair- patchy/widespread, inflamed/noninflammed?, scarring/nonscarring?, exclamation mark hairs?, white hair?
  • Beard, brows, eyelashes, body hair
  • Nails
  • Don’t miss vitiligo!
  • Examine thyroid
  • Check for conjunctival pallor

ICE and Explanation (2 mins)

For example:

“There are many causes of hair loss but I suspect you may have a condition called Alopecia areata.  Hair is lost because it is affected by inflammation. The cause of this inflammation is unknown but it is thought that the immune system may attack the growing hair. Stress occasionally appears to be a trigger. It is hard to predict how much hair loss will occur. Regrowth can over months to years but cannot be guaranteed. If less is lost initially then the chance of regrowth is high at one year.  Sometimes the hair regrows white. I’ll refer you to dermatology who specialise in this condition. They may do a scrape from your hair to rule out fungal infection and some blood tests. There are some treatments available such as steroid creams or injections.  Some individuals with alopecia areata prefer to wear a wig while they wait for recovery. You may find that joining a patient support group and meeting other people with alopecia areata will help.  I can arrange this for you if you would like”


Alopecia areata is a chronic inflammatory disease that affects the hair follicle and sometimes the nail. It is a common cause of non-scarring hair loss that can occur at any age.  It usually causes small, round patches of baldness on the scalp, although hair elsewhere can be affected such as the beard, eyebrows, eyelashes, body and limb hair.  If it involves the whole scalp the condition is called alopecia totalis.  If it involves the whole body and scalp this is called alopecia universalis. Short broken hairs (known as exclamation mark hairs) are frequently seen around the margins of expanding patches of alopecia areata.

Poor prognosis = severe, nail involvement, atopy, young, other autoimmune conditions



Bloods-FBC, TFT, iron/ferritin, glucose, ANA for lupus, Syphilis serology

Fungal culture

Dermoscopy: dystrophic hairs with fractured tips (exclamation mark hairs) and hairs fractured before emergence from the scalp (cadaverized hairs).

Skin biopsy if diagnosis unclear



  • Mild- no treatment, reassure
  • Topical potent corticosteroid or intralesional triamcinolone
  • Dithranol (anthralin) for limited patchy alopecia areata but no convincing evidence that this is effective
  • Minoxidil 5%- but no convincing evidence that this is effective
  • If severe: topical immunotherapy, systemic steroid but side effects, PUVA
  • Trigger control eg. Stress
  • Emotional support, patient support groups, wig


Causes of Hair Loss:

  1. Localised non-scarring
    1. Alopecia Areata
    2. Tinea capitis
    3. Trichotillomania
    4. Traction
  2. Diffuse non-scarring
    1. Androgenetic (male/female pattern baldness)
    2. Endocrine- thyroid
    3. Malnutrition- iron, zinc def
    4. Drugs- chemo, hep, warfarin (anagen effluvium)
    5. Telogen effluvium
    6. Secondary syphilis
  3. Scarring
    1. Lichen planus
    2. Discoid lupus erythematosus
    3. Scleroderma morpheoa
    4. Tinea Capitis (can cause scarring or non-scarring alopecia)



Written by Sarah Kennedy


For more information please see the British Association of Dermatologists’ guidelines for the management of alopecia areata 2012


Resources used to make this document include those listed on the webpage and also: