Abstract
Epidermal melanocyte deficit is the basis of Vitiligo. It is a prolonged condition that may be inherited or acquired. Vitiligo affects 1-2 percent of the global population of all races. Several processes have been hypothesized for the breakdown of melanocytes in Vitiligo. These include genetic, autoimmune, oxidative stress, inflammatory mediator production, and melanocyte detachment processes.Vitamin D suppresses UVB-induced apoptosis in keratinocytes and melanocytes by reducing IL-6, IL-8, TNF-a, and TNF-c production. It reduces the autoimmune linked to Vitiligo.We conducted a case-control study in which we compared the level of Vitamin D in patients with Vitiligo and healthy cases. We confirmed our diagnosis with biopsy and utilized the Elisa method to assess the level of Vitamin D. The concentrations of Vitamin D in individuals with Vitiligo were much lower than in controls; however, we did not find a significant effect of vitamin D deficiency on the progression of Vitiligo lesions. Therefore we conclude that Vitamin D is involved in the genesis of Vitiligo, and replenishing the levels may help the patient recover faster.
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