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Dr. Bertram Medical Hair Transplant
眉 髮 醫 學 移 植 中 心 ( 香 港 ) |
( 852 ) 3421-1138
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Alopecia Areata ( AA )
Pathology
It is not contagious. Alopecia areata ( AA ) is an inflammatory non-scarring hair loss disorder. The hair follicles are attacked and injured by own immune system, and is classified as an "Autoimmune Disease" of unknown cause. The scalp is the most commonly affected area, but the beard or any hair-bearing site can be involved.
Inflammatory cells are found around the affected hair follicle. These immune cells "effect" the hair follicle to interrupt hair growth and triggers shedding.
Incidence
AA is the third most common form of hair loss seen by dermatologists. Both males and females of all ages and ethnicities may develop alopecia areata. Overall AA affects 1% of the population (1 in every 100). There is a 2% chance that anyone will develop AA in their lifetime. Those with a history of atopy (asthma, allergic rhinnitis, and atopic dermatitis) or other autoimmune diseases (SLE, vitiligo, rheumatoid arthritis, pernicious anaemia) are at a higher risk.
Genetic Factors
When a patient develops AA before the age of 30, there is over a 20% chance that other family member are also affected. Alopecia areata has been reported to occur concurrently or sequentially in twins.
Terminology
The most common clinical presentations are called alopecia areata, alopecia totalis, and alopecia universalis.
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Alopecia Areata
refers to round to oval patches of hair loss.
Alopecia Barbae
refers to AA affecting only men's beard area.
Alopecia Totalis
refers to loss of all scalp hair.
Alopecia Universalis
refers to loss of all scalp and body hair. |
Diagnostic Features
- One or 2 patches of hair loss usually appears suddenly in matter of days
- The presence of "exclamation hair" around the edge
- The regrowth hairs are usually white or blonde
- Only pigmented hairs are affected
No symptoms or just mild itching and tingling. After shedding the follicle is either "arrested" at growth, or remains in hair cycle resting phase. Regrowth is thus slow and the involved areas may remain bald for months or years. Skin biopsy may be needed to confirm the diagnosis.
Associated changes
The nail may be affected, ranging from small dot depressions in the nail plate (pitting), to thinning or shedding of the nail plate.
Recovery
90% of patients with just one or two patches affecting less than 25% of the scalp will have a full recovery within 2 years, with or without treatment.
Overall 30% of patients with AA will develop extensive loss.
The presence of severe nail abnormalities, entensive scalp involvement, atopy (asthma, allergic rhinnitis, and atopic dermatitis), and onset before puberty, have all been implicated to have poor result.
Alopecia totalis or universalis lasts > 2 years have a particularly low chance of spontaneous regrowth and is less responsive to therapy.
Treatment
Stem cells of the affected follicles are not destroyed and are ready to resume normal hair production. Therapy should target at the immunological background of the disease. Commonly prescribed medications for mild disease when < 50% scalp hair is lost are :
- Anti-inflammatory - topical or intralesional steroid injections
- Topical 5% minoxidil - to promote hair growth
- Extensive case > 50% scalp hair loss, or not responding to above therapy
- Oral steroid
- Psoralen plus ultraviolet A light (PUVA)
- Topical immunotherapy with diphencyprone and squaric acid dibutylester
- Wigs
Many new drugs are currently being investigated. Overall, the future looks bright.
AA and Hair Transplant
We do not recommend hair transplant for AA. The transplanted hairs will be lost on reactivation of this skin condition.
References
1. Bolduc C, Shapiro J. The treatment of alopecia areata. Dermatol Ther 14: 306-316, 2001.
2. Hordinsky M. Clinical presentations of alopecia areata. Dermatol Ther 14: 291-296, 2001.
3. Hordinsky M. Alopecia Areata. In Olsen EA (ed): Disorders of Hair Growth: Diagnosis and Treatment. McGraw-Hill, New York, 2003.
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