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CASE REPORT
Year : 2018  |  Volume : 19  |  Issue : 2  |  Page : 157-160

Co-occurrence of psoriasis, vitiligo, and lichen planus in a single patient


1 Department of Dermatology, Venereology and Leprosy, Bhaskar Medical College, Dr. NTR University of Health Sciences, Vijayawada, Andhra Pradesh, India
2 Department of Pathology, Bhaskar Medical College, Dr. NTR University of Health Sciences, Vijayawada, Andhra Pradesh, India

Date of Web Publication26-Mar-2018

Correspondence Address:
Swathi Neelagiri
Bhaskar Medical College, Dr. NTR University of Health Sciences, Vijayawada, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijpd.IJPD_127_16

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  Abstract 


Psoriasis is a common autoimmune skin disease affecting around 2%–3% of the world population. The disease has an autoimmune and complex genetic background. It may be associated with other autoimmune diseases such as vitiligo, lichen planus, discoid lupus erythematosus, and alopecia areata as reviewed in the literature. There are few case reports about the co-occurrence of one or two autoimmune diseases. Many speculations have been put forward about the pathogenesis of these conditions, but T-cell-mediated autoimmunity and true Koebner phenomenon background play a common etiological cause of co-occurrence of psoriasis, lichen planus, and vitiligo. We report a 9-year-old female patient who presented with psoriasis, lichen planus, and vitiligo lesions. Interestingly, she developed psoriatic plaques on the vitiligo patches in the knee. Histopathological diagnosis was consistent with the concurrence of psoriasis, lichen planus, and vitiligo.

Keywords: Autoimmunity, co-occurrence, Koebner phenomenon, lichen planus, psoriasis, vitiligo


How to cite this article:
Neelagiri S, Janardhan B, Rami Reddy K S, Sreedhar V. Co-occurrence of psoriasis, vitiligo, and lichen planus in a single patient. Indian J Paediatr Dermatol 2018;19:157-60

How to cite this URL:
Neelagiri S, Janardhan B, Rami Reddy K S, Sreedhar V. Co-occurrence of psoriasis, vitiligo, and lichen planus in a single patient. Indian J Paediatr Dermatol [serial online] 2018 [cited 2019 Dec 7];19:157-60. Available from: http://www.ijpd.in/text.asp?2018/19/2/157/206060




  Introduction Top


Psoriasis, lichen planus, and vitiligo are common skin problems affecting around 2–3%, 1% and 0.1%–2%, respectively, of the world population. Many speculations have been put forward about the pathogenesis of these conditions, but T-cell-mediated autoimmunity and true Koebner phenomenon background play a common etiological role. The literature has been reviewed about the cohabitation of vitiligo and lichen planus [1],[2] and coexistence of vitiligo and psoriasis,[2],[3],[4] but the association of these three conditions together has been found in our patient.


  Case Report Top


A 9-year-old female patient, who was accompanied by her mother, presented with raised, reddish skin lesions over the left forearm for 2 years, associated with itching and exacerbation in winters. After 1 year, the patient had an injury over the right knee, which healed with white patches. Since then, similar white- and light brown-colored patches appeared on the right side of the body at different sites, involving leg, thigh, mons pubis, and trunk within a period of 8 months. For 6 months, the patient has developed raised purple-colored lesions over both legs, left knee, thighs, and trunk which is associated with itching. Recently, for the past 3 months, the patient has been developing reddish lesions on the white patches present over the injured site on the right knee, which are similar in morphology to the lesions on the left forearm. There was no history of fever, sore throat, jaundice, or arthralgia.

The systemic examination was normal. On cutaneous examination, multiple well-defined, bilaterally asymmetrical erythematous plaques of size varying approximately from 1 cm × 2 cm to 6 cm × 4 cm with silvery-white scales present over the extensor aspects of the left forearm and right knee [Figure 1] and [Figure 2]. Woronoff's ring was seen on the left forearm plaque, and the Auspitz sign was positive. Multiple unilaterally, well-defined to ill-defined depigmented and hypopigmented patches of size varying from approximately 0.5 cm × 2 cm to 5 cm × 6 cm with leukotrichia were present over the right side of the body, without crossing the midline [Figure 2] and [Figure 3]. Koebnerization is present. Multiple well-defined violaceous, flat-topped, papules and plaques present over the dorsal aspect of both feet, anterior and posterior aspect of both legs and thighs. Similar lesions are seen over the abdomen and upper chest. [Figure 3]. Wickham's striae were seen. Scalp, nails, and oral and genital mucous are normal.
Figure 1: Erythematous plaque with scaling on the left forearm

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Figure 2: Colocalization of psoriasis and vitiligo

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Figure 3: Co-occurrence of psoriasis, vitiligo, and lichen planus

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In Wood's lamp examination, accentuation was seen at the margins of depigmented patches. All relevant investigations, including antistreptolysin O titers, thyroid function test, anti-hepatitis C virus (HCV), venereal disease research laboratory, hepatitis B surface antigen, and HIV, were done and are within normal limits. A skin biopsy was taken from colocalized erythematous plaque and depigmented patch and from violaceous papule. Histopathological examination (HPE) from erythematous plaque revealed acanthosis, parakeratosis, Munro's microabscesses, elongation of the rete ridges and suprapapillary thinning of the epidermis, which are features suggestive of psoriasis; and HPE from the depigmented patch revealed total loss of melanocytes in the basal layer, confirmed by S-100 protein stain which was negative, suggestive of vitiligo [Figure 4] and [Figure 5]. Histopathology of violaceous papule revealed orthokeratosis, sawtooth rete ridges, vacuolar alteration in the basal layer, and band-like lymphocytic infiltrate which are features suggestive of lichen planus [Figure 6]. The patient was treated with emollients, topical corticosteroids, and narrowband ultraviolet B phototherapy.
Figure 4: High power (×40): Acanthosis, parakeratosis, Munro's microabscesses, elongation of the rete ridges, and suprapapillary thinning of the epidermis

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Figure 5: High power (×40): S-100 protein and immunoperoxidase stain is negative, confirms loss of melanocytes

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Figure 6: High power (×40): Orthokeratosis, Sawtooth rete ridges, band-like lymphocytic infiltrate, vacuolar alteration of the basal layer

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  Discussion Top


Psoriasis, lichen planus, and vitiligo are common dermatological problems in the general population.

Psoriasis is a common inflammatory skin disease characterized by T-cell-mediated hyperproliferation of keratinocytes. It has been reported to begin in children before the age of 16 years in 25%–45% of patients, in 10% before the age of 10 years, and at 2% before the age of 2 years. Despite the advances in the last decades, the cause of psoriasis is still unknown. Recent data strongly indicate that human leukocyte antigen (HLA)-Cw0602 is the susceptible allele in this locus.[5] Three antimicrobial peptides and proteins, namely, cathelicidin, s100 protein, and defensins modulate and trigger host immune response in psoriasis acting as interplay between innate and adaptive immune mechanisms.[6] T-helper (Th) 17/interleukin (IL-23) pathway and IL-22 have been found to play a prominent role in psoriasis pathogenesis.[7]

Vitiligo is an acquired disease characterized by the development of depigmented areas of skin and substantial loss of functioning epidermal and/or hair follicle melanocytes. Many studies report that most cases of vitiligo are acquired, but the exact prevalence in pediatric age group is unknown. Howitz et al. in Denmark found that approximately 25% of patients noted the onset of vitiligo before the age of 10 years.[8] With recent advances, dendritic cells and Langerhans cells secrete IL-1β and IL-18 through the increased expression of NLRP-1 inflammasome mediated through caspase-1. IL-17 cells induced by IL-1β have been detected in increased numbers in serum of patients with vitiligo. These changes induce a proinflammatory state in vitiligo.[9],[10] Regulatory T-cells are reduced in number and have less ability to suppress CD8+ cells.[11] The damage-associated molecular patterns (DAMPs) provide the initiating danger signal in vitiligo.[12]

While lichen planus most commonly presents in middle-aged adults, childhood presentations are well described. It has been hypothesized that the external factors such as stress, anxiety, HCV infection, hypothyroidism, Helicobacter pylori infections, and drugs (beta-blockers and lithium) have been implicated. Although the exact etiology of lichen planus is unknown, genetic linkage studies have been established HLA association between familial lichen planus and HLA-B7.[13] HLA-DR1 seems to be frequently associated with cutaneous lichen planus regardless of ethnicity. Recently, Danielsson et al. demonstrated increased expression of cyclooxygenase-2, a biomarker for autoimmunity in patients with oral lichen planus, suggesting an autoimmune pathogenesis.[14] More recently, numerous cytokines such as interferon-γ, tumor necrosis factor alpha (TNF-α), IL-1α, IL-6, and IL-22 associated with Th cell response have been implicated to have a role in the pathogenesis.[15] Levels of IL-31 which is believed to have a role in T-cell-mediated itch is seen to be elevated in lesions of lichen planus.

Although the pathogenesis of the colocalization between these two diseases, psoriasis and vitiligo, are still not well understood, Sandhu et al.[4] reported no increased incidence of concurrence and they regarded it as a simple coincidence. Until now, cytokines, autoimmunity, the Koebner phenomenon, or decreased melanocytes have been studied as the pathogenic factors for each disease. One of the hypotheses connecting these three diseases is increasing in the production of proinflammatory molecules such as IL-1, IL-6 and IL-8, TNF-α, nuclear factor-β, and vasoactive intestinal peptides.

In conclusion, we report the co-occurrence of these three diseases, psoriasis, lichen planus, and vitiligo, occurring in a single patient by the common etiological background of autoimmunity and Koebner phenomenon.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Sardana K, Sharma RC, Koranne RV, Mahajan S. An interesting case of colocalization of segmental lichen planus and vitiligo in a 14-year-old boy. Int J Dermatol 2002;41:508-9.  Back to cited text no. 1
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2.
Ujiie H, Sawamura D, Shimizu H. Development of lichen planus and psoriasis on lesions of vitiligo vulgaris. Clin Exp Dermatol 2006;31:375-7.  Back to cited text no. 2
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Berger TG, Kiesewetter F, Maczek C, Bauer N, Lueftl M, Schuler G, et al. Psoriasis confined strictly to vitiligo areas – A Koebner-like phenomenon? J Eur Acad Dermatol Venereol 2006;20:178-83.  Back to cited text no. 3
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Sandhu K, Kaur I, Kumar B. Psoriasis and vitiligo. J Am Acad Dermatol 2004;51:149-50.  Back to cited text no. 4
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Gudjónsson JE, Kárason A, Antonsdóttir AA, Rúnarsdóttir EH, Gulcher JR, Stefánsson K, et al. HLA-Cw6-positive and HLA-Cw6-negative patients with psoriasis vulgaris have distinct clinical features. J Invest Dermatol 2002;118:362-5.  Back to cited text no. 5
    
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Batycka-Baran A, Maj J, Wolf R, Szepietowski JC. The new insight into the role of antimicrobial proteins-alarmins in the immunopathogenesis of psoriasis. J Immunol Res 2014;2014:628289.  Back to cited text no. 6
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Hao JQ. Targeting interleukin-22 in psoriasis. Inflammation 2014;37:94-9.  Back to cited text no. 7
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Howitz J, Brodthagen H, Schwartz M, Thomsen K. Prevalence of vitiligo. Epidemiological survey on the Isle of Bornholm, Denmark. Arch Dermatol 1977;113:47-52.  Back to cited text no. 8
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Wang CQ, Cruz-Inigo AE, Fuentes-Duculan J, Moussai D, Gulati N, Sullivan-Whalen M, et al. Th17 cells and activated dendritic cells are increased in vitiligo lesions. PLoS One 2011;6:e18907.  Back to cited text no. 9
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Khan R, Gupta S, Sharma A. Circulatory levels of T-cell cytokines (interleukin [IL]-2, IL-4, IL-17, and transforming growth factor-ß) in patients with vitiligo. J Am Acad Dermatol 2012;66:510-1.  Back to cited text no. 10
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Ben Ahmed M, Zaraa I, Rekik R, Elbeldi-Ferchiou A, Kourda N, Belhadj Hmida N, et al. Functional defects of peripheral regulatory T lymphocytes in patients with progressive vitiligo. Pigment Cell Melanoma Res 2012;25:99-109.  Back to cited text no. 11
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Mosenson JA, Zloza A, Klarquist J, Barfuss AJ, Guevara-Patino JA, Poole IC. HSP70i is a critical component of the immune response leading to vitiligo. Pigment Cell Melanoma Res 2012;25:88-98.  Back to cited text no. 12
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Copeman PW, Tan RS, Timlin D, Samman PD. Familial lichen planus. Another disease or a distinct people? Br J Dermatol 1978;98:573-7.  Back to cited text no. 13
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14.
Danielsson K, Ebrahimi M, Wahlin YB, Nylander K, Boldrup L. Increased levels of COX-2 in oral lichen planus supports an autoimmune cause of the disease. J Eur Acad Dermatol Venereol 2012;26:1415-9.  Back to cited text no. 14
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Chen J, Feng J, Chen X, Xu H, Zhou Z, Shen X, et al. Immunoexpression of interleukin-22 and interleukin-23 in oral and cutaneous lichen planus lesions: A preliminary study. Mediators Inflamm 2013;2013:801974.  Back to cited text no. 15
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]



 

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