There appears to be a genetic predisposition to vitiligo, consistent with a polygenic disorder, and up to one-third of patients report a family history of hypopigmentation.5,6 No definitive precipitating factor responsible for initiating vitiligo has been established, and the basic pathogenesis in general still remains unknown. Current hypotheses range from intrinsic melanocyte dysfunction and/or death to destruction mediated by autoantibodies. Many vitiligo patients also exhibit other autoimmune disorders and the presence of serum melanocyte-specific autoantibodies appears to correlate with the extent and activity of the disease.7,8

The development of vitiligo patches over friction areas may be due to Koebner phenomenon in response to local trauma.

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