An Update on New and Emerging Options for the Treatment of Vitiligo

B. H. Mahmoud, MD, PhD; C. L. Hexsel, MD; I. H. Hamzavi, MD


Skin Therapy Letter. 2008;13(2):1-6. 

In This Article

Abstract and Introduction

Vitiligo is an acquired leukoderma that results from the loss of epidermal melanocytes, and is characterized by macules and patches of depigmented skin. With a relatively high rate of prevalence, vitiligo occurs in localized, generalized, or segmental patterns; it can run a rapidly progressive course or remain stationary. The pathogenesis of vitiligo is not yet fully understood, but the autoimmune hypothesis is the most commonly accepted one, based on which, many treatment modalities have been described. Although many therapeutic options exist and new modalities are still emerging, treatment challenges persist, as not all patients respond to available therapies. Variables that affect the choice of treatment include the extent, distribution, and progression rate of the lesions. Another challenge is the lack of a standardized scoring system, which hampers the production of level 1a evidence studies for the treatment of this condition.

The worldwide prevalence of vitiligo is estimated to range between 0.5% and 4%.[1] These depigmented macules were first described more than 3,000 years ago in pre-Hindu Vedic and ancient Egyptian texts.[2]

The pathogenesis of vitiligo is complex and not yet fully understood, but it is believed to involve a combination of autoimmune, genetic, and environmental factors. The autoimmune hypothesis suggests that antibodies develop against melanocyte surface antigens.[3] Gauthier, et al. recently proposed the melanocytorrhagy hypothesis, which is based on an in vivo observation of melanocyte detachment from the basal layer, followed by transepidermal migration, which in turn triggers melanocyte death.[4] In addition, the neural, self-destruct, and biochemical hypotheses have also been proposed.[1]


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