Association of anticonvulsant hypersensitivity syndrome with Herpesvirus 6, 7

Oskay, Tuğba; Karademir, Asli; Ertürk, Özcan

doi:10.1016/j.eplepsyres.2006.02.006

Cited by 40 publications

(28 citation statements)

References 27 publications

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“…These viruses have been demonstrated to be involved in the flare-up and severity of this syndrome; therefore, the absence of a detectable HHV-6 and HHV-7 reactivation may have accounted for the milder form of disease in our case [19, 20]. …”

Section: Discussionmentioning

confidence: 99%

Granulomatous interstitial nephritis associated with atypical drug-induced hypersensitivity syndrome induced by carbamazepine

et al. 2011

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We report the case of a 70-year-old female patient with granulomatous interstitial nephritis (GIN) induced by carbamazepine (CBZ). The patient had a 22-year history of bipolar disorder. Approximately 50 days before admission to our hospital, she was switched from valproic acid to 200 mg/day CBZ for mood swings. Forty days later, she presented with mild transient platelet depletion and liver dysfunction along with a C-reactive protein (CRP) level of 2.65 mg/dL. At that time, she discontinued CBZ without consulting the doctor. She subsequently developed high fever and a pruritic maculopapular rash. Laboratory tests revealed an elevated CRP level (11.98 mg/dL) and serum creatinine (sCr) of 1.6 mg/dL. Hence, she was admitted to our hospital, where she showed eosinophilia and immunoglobulin suppression. She was diagnosed with atypical drug-induced hypersensitivity syndrome (DIHS). All drugs prescribed by the previous doctor were discontinued. A lymphocyte transformation test showed CBZ positivity; a renal biopsy revealed many granulomatous lesions connected to arterioles, without angionecrotic findings. The patient had no history of allergic disorders or tuberculosis. Because of psychological instability, we treated her conservatively without steroid administration. She had a good recovery except for mild residual renal insufficiency (sCr, 1.0 mg/dL). Although granuloma formation has been observed in kidney biopsy specimens of rare cases with DIHS, no previous studies have reported on the relationship between arterioles and granuloma formation.

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Section: Discussionmentioning

confidence: 99%

Granulomatous interstitial nephritis associated with atypical drug-induced hypersensitivity syndrome induced by carbamazepine

et al. 2011

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“…The exact mechanism by which aromatic anti-convulsant drugs trigger T-cell activation and subsequently cause AHS is not clearly elucidated but is thought to involve at least 3-step consequent mechanisms: First, insufficient microsomal epoxide hydroxylase (MEH) enzyme activity in patients' lymphocytes cannot completely detoxify the metabolites of aromatic amine anticonvulsants, which leads to cell death and antigen formation (Knutsen et al, 1986;Pichler, 2003); Secondly, certain human leukocyte antigen (HLA) subtyping on the antigen-presenting cells owns higher affinity to the antigen (Chung et al, 2004;Kano et al, 2004;Krauss, 2006); Thirdly, reactivation of herpes-type viruses in patients worsens AHS (Bohan et al, 2007;Kano et al, 2004;Oskay et al, 2006). Lymphoproliferative tests for phenobarbital, phenytoin, carbamazepine and lamotrigine.…”

Section: Discussionmentioning

confidence: 99%

Alopecia Areata Universalis After Phenobarbital-Induced Anti-Convulsant Hypersensitivity Syndrome

Huang

Hsieh

Hsiao

et al. 2009

Immunological Investigations

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Alopecia is an adverse effect in those patients taking aromatic anti-convulsant drugs but is rarely reported after discontinuing such medications in the convalescent status of anti-convulsant hypersensitivity syndrome (AHS). A 3-year-old boy developed alopecia areata (AA) universalis in the convalescent status of phenobarbital-induced AHS, compatible to the evidences of increased lymphocyte proliferation and increased dead cells percentages while his peripheral blood mononuclear cells were incubated with phenobarbital. Skin histology revealed peri-follicular, peri-bublar and supra-bublar lymphocyte infiltration. By searching for the key words AHS, alopecia areata (AA, punctuate absence of terminal scalp hair), AA totalis (complete absence of terminal scalp hair), and AA universalis (total loss of terminal scalp and body hair) using PubMed, only 2 cases, to date, developed alopecia in the convalescent status of phenobarbital-induced AHS. Among these 3 cases, all had favorable prognosis despite having jaundiced hepatitis. Their hair grew back after 2-3 months steroid therapy. Alopecia does rarely develop in the convalescent status of phenobarbital-induced AHS after stopping phenobarbital and its mechanism is related to lymphocyte infiltration into the peri-bulbar, supra-bulbar and peri-follicular regions.

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“…Moreover, among patients receiving penicillins and other antimicrobial agents, the incidence of rashes is significantly higher in those with infectious mononucleosis [3]. For carbamazepine and other anticonvulsants, the association between reactivation of HHV, in particular HHV 6 and 7, and the development of hypersensitivity syndrome has been previously reported [15]; the reactivation of HHV has been associated even with hypersensitivity syndromes caused by other molecules like cyanamide [16] or mexiletine hydrochloride [17]. For all these drug-related hypersensitivity reactions, virus-induced immune modulation has been proposed as the triggering factor [5].…”

Section: Discussionmentioning

confidence: 99%

Carbamazepine Hypersensitivity Syndrome Triggered by a Human Herpes Virus Reactivation in a Genetically Predisposed Patient

Calligaris

Stocco

Iudicibus

et al. 2009

Int Arch Allergy Immunol

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A case of severe hypersensitivity syndrome, triggered by carbamazepine in the presence of a concomitant active human herpes virus (HHV) 6 and 7 infection is described. To further understand the molecular mechanism of this adverse reaction, analyses of the genetic variants of human leukocyte antigen (HLA) and of the epoxide hydrolase gene (EPHX1), previously associated with carbamazepine hypersensitivity, were performed. A lymphocyte transformation test (LTT) was conducted in order to detect drug-specific lymphocytes. In the hypersensitive patient, 2 genetic factors previously associated with intolerance to carbamazepine were detected: the allele HLA-A*3101 and homozygosity for the variant allele of SNP rs1051740 in EPHX1. Drug-specific lymphocytes could be detected by LTT when the HHV was active (positive PCR for viral DNA and increased anti-HHV 6 IgG titer), but not when it was no longer active. In conclusion, we document a case of severe carbamazepine hypersensitivity triggered by viral reactivation in a patient presenting the interaction of 2 unfavorable genetic factors.

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Association of anticonvulsant hypersensitivity syndrome with Herpesvirus 6, 7

Cited by 40 publications

References 27 publications

Granulomatous interstitial nephritis associated with atypical drug-induced hypersensitivity syndrome induced by carbamazepine

Granulomatous interstitial nephritis associated with atypical drug-induced hypersensitivity syndrome induced by carbamazepine

Alopecia Areata Universalis After Phenobarbital-Induced Anti-Convulsant Hypersensitivity Syndrome

Carbamazepine Hypersensitivity Syndrome Triggered by a Human Herpes Virus Reactivation in a Genetically Predisposed Patient

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