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Alopecia Areata 1_1113 Derm Dx
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Alopecia Areata 2_1113 Derm Dx
A 45-year-old otherwise healthy patient complains of several patches of hair loss.
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Alopecia areata (AA) is characterized by the sudden onset of discrete areas of non-scarring hair loss on the scalp. Although the etiology is unknown, a combination of genetic and environmental factors is thought to trigger the disease. In the United States, prevalence is 0.1% to 0.2%, and about 20% of patients report having a family history of AA.
AA is thought to be an autoimmune disease specific to hair. Experiments with mice suggest an interaction between cytoxic T-lymphocytes and follicular human leukocyte antigens.
AA is also associated with other autoimmune disorders, such as atopy, autoimmune thyroid disease, vitiligo, inflammatory bowel disease and autoimmune polyendocrinopathy syndrome type 1.
The disorder most commonly presents as round patches of hair loss, revealing smooth scalp underneath. In some cases, hair regrowth occurs within a couple of months, but recovery may not be complete or permanent. In addition, new hair may have a different color or texture (e.g. fine and white), and patients often experience further hair loss from the same or different lesions.
Other presentations of AA include total hair loss of the scalp (alopecia totalis), total body hair loss (alopecia universalis) and band-like hair loss along the scalp (ophiasis pattern). Nail dystrophy (e.g., pitting, trachyonychia, onycholysis) is common and may even occur after resolution of AA.
Patients with limited involvement AA are most likely to have total permanent regrowth of hair whereas patients with extensive hair loss, family history of AA, nail dystrophy and other autoimmune diseases are less likely to recover lost hair.
Diagnosis & Treatment
AA diagnosis is usually based on history and examination. Trichoscopy will reveal yellow dots and “exclamation point” hairs.
If history and exam are inadequate, a scalp biopsy may be helpful in differentiating AA from other diseases, such as tinea capitis, trichotillomania, telogen effluvium, androgenetic alopecia and secondary syphilis.
Histology will show a peribulbar lymphocytic infiltrate “swarm of bees,” no scarring and vellus-like hair follicles.
Treatment controls, but does not cure AA. Treatment development is often hindered by the unpredictable nature of AA. For example, some patients totally recover within 1 year without treatment, whereas others end up with chronic disease.
For patients older than 10 years with less than 50% scalp involvement, repeat intralesional corticosteroid injections — 3 to 5 mg/mL of triamcinolone acetonide — every 4 to 8 weeks are the treatment of choice and hair regrowth is seen within 8 weeks.
However, atrophy may occur with increased dosage and inadequate depth of injection, and steroid injections do not preclude the possibility of recurrent hair loss.
For patients aged older than 10 years with more than 50% scalp involvement, treatment options are less promising but include 5% topical minoxidil solution with or without topical glucocorticoids, topical immunotherapy with diphenylcyclopropenone or squaric acid dibutylester, topical anthralin, oral glucocorticoids or scalp prosthesis.
For patients younger than 10 years, who may not tolerate the pain of intralesional corticosteroid injections, 5% topical minoxidil solution and/or topical glucocorticoid can be used, as well as topical anthralin.
For eyebrows and beards, intralesional glucocorticoids and/or 5% topical minoxidil solution may be used. Eyeglasses and wigs can also serve as cosmetic enhancement.
Vicky Zhen Ren is a medical student at Baylor College of Medicine.
Adam Rees, MD, is a graduate of the University of California Los Angeles School of Medicine and a resident in the Department of Dermatology at Baylor College of Medicine also in Houston.
References
- Bolognia JL, Jorizzo JL and Schaffer JV. “Chapter 69: Alopecias.” Dermatology. Philadelphia, PA: Elsevier Saunders, 2012.
- Habif TP. “Chapter 24: Hair Diseases.” Clinical Dermatology: A Color Guide to Diagnosis and Therapy. Edinburgh, UK: Mosby/Elsevier, 2009.