Alopecia areata

Author: Faculty Reviewer:

Publish date: Posted on
Last updated: March 20, 2022

Keywords #

alopecia areata
alopecia
non-scarring
non-cicatricial
hair loss

Diagnosis #

Alopecia areata(AA),is anon-scarring, patterned hair loss disorder that is seen in approximately0.1-0.2% of the population[1]. Although the exact etiology is unknown, it is thought to be a primarily T-cell driven process resulting in autoimmune attack of the hair follicle. AA classically presents as sudden onset of round or oval patches of hair loss on the scalp. The course of AA is unpredictable. While over half of patients diagnosed with AA will recover within 1 year, relapses are common.Factors that have been associated with a worse prognosis include younger age of onset and extent of disease[2].

Key Concepts #
  • Alopecia areata is an inflammatory disease of the hair follicle.•It classically presents as non-scarring circular or oval patches of hair loss, but can progress rapidly to involve every hair on the head and body in its most severe form.
  • Associated nail abnormalitiesare common.
  • First-line treatment for limited disease includes intralesional corticosteroids.
  • Systemic immunosuppressant and platelet-rich plasma therapies are options for extensive or refractory disease.
Epidemiology #

The cumulative lifetime incidence of AA is estimated to be about 2%[3]. It affects both sexes equally and can be seen in all age groups[4]. One in every five individuals has a family history of the disease[5].

Clinical Features #
  • Sudden onset of one or more well-demarcated circular or oval patches of non-scarring hair loss without significant underlying inflammation[6].
  • Patches of hair loss classically develop on the scalp, but can occur in any hair-bearing area [4].
  • A subset of patients can progress to total scalp hair loss (alopecia totalis) or total body hair loss (alopecia universalis).
  • There are associated nail abnormalities includingpitting (most common), longitudinal ridging, trachyonychia (sandpaper nails), onycholysis (splitting at the ends), and koilonychia (spoon shaped nails)[2, 6].
Differential Diagnoses #
  • Tinea capitis
  • Secondary syphilis
  • Telogen effluvium
  • Trichotillomania
  • Temporal triangular alopecia
Diagnostic Workup #

The diagnosis of AA can usually be made clinically through history and physical examination. Trichoscopy will classically show “exclamation point” hairs at the periphery of the alopecia patches, as well as regular round yellow dots[2]. Biopsies are generally not indicated unless the presentation is unusual. In cases where a biopsy is necessary, histology will show aperibulbar lymphocytic inflammation.

Treatment #

Various combinations of topical, intralesional, and systemic therapies have all been utilized for the treatment of AA. Treatment decisions are based on patient age and extent of disease. For classic patchy AA, most commonly used therapeutic regimens include potent topical or intralesional corticosteroids. Topical minoxidil (2% or 5%) and topical anthralin (0.5-1%) are also options. For more extensive or refractory disease, treatment options include short courses of systemic corticosteroids, topical immunotherapies such as squaric acid dibutylester and diphenylcyclopropenone, methotrexate, cyclosporine, azathioprine, or oral janus kinase inhibitors including tofacitinib, ruxolitinib, and baricitinib[5, 7]. Platelet-rich plasma and injectable platelet-rich fibrin have shown promise as an emerging therapy as well[8].  

It is important to note that no treatment modalities have been shown to reliably induce sustained remission. No treatment may be an appropriate course for a subset of patients[5, 7] 

References #
  1. Safavi, K., Prevalence of alopecia areata in the First National Health and Nutrition Examination Survey. Arch Dermatol, 1992. 128(5): p. 702.
  2. Strazzulla, L.C., et al., Alopecia areata: Disease characteristics, clinical evaluation, and new perspectives on pathogenesis. J Am Acad Dermatol, 2018. 78(1): p. 1-12.
  3. Mirzoyev, S.A., et al., Lifetime Incidence Risk of Alopecia Areata Estimated at 2.1% by Rochester Epidemiology Project, 1990–2009. Journal of Investigative Dermatology, 2014. 134(4): p. 1141-1142.
  4. Wasserman, D., et al., Alopecia areata. Int J Dermatol, 2007. 46(2): p. 121-31.
  5. Messenger, A.G., et al., British Association of Dermatologists’ guidelines for the management of alopecia areata 2012. Br J Dermatol, 2012. 166(5): p. 916-26.
  6. Alkhalifah, A., et al., Alopecia areata update: part I. Clinical picture, histopathology, and pathogenesis. J Am Acad Dermatol, 2010. 62(2): p. 177-88, quiz 189-90.
  7. Strazzulla, L.C., et al., Alopecia areata: An appraisal of new treatment approaches and overview of current therapies. J Am Acad Dermatol, 2018. 78(1): p. 15-24.
  8. Hesseler MJ, Shyam N. Platelet-rich plasma and its utilities in alopecia: A systematic review. Dermatol Surg. 2020. 46(1): p. 93-102.