Alopecia Areata


Alopecia Areata

Primary Care Visit Report   

 A 45-year-old female with past history of scleroderma, autoimmune thyroiditis, and rheumatoid arthritis presented with two patches of  hair loss   on her scalp. The patient noticed an area with complete hair loss on the right side of her scalp which was small initially and gradually grew larger over the 10 days preceding her visit. She had also noticed a second  bald patch   forming in an adjacent area of the scalp. The patient reported a “prickly” feeling in the areas of hair loss. 

 Vitals were  normal  . On exam, there was a 5 cm × 3 cm area of alopecia in the right parietal scalp and a 3 cm × 1.5 cm area of alopecia in the superior occiput. The central area of alopecia patches had scant hair or hair follicles visible. Thinning hair was present at the periphery of the alopecia patches. 

 Given the patient’s history of multiple  autoimmune diseases  , she was referred to a dermatologist for biopsy and treatment of the alopecia. 

     Differential Dx   

    Alopecia areata  

   Telogen effl uvium    

  Tinea capitis  


  Traction alopecia     

     Favored Dx   

 Sudden onset  hair loss   in a middle-aged woman accompanied by additional autoim-mune pathology is consistent with a diagnosis of alopecia areata.  


  Alopecia areata (AA)   is an autoimmune  disease   marked by sudden onset, non- scarring hair loss. The condition results from damage to hair follicles in the anagen (growth) phase, driven by autoreactive CD8+ T-cells, that disrupts the normal  hair cycle   [ 1 ,  2 ]. Normal  hair follicle  s go through periods of active hair growth (anagen), then follicular involution (catagen), and then rest (telogen). In AA, the peribulbar follicular infl ammation causes the actively growing hair follicle to prematurely tran-sition into catagen and telogen phases thus resulting in lack of hair growth/ hair loss  . 

 The etiology of AA is multifactorial, and involves genetic and environmental fac-tors. The concordance rate in monozygotic twins is about 55 % [ 2 ]. There is family 

history of AA ranging in 10–42 % of cases, and that estimate is higher for early- onset AA [ 3 ]. AA is thought to be polygenic, and the involved gene loci may be located on chromosome 21, as there is an association with Down syndrome (trisomy 21) [ 3 ,  4 ]. The frequency of AA is equivalent across genders, and it can occur at any age, although it is more common in younger ages [ 3 ,  4 ]. The prevalence of the disease is about 0.2 %, and there is a 2 % lifetime risk of developing AA at some point [ 3 – 5 ]. AA is the most common cause of hair loss in childhood. 

 Alopecia areata is associated with a number of concomitant  autoimmune  diseases  , including  Hashimoto’s thyroiditis  , Grave’s disease, Addison’s, pernicious anemia, insulin-dependent diabetes mellitus, vitiligo, atopic diseases (including asthma, allergic rhinitis, and atopic dermatitis), and celiac disease [ 2 ,  3 ,  5 ]. The most common association is with Hashimoto’s thyroiditis, although the minority of AA cases present with additional autoimmune disorders [ 3 – 5 ]. AA is also a com-mon fi nding in  vitamin-D   defi cient individuals [ 6 ,  7 ]. AA is organ-specifi c and lim-its its effects to the hair follicle, and sometimes the nails. Alopecia totalis is full loss of scalp hair, and it occurs in 5 % of individuals suffering from AA. Total body  hair loss  , or alopecia universalis, occurs in 1 % of AA patients at some point in the course of their disease [ 3 ]. Although the condition tends to be chronic, hair follicles are not permanently damaged, and hair regrowth is possible [ 2 ].  


 Alopecia areata typically presents as asymptomatic, suddenonset  hair loss  , most commonly on the scalp, beard, and eyebrows. The hair loss occurs in well circumscribed round or oval patches. Sometimes patients describe stressful life events prior to onset [ 2 ]. A common characteristic of AA is the presence of “excla-mation point” hairs, also called  point noir hairs, which appear as black dots within the patch. The black dots represent hairs that were broken before exiting the follicle, and are subsequently pushed out. 

 In many cases AA presents with nail fi ndings. Nail fi ndings may precede, appear with, or follow AA onset. Typical nail fi ndings are small pits or indentations, red spots on the lunulae, and/or vertical ridges. Nail abnormalities are associated with more widespread AA [ 4 ].  


 The presence of characteristic AA features of well-circumscribed  bald patches  ,  excla-mation point hairs  , and nail fi ndings in the physical examination are usually suffi cient to make a diagnosis. Positive family history would further support a diagnosis. There are no blood tests to confi rm or rule out AA; however, if there is evidence to support a thyroid disorder (e.g., positive family history, exam fi ndings),  TSH   and  ANA tests   

would be relevant. A  biopsy   may be done if the diagnosis is unclear. Expected fi ndings would be lymphocytic infi ltrates surrounding the hair follicles, and a marked increase in catagen and telophase hair follicles [ 3 ].  


 There is no cure for  AA  , and there is very little evidence-based guidance to help determine appropriate treatment [ 2 ,  3 ]. Treatment should be determined by disease extent, duration, and activity, as well as the potential distress it can cause to patients. In some cases, treatment may not be necessary, as 50 % of patients with limited disease lasting less than a year may experience spontaneous regrowth [ 8 ]. However, AA can have devastating psychological effects on patients, and they will likely  prefer treatment. Part of the treatment discussion should include setting patient expectations, as treatment does not always work, and several studies defi ne treat-ment success as >50 % hair regrowth [ 9 ]. There are numerous available treatment approaches, including topical, intralesional, and systemic  corticosteroids  , topical  immunomodulators  , biologics, minoxidil, anthralin, and photochemotherapy. First line treatments are topical and intralesional corticosteroids. 

 Super potent (class I) and potent (class II)  corticosteroids   have demonstrated success in treating mild AA [ 8 ,  9 ]. Multiple formulations (cream, lotion, ointment, foam, solution) are available, but one study indicated foam had superior therapeutic effects [ 8 ,  10 ]. Additionally, topical corticosteroids may be more effective when treatment occurs under occlusion [ 3 ,  11 ]. Clobetasol propionate 0.05 % (Class I) or betamethasone valerate 0.1 % foam (Class III) may be applied twice daily, or once nightly under occlusion of plastic wrap. In areas of the body that are diffi cult to wrap, for example the scalp, an adhesive like a bandaid or fabric tape may be used. This should occur on a discontinuous schedule to avoid extensive local skin atrophy, for example on 5 days per week for 4–6 months, depending on improvement. An alternative schedule is twice daily application for 2 weeks, followed by 2 weeks without treatment, for 4–6 months. One study found that  Pacrolimus   1 % had equiv-alent effi cacy as clobetasol 0.05 %, with fewer side effects [ 8 ]. Hair regrowth may be observed within anywhere from 6 to 24 weeks. 

  Intralesional corticosteroid         injections are  fi rst-line therapy   for mild to moderate AA, with less than 50 % involvement [ 3 ]. It would not be appropriate treatment for individuals with alopecia totalis. Injections are administered at a concentration of 5–10 mg/cc and may help achieve local regrowth within 4–8 weeks [ 3 ]. Injections are administered every 4–6 weeks; however, many patients experience reversible atrophy of adjacent subcutaneous fat, which presents as dents in the skin at the injection sites. Repeated injections on the same sites may lead to permanent skin atrophy [ 4 ]. If no improvement is noted after four treatments, alternative approaches should be investigated.   Patients who do not respond to topical or  intralesional corticosteroids      may be referred to dermatology. Extensive disease, and patients with alopecia totalis or alopecia universalis should also be referred to a specialist, where alternate therapies may be explored.  


 The clinical course of AA is variable and unpredictable. Most of the treatment studies have evaluated short-term outcomes, and those who studied outcomes beyond 6 months indicated that treatment does not infl uence the long-term prognosis of dis-ease [ 9 ]. For patients with limited, patchy disease, the prognosis is better, and hair often spontaneously regrows. Increased severity, alopecia totalis, and alopecia uni-versalis are associated with poorer prognosis [ 3 ,  4 ]. Overall, 25 % of patients with AA experience a single event of  hair loss   [ 3 ]. For most patients; however, it is a chronic, relapsing condition.   

Questions for the Dermatologist 

When you do bloodwork to rule out autoimmune systemic disorders and you find nothing abnormal, do you then just assume the AA is idiopathic? Or should the patient continue to have their blood checked for some time period afterwards?

If there are no abnormal fi ndings in the blood work, you would assume the condition is idiopathic. If the TSH and ANA tests were negative and there are no interesting fi ndings in a review of systems, there is no need to redo blood tests. If there are additional symptoms to support presence of an autoimmune disorder, it would be worthwhile to order tests again.

– If the patient is found to have autoimmune thyroiditis, is it necessary for that to get treated/controlled before the hair will grow back?

No, treatment of any concomitant autoimmune disorder would not affect AA. AA has a higher prevalence in autoimmune and thyroid conditions. However, presence of Hashimoto’s thyroiditis , for example, is only indicative of a propensity for autoimmune disorders generally.

– Do any of the treatments (e.g., intralesional steroid injections and topical steroids) work any better than doing nothing and seeing if the hair grows back on its own?

Yes, treatments have better results than no intervention. Intralesional steroid injections and topical steroids have double-blinded, placebo-controlled studies indicating benefi ts over no treatment. They can grow hair back faster, or make hair loss slower.

–  When the hair grows back, does it grow back with normal thickness and color, or does it grow back thinner?  

 The hair often grows back thinner, or as short, fi ne vellus hair to begin with. The hair may be white initially but it will eventually repigment and become thicker. 

–  If alopecia areata recurs, is it usually in the same spot as the fi rst time? If it does occur in the same spot, does that make it less likely the hair will grow back?  

 AA can appear anywhere on the body, including the beard in men, regardless of where the fi rst patch occurred. Even if it recurs in the same spot, responders to therapy in the fi rst go-round are more likely to respond to subsequent treatment.     


 1.   Xing L, Dai Z, Jabbari A, Cerise JE, Higgins CA, Gong W, de Jong A, Harel S, DeStefano GM, Rothman L, Singh P, Petukhova L, Mackay-Wiggan J, Christiano AM, Clynes R. Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition. Nat Med. 2014;20(9):1043–9.

 2.    Hordinsky MK. Overview of alopecia areata. J Investig Dermatol Symp Proc. 2013;16(1): S13–5.

 3.    Otberg N, Shapiro J. Chapter 88. Hair growth disorders. In: Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K, editors. Fitzpatrick’s dermatology in general medicine. 8th ed. New York: McGraw-Hill; 2012. Available from:    . Accessed 23 Mar 2015.

 4.    Freyschmidt-Paul P, McElwee K, Hoffmann R. Alopecia areata. In: Hertl M, editor. Autoimmune diseases of the skin: pathogenesis, diagnosis, management. 3rd ed. New York: Springer; 2011. p. 463–96.

 5.   Lyakhovitsky A, Shemer A, Amichai B. Increased prevalence of thyroid disorders in patients with new onset alopecia areata. Australas J Dermatol. 2014. doi:  10.1111/ajd.12178    .  

 6.   Mahamid M, Abu-Elhija O, Samamra M, Mahamid A, Nseir W. Association between vitamin D levels and alopecia areata. Isr Med Assoc J. 2014;16(6):367–70.

 7.   Kim DH, Lee JW, Kim IS, Choi SY, Lim YY, Kim HM, Kim BJ, Kim MN. Successful treat-ment of alopecia areata with topical calcipotriol. Ann Dermatol. 2012;24(3):341–4.

 8.    Hordinsky M, Donati A. Alopecia areata: an evidence-based treatment update. Am J Clin Dermatol. 2014;15(3):231–46.

 9.   Delamere FM, Sladden MM, Dobbins HM, Leonardi-Bee J. Interventions for alopecia areata. Cochrane Database Syst Rev. 2008;2, CD004413.

    10.    Tosti A, Iorizzo M, Botta GL, Milani M. Effi cacy and safety of a new clobetasol propionate 0.05% foam in alopecia areata: a randomized, double-blind placebo-controlled trial. J Eur Acad Dermatol Venereol. 2006;20(10):1243–7.

    11.   Tosti A, Piraccini BM, Pazzaglia M, Vincenzi C. Clobetasol propionate 0.05% under occlusion in the treatment of alopecia totalis/universalis. J Am Acad Dermatol. 2003;49(1):96–8.

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