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Vitiligo

Abstract

Vitiligo is an acquired depigmenting disorder that affects 0.5% to 2% of the world population. Three different forms are classified according to the distribution of lesions; namely non-segmental, segmental and mixed vitiligo. Vitiligo is associated with polymorphisms in genes involved in the immune response and in melanogenesis. However, environmental factors are required for the development of manifest disease. In general, the diagnosis is clinical and no laboratory tests or biopsies are required. Metabolic alterations are central to current concepts in pathophysiology. They induce an increased generation of reactive oxygen species and susceptibility to mild exogenous stimuli in the epidermis. This produces a senescent phenotype of skin cells, leads to the release of innate immune molecules, which trigger autoimmunity, and ultimately causes dysfunction and death of melanocytes. Clinical management aims to halt depigmentation, and to either repigment or depigment the skin, depending on the extent of disease. New therapeutic approaches include stimulation of melanocyte differentiation and proliferation through α-melanocyte-stimulating hormone analogues and through epidermal stem cell engineering. Several questions remain unsolved, including the connection between melanocyte depletion and stem cell exhaustion, the underlying degenerative mechanisms and the biological mediators of cell death. Overall, vitiligo is an excellent model for studying degenerative and autoimmune processes and for testing novel approaches in regenerative medicine. For an illustrated summary of this Primer, visit: http://go.nature.com/vIhFSC

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Figure 1: The hair follicle unit.
Figure 2: The melanocyte and its environment.
Figure 3: Treatment target in interferon signalling.
Figure 4: Typical presentation of vitiligo.
Figure 5: Differential diagnosis of vitiligo.
Figure 6: Management algorithm for the treatment of vitiligo.
Figure 7: Determinants of quality of life in vitiligo.
Figure 8: Vitiligo as a model for autoimmune and degenerative diseases.

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Acknowledgements

Introduction (M.P.); Epidemiology (K.E., I.H., D.P.); Mechanisms/pathophysiology (M.L.D., M.P., J.E.H.); Diagnosis, screening and prevention (K.E., I.H., D.P., A.T.); Management (K.E., A.T.); Quality of life (I.H., D.P., M.P.); Outlook (M.P.); overview of Primer (M.P.).

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Introduction (M.P.); Epidemiology (K.E., I.H., D.P.); Mechanisms/pathophysiology (M.L.D., M.P., J.E.H.); Diagnosis, screening and prevention (K.E., I.H., D.P., A.T.); Management (K.E., A.T.); Quality of life (I.H., D.P., M.P.); Outlook (M.P.); overview of Primer (M.P.).

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Correspondence to Mauro Picardo.

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Competing interests

M.P. received research grants from Giuliani, Cantabria, Stealth Peptides, Fidia, and he was speaker for Pierre Fabre. J.E.H. received research grants from AbbVie, Sanofi/Genzyme, Combe, Gliknik; he was consultant for Pfizer and Biomedical System; he was a speaker for Alkem Pharmauceticals. I.H. was an investigator for Clinuvel, Estee Lauder, and Ferndale Laboratories and he received equipment from Canfield. A.T. received research grants from Galderma and Astellas. M.L.D. and D.P. declare no competing interests.

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Picardo, M., Dell'Anna, M., Ezzedine, K. et al. Vitiligo. Nat Rev Dis Primers 1, 15011 (2015). https://doi.org/10.1038/nrdp.2015.11

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