Carbamazepine Induced Ebstein-Barr Virus Reactivation: A Rare Manifestation of Anticonvulsant Hypersensitivity Syndrome

Carbamazepine (CBZ) is an antiepileptic drug which has multiple mechanisms of action including stabilization of the inactivated stage of the voltage-gated sodium channels, potentiating gamma-amino butyric acid (GABA) receptors as a GABA antagonist, as well as the serotonin releasing affect. It is effective in neuropathic pain syndromes such as post-herpetic neuralgia and trigeminal neuralgia, as well as epilepsy. We presented a 29-year-old female patient with the diagnosis of trigeminal neuralgia (TN) who experienced a reactivation of the latent Ebstein-Barr Virus (EBV) infection in terms of anticonvulsant hypersensitivity syndrome after CBZ use, who gave her approval to publish her data. Since the clinical and serological findings of EBV re-infection resolved after the discontinuation of the drug, this clinical and serological manifestation was attributed to CBZ. Since common side-effects of CBZ are drowsiness, dizziness, headaches, skin reactions, cognitive dysfunctions, we reported an activation of EBV infection due to CBZ consumption as a rare side-effect of the drug.

Patch testing and cross sensitivity study of adverse cutaneous drug reactions due to anticonvulsants: A preliminary report

AIM To evaluate the utility of patch test and cross-sensitivity patterns in patients with adverse cutaneous drug reactions(ACDR) from common anticonvulsants. METHODS Twenty-four(M:F = 13:11) patients aged 18-75 years with ACDR from anticonvulsants were patch tested 3-27 mo after complete recovery using carbamazepine, phenytoin, phenobarbitone, lamotrigine, and sodium valproate in 10%, 20% and 30% conc. in pet. after informed consent. Positive reactions persisting on D3 and D4 were considered significant. RESULTS Clinical patterns were exanthematous drug rash with or without systemic involvement(DRESS) in 18(75%), Stevens-Johnsons syndrome/toxic epidermal necrolysis(SJS/TEN) overlap and TEN in 2(8.3%) patients each, SJS and lichenoid drug eruption in 1(4.2%) patient each, respectively. The implicated drugs were phenytoin in 14(58.3%), carbamazepine in 9(37.5%), phenobarbitone in 2(8.3%), and lamotrigine in 1(4.7%) patients,respectively. Twelve(50%) patients elicited positive reactions to implicated drugs; carbamazepine in 6(50%), phenytoin alone in 4(33.3%), phenobarbitone alone in 1(8.3%), and both phenytoin and phenobarbitone in 1(8.33%) patients, respectively. Cross-reactions occurred in 11(92%) patients. Six patients with carbamazepine positive patch test reaction showed cross sensitivity with phenobarbitone, sodium valproate and/or lamotrigine. Three(75%) patients among positive phenytoin patch test reactions had cross reactions with phenobarbitone, lamotrigine, and/or valproate. CONCLUSION Carbamazepine remains the commonest anticonvulsant causing ACDRs and cross-reactions with other anticonvulsants are possible. Drug patch testing appears useful in DRESS for drug imputability and cross-reactions established clinically.

Phenytoin Induced Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS): Case Report

Background: Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a rare and potentially life-threatening condition. It presents a long prodromal period, extensive rash, fever, lymphadenopathy, hematologic abnormalities (eosinophilia with or without atypical lymphocytosis), and internal organ involvement. Purpose: To describe a case of phenytoin induced DRESS syndrome, presenting diagnostic and management challenges of clinical interest. Methods: The Consensus-based Clinical Case Reporting Guideline Development (CARE) was observed for data analysis in case reports. Case Report: A 22-year-old man, using phenytoin for 60 days, sought medical attention due to fever and maculopapular cutaneous lesions. He presented lymphocytosis with eosinophilia and severe acute hepatitis 24 hours after admission day. Hepatic transaminases returned to reference levels after phenytoin withdrawal, and eosinophilia and cutaneous manifestations did not respond well to systemic steroids. A forearm biopsy showed findings suggestive of severe cutaneous adverse reaction. The patient’s microscopic and clinical characteristics meet all criteria in the scoring systems of Bocquet et al., Registry of Severe Cutaneous Adverse Reaction (RegiSCAR), and Japanese Research Committee on Severe Cutaneous Adverse Reaction (J-SCAR), being highly suggestive of DRESS syndrome very probably caused by phenytoin. The complete remission of symptoms was achieved weeks after admission. Conclusions: DRESS syndrome is a defiant reaction. Clinicians must be aware of potential causative drugs and perform a complete clinical examination using the available resources, including laboratory tests and histopathological assessment. The clinical remission relies on the withdrawal of the culprit drug. Particular attention should be given to the involvement of internal organs.

Severe cutaneous adverse drug reactions： a review on epidemiology, etiology, clinical manifestation and pathogenesis

Purpose To review the current progress in epidemiology, etiology, clinical manifestation, and pathophysiology of severe cutaneous adverse drug reactions （SCADRs）. Data sources Data were acquired by using Blackwell-Synergy, PubMed, original articles published in the main Chinese journals and related medical textbooks materials. Study selection and data extraction Throughout the literature review 49 articles were selected. Results SCADRs cases are rare, however, the implication is life threatening with significant mortality rates. Epidemiology studies have shown various incidences from different regions, gender, age, race and concurrent illness. There are typical signs and symptoms for each type of SCADRs, but this is not always so. Drugs associated with inducing SCADRs are anticonvulsants, antibiotics, NSAIDs and antirheumatic drugs. In some countries, especially in Asia, traditional drugs are often the cause of SCADRs. Genetic polymorphisms and viral infections are predisposition factors of SCADRs. Patients with certain genetic alleles and underlying diseases are vulnerable to SCADRs. The exact pathogenesis of SCADRs is not well defined. Nonetheless, recent study showed that reactive metabolites and immunological processes have a significant role in SCADRs. Conclusions The different SCADRs reactions are attributed by different intrinsic factors, such as genetic polymorphisms, gender, age and race as well as extrinsic factors, such as underlying diseases. Different regions and culprit drugs also play a role in the various types of SCADRs.