The genetics and epidemiology of generalized vitiligo

vitiligo Generalized vitiligo (GV) is the most common depigmentation disorder, in which acquired multifocal patches of white skin and overlying hair result from loss of melanocytes in the involved areas (Figure 1) [1,2]. Th e prevalence of GV is approximately 0.5% in various populations [3], with an average age of onset at about 24 years and occurring with approximately equal frequency in males and females [4]. Th e concordance of GV in monozygotic twin-pairs is approximately 23% [4], and epidemiological evidence indicates that GV is a complex trait involving multiple genes and unknown environmental factors [3]. Many hypotheses have been proposed to account for melanocyte loss in GV [1]. Most current evidence supports an autoimmune basis of disease [5], though the triggers of the autoimmune response remain unknown. Among European-derived white individuals with GV, about 15% to 25% have at least one additional conco mitant autoimmune disease, particularly autoimmune thyroid disease (Hashimoto’s thyroiditis and Graves’ disease), pernicious anemia, rheumatoid arthritis, psori asis, type 1 diabetes, Addison’s disease and systemic lupus erythe matosus; these diseases also occur at increased frequencies in fi rst-degree relatives of patients with GV, whether or not those relatives have GV them selves [4]. Together, these fi ndings indicate that patients with GV and their close relatives have inherited susceptibility to this specifi c diathesis of autoimmune diseases, mediated by shared susceptibility genes.