Pseudolymphoma syndrome revisited.

Anticonvulsants have long been recognized as a cause of hypersensitivity reactions. Phenytoin hypersensitivity can be traced to 1916, when phenylethylhydantoin (phenytoin sodium), which was used to treat children with Sydenham chorea, was found to induce a hypersensitivity reaction. Phenytoin was then known as a “nerve sedative,” and the hypersensitivity reaction, “nirvanol sickness,” resolved on discontinuation of the hydantoin. 1 The constellation of systemic manifestations was first described as the Dilantin sensitivity syndrome in 1950. The syndrome was referred to as anticonvulsant hypersensitivity syndrome (AHS) in 1988, after its occurrence was found to be related to antiepileptic drugs other than phenytoin. Antiepileptic drugs have been implicated as etiologic agents for a variety of dermatologic eruptions, including allergic or leukocytoclastic vasculitis, StevensJohnson syndrome (erythema multiforme major), and toxic epidermal necrolysis. These dermatoses exhibit clear diagnostic features that differentiate them from AHS.