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Year : 2001  |  Volume : 67  |  Issue : 4  |  Page : 214-215

Vitiligo and psoriasis: Coexistence with colocalization

Department of Dermatology, Venereology & Leprosy BLDEA's SBMP Medical College, Bijapur - 586 103, India

Correspondence Address:
Department of Dermatology, Venereology & Leprosy BLDEA's SBMP Medical College, Bijapur - 586 103, India


A 20-year-old male patient with vitiligo who developed psoriasis is reported here. There was co-existence of both diseases and co-habitation lesions at places. Clinical heterogenicity of both diseases and new conclusions are discussed.

How to cite this article:
Inamadar AC, Sampagavi V V, Athanikar S B, Patil M N, Deshmukh N S. Vitiligo and psoriasis: Coexistence with colocalization. Indian J Dermatol Venereol Leprol 2001;67:214-5

How to cite this URL:
Inamadar AC, Sampagavi V V, Athanikar S B, Patil M N, Deshmukh N S. Vitiligo and psoriasis: Coexistence with colocalization. Indian J Dermatol Venereol Leprol [serial online] 2001 [cited 2020 Dec 5];67:214-5. Available from:

   Introduction Top

Vitiligo has been associated with many conditions.[1] Anatomical co-habitation of psoriasis and vitiligo has been reported.[2],[3] A case of long standing vitiligo, developing psoriasis, with few co-habitation lesions and new conclusions are reported herein.

   Case Report Top

A 20-year-old male was on PUVA therapy for vitiligo vulgaris since one year. Patient noticed red, scaly elevated skin lesions for the past 2 months. Cutaneous examination revealed well defined, erythematous papules and plaques with silvery white scales over scalp and extremities. At places there was co-habitation of psoriatic lesions over vitiligo patches [Figure - 1]. Auspitz sign was positive. A clinical diagnosis of coexistent vitiligo and psoriasis was made. Skin biopsy was done from colocalized lesion. HPE revealed hyperkeratosis, parakeratosis, hypogranulosis, and elongation of rete ridges with suprapapillary thinning of the epidermis. There was an absence of melanocytes in the basal cell layer, confirmed by special stainig. Perivascular lymphocytic infiltration was noted in the dermis. The features were consistent with colocalized vitiligo and psoriasis.

   Discussion Top

It is not suprising to see association of vitiligo and psoriasis as they affect 1% to 3% of the population normally.[4],[5] The hypothesis that generalised vitiligo is an autoimmune process is based principally on its association with other presumably immunologic disorders4 and demonstration of antimelanocyte antibody.[6] The serendipitous observation that treatment with cyclosporine dramatically improved psoriasis[7] provided the first strong evidence that the disorder had an immune cause and there is increasing support for the idea that psoriasis is a T cell mediated autoimmune disease.[8] Co-habitation of two disorders which possess a prominent immunological component in their pathogenesis may offer a clue as to their causation, although such hopes have not been fulfilled in the earlier cases reported.[2],[3]
The curious cohabitation of a psoriatic lesion over a PUVA treated vitiligo patch in our patient has raised speculation on the role of T-cell activation in the development and persistence of psoriatic lesions. PUVA greatly reduces the number of activated T cells in the psoriatic skin by inducing T cell apoptosis, often resulting in long standing remissions.[9] So our patient should not have developed psoriatic lesions on the PUVA treated vitiligo patch. This paradox can be explained by the clinical heterogenicity of psoriasis, the apparent multigenic pattern of inheritance and a combination of variables involved in the development of psoriasis.
An alternative explanation can be on the basis of Koebner phenomenon, which is consistent with the immune surveillance paradigm.[10] PUVA destroys keratinocytes, lymphocytes and fibroblasts in culture.[4] Preformed interleukin 1 alpha is released from keratinocytes after minor trauma[11] (? PUVA in the present case). Cutaneous lymphocyte antigen (CLA) positive T cells are recruited from peripheral blood by interleukin 1 alpha initiated inflammation, and CLA positive T cells whose antigen receptor is specific for the putative psoriatic auto antigen in skin will be activated insitu. The subsquent release of type 1-Tcell cytokines results in further inflammation, the recruitment of additional CLA positive T cells, and ultimately the development of psoriatic lesion in susceptible persons.[12]
Dhar et al[13] conclude that, there could be structural similarities between anti stratum corneum antibodies and anti melanocyte antibodies and also a common neuropeptide might be responsible for cohabitation of vitiligo and psoriasis.
In conclusion, we report the co-existence of vitiligo and psoriasis with few colocalized lesions. Many pigment cell biologists and dermatologists have concluded that vitiligo is an autoimmune disease and psoriasis, the T cell mediated skin disease, may be associated. Whether their interpretation of the association is valid is uncertain. This requires further insight into their pathogenesis, as we believe that psoriasis and vitiligo are spectra of diseases with varied etiology for varied clinical presentation. 

   References Top

1.Nordlund JJ, Lerner AB. Vitiligo: Its relationship to systemic disease In: Moschella S(Ed) : Dermatology update. Elsevier, North Holland, 1997:411.  Back to cited text no. 1    
2.De Moragas JM, Winkelmann RK. Psoriasis and vitiligo. Int J Dermatol 1970: 101: 235-237.  Back to cited text no. 2    
3.Menter A, Boyd AS, Silverman AK. Guttate psoriasis and vitiligo anatomic cohabitation. J Am Acad Dermatol 1989;20:698-700.  Back to cited text no. 3  [PUBMED]  
4.Nordlund JJ. Vitiligo. In: Pathogenesis of Skin Disease (Ed: Thiers and Dobson), Churchill Livingstone, New York, 1986, 99-127.  Back to cited text no. 4    
5.Arndt KA. Manual of Dermatology Therapeutics, 5th ed. Little Brown and Company, 1995; 149-159.  Back to cited text no. 5    
6.Herkz KC, Gazze LA, Kirkpatric CA, et al.Autoimmune vitiligo: detection of antibodies to melanin producing cells. N Eng 3 Med 1997; 297:634-636.  Back to cited text no. 6    
7.Ellis CN, Fradin MS, Messana JM, et al. Cyclosporine for plaque type psoriasis: results of a multidose, double blind trial. N Eng J Med 1991; 324: 277-284.  Back to cited text no. 7    
8.Gottlieb SL, Gilleaudeau, Johnson R, et al. Response of psoriasis to a Lymphocyte selective toxin (DAB 389IL-2) suggests a primary immune, but not keratinocyte, pathogenic basis. Nat Med 1995;1: 442-447.  Back to cited text no. 8    
9.Genestier L, Paillot R, Fournel 5, et al. Immunosupressive properties of methotrexate:apoptosis and clonal detection of activated peripheral T cells. 3 Clin Invest 1998;102:322-328.  Back to cited text no. 9    
10.Melsko JW, Bernhard JD, Stern RS. The Koebner (isomorphic) response in psoriasis: associations with early age at onset and multiple previous therapies. Arch Dermatol 1983;119:655-659.  Back to cited text no. 10    
11.Lee RT, Briggs WH, Chery GC et al. Mechanical deformation promotes secretion of IL-1 alpha and IL-1 receptor antagonist. J Immunol 1997; 159:5084-5088.  Back to cited text no. 11    
12.Robert C, Kupper TS. Inflammatory skin diseases T cells, and immune surveillance, N Engl J Med 1991; 341:1817-1828.  Back to cited text no. 12    
13.Dhar S, Malakar S, Dhar S. Colocalization of vitiligo and psoriasis in a 9-year old boy: Paed Dermatol 1999;1: 242-243.  Back to cited text no. 13    


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