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Pathophysiology of vitiligo

Pathophysiology of vitiligo ELSFVIER Pathophysiology JEROME CASTANET, MD JEAN-PAUL ORTONNE, MD of Vitiligo itiligo is a common skin and hair disorder affecting approximately l-4% of the world’s population and characterized by circumscribed white spots on the skin that tend to enlarge centrifugally over time .1,2 The course of vitiligo on a case by case basis is unpredictable. The natural course of the disease is usually one of slow progression, but it may stabilize or exacerbate rapidly. Some degree of spontaneous or sun-induced repigmentation is not uncommon in vitiligo, but complete and stable repigmentation is a rare event. The characteristic histological picture is the total absence of melanin and melanin-forming cells, or melanocytes, with an otherwise normal dermis and epidermis. The etiology is unknown, and several hypotheses have been proposed to explain the loss of melanocytes. The autocytoxic hypothesis supposes that intermediate metabolites in the melanin synthesis are melanocytotoxic. The neural hypothesis suggests that accumulation of some neurochemical mediator causes decreased melanin production. The autoimmune hypothesis is the most prevalent, and it is based mainly on the presence of melanocyte-specific antibodies that are able to induce necrosis of cultured human melanocytes:’ Recent advances in melanocyte research, due largely to the availability of http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinics in Dermatology Elsevier
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