Vitiligo is a common idiopathic acquired or inherited disease with loss of normal melanin pigments and functioning melanocytes from otherwise healthy looking skin. Clinically, vitiligo can be grouped into several unique types (Figure 1, Figure 2. The localized type includes focal and segmental vitiligo. Generalized types are vitiligo vulgaris, acrofacial vitiligo, and universal vitiligo. A genetic predisposition is considered.<sup>13 Das S.K., Majumder P.P., Chakraborty R. , y al. Studies on vitiligo. I. Epidemiological profile in Calcutta, India Genet Epidemiol 1985 ;  2 : 71-78  [cross-ref]

Haga clic aquí para ir a la sección de Referencias, 46 Ortonne J.P., Bose S.K. Vitiligo: Where do we stand? Pigment Cell Res 1993 ;  6 : 61-72  [cross-ref]

Haga clic aquí para ir a la sección de Referencias</sup>

The leukoderma of vitiligo does not contain any functioning melanocytes.<sup>35 Le Poole I.C., Van den Wijngaard R.M., Westerhof W. , y al. Presence or absence of melanocytes in vitiligo lesions: An immunohistochemical investigation J Invest Dermatol 1993 ;  100 : 816-822

Haga clic aquí para ir a la sección de Referencias</sup> Pathogenesis of vitiligo leukoderma is still unknown, but currently three major theories have been proposed.<sup>11 Chakraborty D.P., Roy S., Chakraborty A.K. Vitiligo, psoralen, and melanogenesis: Some observations and understanding Pigment Cell Res 1996 ;  9 : 107-116  [cross-ref]

Haga clic aquí para ir a la sección de Referencias</sup> One is the neural theory, that presupposes that there is a chemical mediator liberated at the nerve endings that destroys the melanocytes or inhibits the production of melanin pigments. A second theory proposes that melanocytes are destroyed either by themselves through generation of melanin precursors (or metabolites) or by surrounding keratinocytes that liberate chemicals that cause oxidative stresses. In normal melanocytes there is some defense or scavenging mechanism against these cytotoxic melanin precursors or chemicals generating oxidative stresses, but there is a defect in this defense process (mechanism) in vitiligo melanocytes (Figure 3).<sup>26 Jimbow K., Chen H., Park J.S. , y al. Vitiligo leukoderma: Abnormal retention of TRP-1 due to protein-protein interaction with calnexin, melanogenesis chaperone, leading to melanocyte apoptosis J Invest Dermatol 1995 ;  104 : 664

Haga clic aquí para ir a la sección de Referencias</sup> The third theory is the autoimmune hypothesis, which speculates that vitiligo is an autoimmune disease. Vitiligo patients develop autoantibodies against melanocytes.<sup>9 Bystryn J.C., Naughton C.K. The significance of vitiligo antibodies J Dermatol 1985 ;  12 : 1-9

Haga clic aquí para ir a la sección de Referencias, 39 Naughton G.K., Eisinger M., Bystryn J.C. Antibodies to normal human melanocytes in vitiligo J Exp Med 1983 ;  158 : 246-251  [cross-ref]

Haga clic aquí para ir a la sección de Referencias</sup> In metastatic melanoma patients, depigmented macules similar or identical to vitiligo leukoderma can be developed by destruction of melanocytes through the interaction with cytolytic T-lymphocytes, which are activated by tyrosinase gene family proteins<sup>7 Brichard V., Van Pel A., Wolfel T. , y al. The tyrosinase gene codes for an antigen recognized by autologous cytolytic T lymphocytes on HLA-A2 melanomas J Exp Med 1993 ;  178 : 489-495  [cross-ref]

Haga clic aquí para ir a la sección de Referencias, 56 Wang R.F., Robbins P.F., Kawakami Y. , y al. Identification of a gene encoding a melanoma tumor antigen recognized by HLA-A31-restricted tumor-infiltrating J Exp Med 1995 ;  181 : 799-804  [cross-ref]

Haga clic aquí para ir a la sección de Referencias</sup> and other melanogenesis-associated proteins.<sup>4 Bakker A.B., Schreurs M.W., De Boer A.J. , y al. Melanocyte lineage-specific antigen gp100 is recognized by melanoma-derived tumor-infiltrating lymphocytes J Exp Med 1994 ;  179 : 1005-1009  [cross-ref]

Haga clic aquí para ir a la sección de Referencias</sup>