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 Table of Contents  
CASE REPORT
Year : 2013  |  Volume : 5  |  Issue : 1  |  Page : 50-52  

Colocalization of vitiligo and alopecia areata: Coincidence or consequence?


Department of Dermatology, GGS Medical College, Faridkot, Punjab, India

Date of Web Publication6-Jul-2013

Correspondence Address:
Jyotisterna Mittal
102, Good Earth Colony, B/s New Moti Palace, Patiala, Punjab - 147 001
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-7753.114705

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   Abstract 

Both alopecia areata (AA) and vitiligo are autoimmune diseases, and their coexistence in the same patient is not uncommon, as vitiligo has been reported to occur in 4.1% of patients of AA. We present a case of a 15-year-old male child who had vitiligo and later developed AA over the existing lesions of vitiligo over face and scalp and have attempted to elucidate the current understanding of mechanisms of coexistence of these two diseases.Our case lends support to the hypothesis that AA and vitiligo share a common pathogenic pathway including autoimmune response against some common antigens like those derived from the bulb melanocytes. Stimulation of proinflammatory T-helper(Th)-1 cell mediated immunological response or inactivation of a suppressor T-cell mediated response could be the common underlying phenomenon. However, the striking rarity of colocalization of these two diseases has led to the recent debate over current understanding of their pathogenesis, and whether this association is merely a coincidence.As both AA and vitiligo are frequent and chronic dermatological disorders, it is of utmost importance to gain more understanding into their pathogenic mechanisms so that more definitive treatment modalities may be devised and the quality of life of these patients can be improved.

Keywords: Alopecia areata, colocalization, vitiligo


How to cite this article:
Kumar S, Mittal J, Mahajan B B. Colocalization of vitiligo and alopecia areata: Coincidence or consequence?. Int J Trichol 2013;5:50-2

How to cite this URL:
Kumar S, Mittal J, Mahajan B B. Colocalization of vitiligo and alopecia areata: Coincidence or consequence?. Int J Trichol [serial online] 2013 [cited 2019 Dec 12];5:50-2. Available from: http://www.ijtrichology.com/text.asp?2013/5/1/50/114705


   Introduction Top


Both alopecia areata (AA) and vitiligo are autoimmune diseases, and their coexistence in the same patient is not uncommon, as vitiligo has been reported to occur in 4.1% of patients of AA and is about 4 times more common in patients with AA than in the general population. [1] However, their colocalization over the same site is exceedingly rare, with less than five cases being reported in the literature. [2],[3],[4] We present a case of a 15-year-old male child who had vitiligo and later developed AA over the existing lesions of vitiligo over face and scalp and have attempted to elucidate the current understanding of mechanisms of coexistence of these two diseases.


   Case Report Top


A 12-year-old boy presented to the skin outpatient department with history of depigmented areas on the scalp, face, neck, arms and legs for 5 years. He also gave a history of development of patchy loss of hair over some of these lesions for 3 years. There was no previous history of any trauma or medications. Family history was not relevant. On examination, there were depigmented macules over the scalp, forehead, eyebrows, periorbital, perioral, preauricular regions, neck, elbows, hands, feet, shins, nose, chin, hands, knees and feet [Figure 1] and [Figure 2]. Patches of hair loss were seen, limited to some of these depigmented areas over the vertex and occipital region of the scalp and eyebrows [Figure 3]. Other body areas were not affected by patchy hair loss. Clinically, the diagnosis of vitiligo with AA was made. On histopathological examination [Figure 4] of the skin biopsy specimen obtained from the scalp, dense peribulbar infiltrate was seen in the dermis. Other features were in keeping with the diagnosis of AA. Additionally, the basal layer of the epidermis was almost devoid of pigment, [Figure 5] confirming the diagnosis of vitiligo over the same site.
Figure 1: Depigmented macules over the scalps forehead, eyebrows, periorbital, perioral, preauricular regions, nose and chin

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Figure 2: Depigmented macules over the hands and feet

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Figure 3: Patches of alopecia over some of the depigmented areas over the scalp

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Figure 4: Histopathological examination of scalp biopsy: Dense peribulbar infiltrate in dermis and other features in keeping with the diagnosis of alopecia areata

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Figure 5: Basal layer of the epidermis over the same site is almost devoid of pigment, confirming the diagnosis of vitiligo

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   Discussion Top


AA is a non-scarring, autoimmune, inflammatory hair loss on the scalp, and/or body. Both AA and vitiligo are clubbed under the spectrum of autoimmune disorders. This is evidenced by the presence of antibodies in both these diseases and their frequent association with other autoimmune disorders, such as thyroid diseases, diabetes mellitus, bullous pemphigoid, pemphigus vulgaris, lichen planus or pernicious anemia etc. [1],[5] In case of AA, the autoreactive T-lymphocytes are predominantly present in the peribulbous inflammatory infiltrate and are directed against an unknown antigen of the hair follicle. [6] Some common factors that appear to be implicated in the etiopathogenesis of both these diseases are autoimmunity, genetic pre-disposition, environmental factors, and emotional or physical stress.

Our case lends support to the hypothesis that AA and vitiligo share a common pathogenic pathway including autoimmune response against some common antigens like those derived from the bulb melanocytes. Melanocytes-derived peptide antigens released during vitiligo pathogenesis could act as auto-antigens not only for vitiligo, but also for AA, and autoimmune Th-cells against them could also trigger a response against the hair follicle melanocytes, thus, pre-disposing to AA. This is evidenced immunohistologically by the findings of helper T-lymphocytes and antibodies against abnormal hair bulb melanocytes in both these diseases. [7],[8],[9] This hypothesis is also supported by the chronological order of vitiligo followed by AA in this patient.

Thus, stimulation of proinflammatory Th-1 cell mediated immunological response or inactivation of a suppressor T-cell mediated response could be the common underlying phenomenon. Moreover, the frequent clinical observation that after AA, the regrown hair is initially white in color may also be due to the coexistent damage to the hair follicle melanocytes in AA. [9] During recovery from vitiligo, pigmentation process starts from follicular and perifollicular region. This is evidence suggesting the common pathogenic processes involved in these two diseases. [10]

However, the colocalization of these two autoimmune diseases is strikingly rare. This has led to the recent debate over the current understanding of their pathogenesis, and whether this association is merely a coincidence. [4] According to the "mosaic of autoimmunity" theory, autoimmune diseases are a result of the complex interplay of various factors like immunological, genetic, hormonal and environmental. This multifactorial etiology brings about diversity in the clinical presentation of autoimmune diseases and may be the cause of rarity of colocalization of these two diseases inspite of some common processes involved in their etiopathogenesis. [11]

Another difference in these two diseases lies in the site of the target melanocytes. While the populations of melanocytes targeted by the autoimmune T-lymphocytes in AA are present in the hair bulb, in case of vitiligo the epidermal melanocytes are involved. Antigenic differences also exist in these two melanocytes populations. [12] These factors may be the cause of the very low incidence of the colocalization of these two diseases even though the common pathogenic mechanisms would suggest otherwise.


   Conclusion Top


As both AA and vitiligo are frequent and chronic dermatological disorders, it is of utmost importance to gain more understanding into their pathogenic mechanisms so that more definitive treatment modalities may be devised and the quality of life of these patients can be improved.

 
   References Top

1.Muller SA, Winkelmann RK. Alopecia areata. An evaluation of 736 patients. Arch Dermatol 1963;88:290-7.  Back to cited text no. 1
    
2.Dhar S, Kanwar AJ. Colocalization of vitiligo and alopecia areata. Pediatr Dermatol 1994;11:85-6.  Back to cited text no. 2
    
3.Adams BB, Lucky AW. Colocalization of alopecia areata and vitiligo. Pediatr Dermatol 1999;16:364-6.  Back to cited text no. 3
    
4.Ramot Y, Thomaidou E, Mali A, Zlotogorski A. An extraordinary colocalization of alopecia areata and vitiligo. Int J Trichology 2010; 2:108-9.  Back to cited text no. 4
    
5.Brenner W, Diem E, Gschnait F. Coincidence of vitiligo, alopecia areata, onychodystrophy, localized scleroderma and lichen planus. Dermatologica 1979;159:356-60.  Back to cited text no. 5
    
6.Hordinsky M, Ericson M. Autoimmunity: Alopecia areata. J Investig Dermatol Symp Proc 2004;9:73-8.  Back to cited text no. 6
    
7.Boissy RE, Spritz RA. Frontiers and controversies in the pathobiology of vitiligo: Separating the wheat from the chaff. Exp Dermatol 2009; 18: 583-5.  Back to cited text no. 7
    
8.Kalish RS, Gilhar A. Alopecia areata: Autoimmunity-The evidence is compelling. J Investig Dermatol Symp Proc 2003; 8: 164-7.  Back to cited text no. 8
    
9.Tobin DJ, Fenton DA, Kendall MD. Ultrastructural observations on the hair bulb melanocytes and melanosomes in acute alopecia areata. J Invest Dermatol 1990; 94: 803-7.  Back to cited text no. 9
    
10.Falabella R, Barona MI. Update on skin repigmentation therapies in vitiligo. Pigment Cell Melanoma Res 2009; 22: 42-65.  Back to cited text no. 10
    
11.Brickman CM, Shoenfeld Y. The mosaic of autoimmunity. Scand J Clin Lab Invest Suppl 2001; 235: 3-15.  Back to cited text no. 11
    
12.Tobin DJ, Bystryn JC. Different populations of melanocytes are present in hair follicles and epidermis. Pigment Cell Res 1996; 9: 304-10.  Back to cited text no. 12
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]


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