By: John Kraft and Charles Lynde, MD, FRCPC

Alopecia Areata

Hair loss or 'alopecia' can be scarring or not. 'Alopecia Areata' is a form of non-scarring alopecia. (check-out the definitions on www.skincareguide.com/glossary ) This means that there is hair loss but the hair follicles are still intact and visible on inspection. It is an autoimmune disease that affects the bulb region of the hair follicle. For some unknown reason, immune cells attack this region of the hair follicle, normally a sight out of bounds for the body's immune surveillance. This attack causes the hair to fall out without causing permanent damage to the hair follicle. It is possible for the hair to regrow in time.

Alopecia areata is relatively common in North America with a prevalence of 0.1-0.2%. 1 in 5 patients has a relative with the disease.

In the normal scalp, 90-95% of hair follicles are in the anagen phase (growing) and the remainder (5-10%) are in the telogen (shedding) phase. Each follicle cycles through the various stages independently. What signals cause a hair follicle to stop growing and enter the telogen phase are currently unknown.

Causes of non-scarring hair loss:

  • severe illness
  • childbirth
  • hormones (i.e. hypothyroidism, androgens)
  • toxins (i.e. anticoagulants, chemotherapy, heavy metals, vitamin A)
  • micronutrient deficiencies (i.e. iron or zinc deficiencies)
  • physical damage to the hair follicle (i.e. 'corn-row' braiding, trichotillomania- obsession with pulling out hair)
  • autoimmune (i.e. alopecia areata),

In alopecia areata, telogen hair loss is mainly localized to the scalp, eyebrows, eyelashes, and beard (although all body hair areas can be affected). Round or oval patches of non-scarring hair loss are typically seen. The hair loss is usually asymptomatic.

There are various patterns of alopecia areata. These include localized alopecia areata, alopecia totalis (loss of all scalp hair), alopecia universalis (loss of all scalp and body hair) and ophiasis pattern alopecia areata (bandlike pattern of hair loss along periphery of temporal and occipital scalp).

Other findings in alopecia areata:

  • nail changes (10-20% of patients): pitting, rough longitudinal ridging, brittleness, dystrophy, onycholysis (nail becomes separated from the nail bed) (See www.fungalguide.com/types/fungal_nail_infections.html )
  • can be associated with other immunologic diseases: Atopy (i.e. allergic rhinitis, asthma, and atopic dermatitis), thyroid diseases, vitiligo, pernicious anemia, Addison's disease, inflammatory bowel disease

The clinical course of alopecia areata is variable. Hair may regrow within months of the first attack. 30% of patients may have regrowth after 6 months, 50% after a year, and 75% after 5 years. Recurrences have been linked to emotional distress. Treating alopecia areata is difficult because of the unpredictability of the disease. The agents used in treatment are designed to suppress the out-of-control immune response that is causing the hair loss.

Localized patchy alopecia areata can be treated with topical or intralesional corticosteroids, topical minoxidil (2 or 5%), anthralin, and combination therapy. Injections of corticosteroids are usually given every 4-6 weeks. One risk of corticosteroid injections includes atrophy (thinning of the skin), but this often resolves with time. The majority of patients will see signs of hair regrowth within 6 weeks.

Treating more extensive alopecia areata may involve the use of topical immunotherapy (i.e. topical diphencyprone applied weekly to induce a contact allergic reaction on the affected area), psoralen plus ultraviolet A light (PUVA), or systemic prednisone.

Results of a scalp biopsy can also influence treatment. When there is little inflammation, 5% topical minoxidil may be the most appropriate therapy, and when there is significant inflammation, the use of corticosteroids in addition to minoxidil may be beneficial. In extensive cases, wigs may be an option while treatment is attempted. Alopecia Areata Support Groups are found in most communities and on the internet. To learn about other skin conditions, click on www.SkinCareGuide.ca .


About the authors:

Charles Lynde, MD, FRCPC is Assistant Clinical Professor, University of Toronto Canada. His special interests include paediatric dermatology, cosmetic procedures, contact dermatitis, skin cancer, psoriasis and clinical trials in acne, eczema, and psoriasis.
John Kraft, HBSc, is a fourth year medical student at the University of Toronto, with an interest in dermatology


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