Abstract

Vitiligo is a common acquired, non-contagious pigmentary disorder characterized by patchy loss of pigmentation from the skin, overlying hair and mucosa caused by the selective destruction of melanocytes. Vitiligo occurs with a frequency of 0.4–2.0% in various populations worldwide, without predilection for sex or race. Patterns of distribution of the disease include the localized, segmental, acrofacial, generalized and universal types. There are three major hypotheses for the pathogenesis of vitiligo: autoimmune, autocytotoxic-metabolic and neural dysfunctional. Autoimmunity remains the most popular hypothesis. The incidence of vitiligo is 10–15 times higher in patients with autoimmune disease. An increase in the frequencies is noted in the case of several autoimmune disorders in vitiligo probands and their first-degree relatives: autoimmune thyroid disease, pernicious anaemia, Addison’s disease, systemic lupus erythematosus, vitiligo, and inflammatory bowel disease. Many circulating autoantibodies reacting with multiple antigens, not only expressed on pigment cells, have been found in the sera of vitiligo patients. This may suggest that humoral response could be secondary to the destruction of melanocytes. Recent research focuses on the melanocyte-specific cytotoxic T-cell immune reaction in melanocyte destruction. Epidemiological studies have shown that vitiligo tends to aggregate in families. The genetics of vitiligo cannot be explained by the simple Mendelian pattern. It is characterized by incomplete penetrance, multiple susceptibility loci and genetic heterogeneity. Historically, the gold standards of treatment of vitiligo have been oral or topical psoralen photochemotherapy and topical corticosteroids. In the past ten years, there have been new therapeutic advances for vitiligo: narrowband UVB phototherapy, topical immunomodulators, and calcipotriol in combination with ultraviolet light.