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Vitiligo: An Update on Pathophysiology and Treatment Options

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Abstract

The pathophysiology of vitiligo is becoming increasingly clarified. In non-segmental vitiligo, early factors include activation of innate immunity, inflammasome activation, oxidative stress, and loss of melanocyte adhesion. Nonetheless, the main mechanism leading to non-segmental vitiligo involves an immune-mediated destruction of melanocytes. Anti-melanocyte-specific cytotoxic T cells exert a central role in the final effector stage. Genetic research revealed a multi-genetic inheritance displaying an overlap with other autoimmune disorders. However, some melanocyte-specific genes were also affected. Segmental vitiligo carries a different pathogenesis with most evidence indicating a mosaic skin disorder. Current management includes topical corticosteroids and immunomodulators. Narrow-band ultraviolet B can be used in patients not responding to topical treatment or in patients with extensive disease. Pigment cell transplantation offers an alternative for the treatment of segmental vitiligo or stable non-segmental lesions. Recent findings have revealed new targets for treatment that could lead to more efficient therapies. Targeted immunotherapy may halt the active immune pathways, although combination therapy may still be required to induce satisfying repigmentation. A recently established core set of outcome measures, new measurement instruments, and biomarker research pave the way for future standardized clinical trials.

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Correspondence to Reinhart Speeckaert.

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This research was supported by a postdoctoral research grant to Reinhart Speeckaert from the Ghent University Special Research Fund (BOF; Grant No. 01P12914) and a research grant to Nanja van Geel from the Scientific Research Foundation-Flanders (FWO Senior Clinical Investigator; Grant No. FWO11/FKM/001).

Conflict of interest

Reinhart Speeckaert and Nanja van Geel have no conflicts of interest directly relevant to the contents of this article.

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Speeckaert, R., van Geel, N. Vitiligo: An Update on Pathophysiology and Treatment Options. Am J Clin Dermatol 18, 733–744 (2017). https://doi.org/10.1007/s40257-017-0298-5

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