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The most relevant feature is keratinocyte damage, with the presence of eosinophilic intracytoplasmic bodies, vacuolar keratinocyte degeneration, dyskeratotic keratinocytes, and confluent keratinocyte necrosis that leads to intraepidermal cleavage with the formation of intraepidermal blisters.18 There may be associated nonleukocytoclastic vasculitis.13 Immunohistochemistry has shown a loss of cytokeratin 10 and increased expression of cytokeratin 14, which would suggest an effect of the drug on keratinocyte differentiation.14 Jain et al.19 hypothesized that the clinical differences between HFS and HFSR could be explained by differences in the etiological and pathogenic mechanisms underlying the 2 conditions

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