Description
Research over the last decade has revealed that the normally pigmented skin of patients with vitiligo is not normal at all, as evidenced by alterations in cutaneous morphology and modifications in cellular and metabolic functions that ultimately drive immune activation against melanocytes. Furthermore, nonlesional skin is in a state of subclinical inflammation until triggered by internal and/or external exposomal events. Therefore, targeting early processes that drive immune dysregulation in normally pigmented skin may avoid or reduce melanocyte loss. Thus, shifting the focus to nonlesional skin may prevent the appearance of clinical manifestations of the disease rather than treating the lesions.