Segmental vitiligo as the possible expression of cutaneous somatic mosaicism: implications for common non-segmental vitiligo

Authors

  • Alain Taïeb,

    1. Service de Dermatologie et Dermatologie Pédiatrique, Centre de Référence des Maladies Rares de la Peau, CHU de Bordeaux, Bordeaux; and Inserm U 876, University of Bordeaux, Bordeaux, France
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  • Fanny Morice-Picard,

    1. Service de Dermatologie et Dermatologie Pédiatrique, Centre de Référence des Maladies Rares de la Peau, CHU de Bordeaux, Bordeaux; and Inserm U 876, University of Bordeaux, Bordeaux, France
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  • Thomas Jouary,

    1. Service de Dermatologie et Dermatologie Pédiatrique, Centre de Référence des Maladies Rares de la Peau, CHU de Bordeaux, Bordeaux; and Inserm U 876, University of Bordeaux, Bordeaux, France
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  • Khaled Ezzedine,

    1. Service de Dermatologie et Dermatologie Pédiatrique, Centre de Référence des Maladies Rares de la Peau, CHU de Bordeaux, Bordeaux; and Inserm U 876, University of Bordeaux, Bordeaux, France
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  • Muriel Cario-André,

    1. Service de Dermatologie et Dermatologie Pédiatrique, Centre de Référence des Maladies Rares de la Peau, CHU de Bordeaux, Bordeaux; and Inserm U 876, University of Bordeaux, Bordeaux, France
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  • Yvon Gauthier

    1. Service de Dermatologie et Dermatologie Pédiatrique, Centre de Référence des Maladies Rares de la Peau, CHU de Bordeaux, Bordeaux; and Inserm U 876, University of Bordeaux, Bordeaux, France
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Alain Taïeb, e-mail: alain.taieb@chu-bordeaux.fr

Summary

Clinical findings in vitiligo challenge the widely accepted organ specific autoimmune pathomechanisms. We draw the attention to the fact that the distribution of segmental vitiligo (SV) fits in at least a subset of patients a pattern usually associated with cutaneous mosaicism. The association of SV to non-segmental vitiligo (NSV) now confirmed by several observations indicates a continuum between the two subsets with shared predisposing genetic factors, including genes operating specifically in the skin. Some pedigrees associating SV and NSV further suggest a mechanism of loss of heterozygosity for a dominant gene controlling part of the cutaneous phenotype. The mosaic hypothesis applies only to SV and to the rare SV-NSV association, but suggests that predisposing genetic factors in common NSV should also be searched directly in the skin. SV would be a good candidate disease to explore as a proof of principle of a new gene discovery strategy useful for multigenic disorders with organ specificity, applicable in priority to chronic inflammatory skin disorders.

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