A 25-year-old man with no significant medical history arrives at the clinic concerned about a bald patch on his head that has been growing in size. There is no family history of hair loss, and he denies hair-pulling, scratching, or trauma to the area. On examination, a well-demarcated, circular, smooth patch of nonscarring hair loss is noted over the parietal scalp. There is no hair loss on any other part of the body.
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Alopecia areata is a prevalent autoimmune disease of the hair follicles leading to nonscarring hair loss, commonly presenting as smooth patches of well-defined hair loss on the scalp. It has been frequently described in the literature since the early 20th century, with numerous studies investigating its etiology and treatment. A variety of presentations have been seen, ranging from small patches of hair loss to total body hair loss, and response to treatment has been found to vary widely among patients.
After androgenetic alopecia, alopecia areata is the second most common cause of hair loss, affecting an estimated 4.5 million people in the United States, with a worldwide prevalence of 0.1% to 0.2% and an estimated lifetime incidence of 2.1%.1-3 Although it is often seen in children and younger adults, individuals of all ages can be affected.3 There is no apparent sex predominance, no significant variance among ethnicities, and hair of all colors can be affected.3,4
Alopecia areata is believed to occur as a result of an autoimmune process directed against follicular melanocytes or matrix keratinocytes in which inflammatory cells attack anagen hair follicles and prematurely propel them into the catagen phase.5 As the hair shaft can then no longer be anchored within the hair canal, it is subsequently shed, leading to visible hair loss.6 Given its underlying autoimmune basis, patients with alopecia areata are at increased risk for other conditions including atopy, vitiligo, thyroid disease, and other autoimmune diseases, as well as depression and anxiety.3,7 Alopecia areata has a strong genetic component, with a family history increasing the risk of developing the condition.7 Likewise, a family history of other autoimmune conditions increases the risk of developing alopecia areata. Patients with Down syndrome have also been found to be at increased risk for alopecia areata.7
The diagnosis of alopecia areata is primarily made clinically, with the classic presentation of well-defined smooth patches of nonscarring hair loss and absence of any notable epidermal changes.8 Although the skin in the observed patch is typically normal, peachy or mildly reddened discoloration can sometimes be seen. Hair loss most commonly involves the scalp, but other areas such as the eyebrows, eyelashes, beard, extremities, or anywhere else on the body may be affected.4 Patches can be single, multiple, or diffuse, and classification of alopecia areata is typically based on this designation. Alopecia areata can present as patchy alopecia; alopecia totalis, where hair loss involves the entire head; or alopecia universalis, where hair loss involves the full body.4,8 The latter two of these diagnoses are commonly observed to have high resistance to treatment.9 Other commonly observed patterns include ophiasis type, which is a band-like hair loss of the parieto-temporo-occipital scalp, or ophiasis inversus (sisaipho), which involves hair loss of the fronto-parieto-temporal scalp.8
Common clinical findings in alopecia areata can include “exclamation mark hairs,” which are short hairs that taper closer to the skin, and nail pitting, an associated clinical finding observed in two-thirds of cases.4 Upon histologic examination, alopecia areata typically involves an infiltrate of lymphocytes surrounding the hair bulb, sometimes described as a “swarm of bees.”5 This finding may be absent in older alopecia areata lesions; therefore, other clues such as eosinophils, melanin and lymphocytes in fibrous tract remnants, and an increase in catagen-telogen follicles may help in diagnosis.5
The differential diagnosis for alopecia areata includes a variety of hair loss conditions, most notably tinea capitis, trichotillomania, and telogen effluvium.4,8 Several clinical features of these conditions can help differentiate them from alopecia areata. The presence of inflammation and scale as well as postauricular lymphadenopathy can help identify tinea capitis. The finding of hairs broken off at different lengths is more consistent with trichotillomania. Diffuse hair loss as opposed to localized hair loss can help distinguish telogen effluvium. Other potential diagnoses to consider include lupus or secondary syphilis, which can be confirmed via serologic testing.8
Although alopecia areata can be treated, no definitive cure is known. Spontaneous remission occurs in approximately 8% to 68% of cases, with the higher remission rates occurring when <25% of the scalp is involved.10 Treatment can often help with hair regrowth and prevent further hair loss.10 Initial treatment may involve topical or intralesional corticosteroids, with the former often preferred for pediatric patients who may not tolerate injections.10 Minoxidil foam or solution is sometimes added as adjuvant therapy. Short, 6-week courses of oral corticosteroids can also be effective for hair regrowth; however, the risk of relapse is high, and long-term use is not advised given the associated side effects. Other treatments including methotrexate and topical immunotherapy, such as diphenylcyclopropenone and squaric acid dibutylester, may be considered in refractory cases.9 New therapies including Janus kinase inhibitors such as tofacitinib, ruxolitinib, and baricitinib are currently under investigation.10 With continued development and study of new treatment options for alopecia areata, it is hoped that more effective hair regrowth and sustained disease control will be attainable.
Our patient was treated with intralesional triamcinolone acetonide (5 mg/mL x 1 cc). At his return visit 6 weeks later, he was noted to have significant hair regrowth and was happy with the results.
Maya Firsowicz, BS, is a medical student; Michelle Eugene Lee, BS, is a medical student; and Christopher Rizk, MD, is a dermatology fellow at Baylor College of Medicine, in Houston, Texas.
- Safavi K. Prevalence of alopecia areata in the First National Health and Nutrition Examination Survey. Arch Dermatol. 1992;128(5):702.
- Mirzoyev SA, Schrum AG, Davis MDP, Torgerson RR. Lifetime incidence risk of alopecia areata estimated at 2.1% by Rochester Epidemiology Project, 1990–2009. J Invest Dermatol. 2014;134(4):1141-1142.
- Fricke ACV, Miteva M. Epidemiology and burden of alopecia areata: a systematic review. Clin Cosmet Investig Dermatol. 2015;8:397-403.
- Finner AM. Alopecia areata: clinical presentation, diagnosis, and unusual cases. Dermatol Ther. 2011;24(3):348-354.
- Peckham SJ, Sloan SB, Elston DM. Histologic features of alopecia areata other than peribulbar lymphocytic infiltrates. J Am Acad Dermatol. 2011;65(3):615-620.
- Gilhar A, Etzioni A, Paus R. Alopecia areata. N Engl J Med. 2012;366(16):1515-1525.
- Goh C, Finkel M, Christos PJ, Sinha AA. Profile of 513 patients with alopecia areata: associations of disease subtypes with atopy, autoimmune disease and positive family history. J Eur Acad Dermatol Venereol. 2006;20(9):1055-1060.
- Alkhalifah A, Alsantali A, Wang E, McElwee KJ, Shapiro J. Alopecia areata update: part I. Clinical picture, histopathology, and pathogenesis. J Am Acad Dermatol. 2010;62(2):177-188.
- Kassira S, Korta DZ, Chapman LW, Dann F. Review of treatment for alopecia totalis and alopecia universalis. Int J Dermatol. 2017;56(8):801-810.
- Strazulla LC, Wang EHC, Avila L, et al. Alopecia areata: an appraisal of new treatment approaches and overview of current therapies. J Am Acad Dermatol. 2018;78(1):15-24.