Update on childhood vitiligo

This review addresses recent changes in the understanding and the treatment of vitiligo vulgaris.

Two target genes for vitiligo have been identified, NACHT-leucine-rich-repeat protein-1 (NALP1), part of the inflammasome cascade, and tyrosinase, the enzyme that produces melanin. Identification of reactive oxidation species has furthered the understanding of melanocyte destruction. Comorbid autoimmune disease, including thyroid autoimmunity seen in 25%, is genetically linked to generalized vitiligo and is noted in both childhood vitiligo patients and their families. Screening for vitamin deficiencies and concurrent autoimmunity can be beneficial to the overall health of the child with vitiligo. About half of all vitiligo vulgaris patients have onset of their illness during childhood, causing increased psychological stress during the formative years. Fortunately, therapy has improved as well, with the development of newer topical agents for vitiligo, including topical calcineurin inhibitors; new topical combinations such as topical corticosteroids and calcipotriene; and new technological advances including narrowband ultraviolet B and excimer laser.

A cyclic approach to therapy should be used wherein topical agents are altered every 6-8 months and technology is used as an alternative after achievement of maximal topical response. With cyclic therapy and early disease intervention, good cosmetic outcomes may be achievable, particularly in localized cases.