Anticonvulsant hypersensitivity syndrome with an epoxide hydrolase defect

Yoo, Ji-Sang; Kang, Alice J.; Chun, Chun; Lee, Myeong Soo

doi:10.1046/j.1365-2133.1999.02639.x

Cited by 20 publications

(14 citation statements)

References 9 publications

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“…It is thought that insufficient detoxification of these metabolites may account for the picture. A hereditary deficiency in epoxide hydrolase function – an enzyme active in the conjugation phase of these drugs – may predispose certain individuals to AHS 10 . Recently, an association between AHS and reactivation of cytomegalovirus has been advanced 11 …”

Section: Discussionmentioning

confidence: 99%

Anticonvulsant hypersensitivity syndrome

Kaminsky¹,

Moreno²,

Díaz³

et al. 2004

Int J Dermatology

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Anticonvulsant hypersensitivity syndrome (AHS) is a rare and potentially fatal reaction characterized by the appearance of fever, skin rash and internal organ involvement. Phenytoin, phenobarbital and carbamazepine are the most frequent aromatic anticonvulsants causing the reaction. This syndrome occurs 1–8 weeks after the initial drug exposure but, even though glucocorticoids appear to be useful in severe cases, discontinuation of the drug has been found to be essential in the resolution of symptoms.

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Section: Discussionmentioning

confidence: 99%

Anticonvulsant hypersensitivity syndrome

Kaminsky¹,

Moreno²,

Díaz³

et al. 2004

Int J Dermatology

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“…If detoxification of this toxic metabolite is insufficient, the toxic metabolite may bind to cellular macromolecules, causing cell necrosis or a secondary immunological response. Anticonvulsant hypersensitivity syndrome has been linked to a defect in the enzyme epoxide hydrolase [72]. It has been suggested that its incidence is highest in elderly black males [73].…”

Section: Hypersensitivity Syndromementioning

confidence: 99%

Impact of phenytoin therapy on the skin and skin disease

Scheinfeld¹

2004

Expert Opinion on Drug Safety

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Phenytoin (diphenylhydantoin; Dilantin), ALZA Corp.) is a highly effective and widely prescribed anticonvulsant agent used in the treatment of focal and tonic clonic generalised seizures. The side effects of phenytoin can occassionally engender significant morbidity. Phenytoin can induce generalised eruptions that include: a maculopapular exanthem, Stevens-Johnson syndrome, generalised exfoliative dermatitis, toxic epidermal necrolysis, vasculitis and fixed drug eruptions. Phenytoin is linked to a hypersensitivity syndrome that manifests with fever, rash and lymphadenopathy. Patients receiving phenytoin may develop pseudolymphoma or, rarely, malignant lymphoma and mycosis fungoides-like lesions. Rarer cutaneous side effects include drug-induced lupus, purple hand syndrome, pigmentary alterations and IgA bullous dermatosis. Phenytoin can effect clotting function and alter vitamin and mineral levels. Prenatal exposure to phenytoin may result in a spectrum of structural, developmental and behavioural changes, known as the fetal hydantoin syndrome. Patients who use phenytoin in the long-term commonly manifest with gingival hyperplasia, coarsening of the facies, and hirsutism.

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“…Anticonvulsant hypersensitivity syndrome is a potentially fatal drug reaction with an estimated incidence of 1 in 10 000 new drug exposures 3031 and fatal anticonvulsant hypersensitivity syndrome occurring in a man with a functional epoxide hydrolase defect has been described 32. Whereas this defect may have resulted from the anticonvulsant drug itself, sepsis, or treatment with corticosteroids, the potential for it to be genetically based is increased by the finding of familial aggregation of phenytoin hypersensitivity33 and concordance of carbamazepine hypersensitivity in MZ twins 34.…”

Section: Epilepsy and Pharmacogeneticsmentioning

confidence: 99%

The clinical impact of epilepsy genetics

Johnson

2001

Journal of Neurology, Neurosurgery &Amp; Psychiatry

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An overemphasis on molecular genetic advances in epilepsy is in danger of missing the major contribution that clinical genetic studies make in predicting the likely benefit of molecular research eVorts. Genetic epidemiology, twin, and family studies suggest that some individual epilepsy genes raise the risk for developing many diVerent types of epilepsy but that specific combinations of these genes determine specific epilepsy phenotypes. Experimental data show how diVerences in drug response can result from inherited diVerences in drug sensitivity and there is emerging data on the genetic basis of harmful adverse drug reactions and teratogenesis. These developments predict a future in which epilepsy is ultimately classified on the basis of its oligogenic architecture, eVective treatments are tailored to the appropriate patient and harmful adverse drug reactions avoided in those who are sensitive.Epilepsy can be classified as idiopathic (where no aetiology other than a genetic predisposition is identified), symptomatic (epilepsy occurring as a result of identified brain lesion), and cryptogenic (where symptomatic epilepsy is suspected but an underlying brain lesion is not identified). With advances in genetics and neuroimaging the prevalence of cryptogenic epilepsy is falling.The role of inheritance in epilepsy is traditionally categorised according to the mechanism of inheritance: (1) mendelian disorders in which epilepsy forms part of the phenotype; (2) idiopathic epilepsies with mendelian inheritance; (3) epilepsies with complex inheritance; (4) idiopathic epilepsies associated with cytogenetic abnormality.There are over 200, individually rare, mendelian disorders in which epilepsy forms part of the phenotype. These include neurocutaneous disorders, neurodegenerative disorders, inherited malformations of cortical development, and an array of inherited metabolic disorders. Examples of recent interest are discussed elsewhere and although important, are not the focus of this editorial.

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Anticonvulsant hypersensitivity syndrome with an epoxide hydrolase defect

Cited by 20 publications

References 9 publications

Anticonvulsant hypersensitivity syndrome

Anticonvulsant hypersensitivity syndrome

Impact of phenytoin therapy on the skin and skin disease

The clinical impact of epilepsy genetics

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