Elsevier

The Lancet

Volume 358, Issue 9293, 10 November 2001, Page 1575
The Lancet

Clinical Picture
Leopard-like vitiligo with capecitabine

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    Similar to NEH, the pathogenesis of ESS is obscure and complicated by its association with targeted therapies that are not conventionally understood to result in direct cytotoxicity; nonetheless, the distribution and histologic findings of both ESS and NEH suggest accumulation, and/or concentrating effects are likely related to the pathogenic cascade. A wide variety of pigmentary alterations are seen with chemotherapeutics (Table 3).2,7,90,93–95,97–99 These alterations range not only by pigmentary pattern (depigmentation vs hyperpigmentation) but also distribution (localized vs diffuse; predominating in the skin, nails, mucosal surfaces, or hair follicles).

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    Chemotherapy-induced inflammation of actinic keratoses was first described in 1962 with the use of systemic fluorouracil, but had never before been linked to capecitabine therapy.217 Other capecitabine-induced cutaneous adverse events described in single case reports include cutaneous and mucosal hyperpigmentation, spotty, “leopard-like” repigmentation of vitiligo in sun-exposed sites,218 radiation recall dermatitis, onycholysis, and onychomadesis.210,219 Tegafur is a prodrug of 5-FU that is given orally.

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