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Thomas B. Fitzpatrick, MD, PhD

Arch Dermatol. 1997;133(12):1591-1592.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

IN DEVELOPING new therapies for vitiligo, it is conducive to try to understand the pathogenesis of vitiligo. A stubborn fact regarding vitiligo is that there are no melanocytes in fully evolved vitiligo macules. So the pathogenesis of vitiligo centers around a mechanism for the destruction of melanocytes. The most favored is an autoimmune hypothesis; this is based on the association of vitiligo with other autoimmune disorders, especially Hashimoto thyroiditis, pernicious anemia, and adrenal insufficiency, and the occurrence of autoantibodies in these patients. Also, the use of oral and topical corticosteroids can induce pigmentation in vitiligo macules.

Because there are no melanocytes in fully developed vitiligo macules, the autoimmune mechanism would appear to involve progressive destruction of melanocytes by autoantibody-dependent cellular cytotoxicity¹ or by cytotoxic T lymphocytes.² In contrast to epidermal melanocytes, melanocytes in the outer root sheath of the hair follicle appear to be immunologically "privileged" and, in . . . [Full Text PDF of this Article]

Author Affiliations
Department of Dermatology Massachusetts General Hospital Blossom Street Boston, MA 02114

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