Eslicarbazepine acetate as a therapeutic option in a patient with carbamazepine-induced rash and HLA-A*31:01

Kay, Lara; Willems, Laurent M.; Zöllner, Johann Philipp; Reif, Philipp S.; Klein, Karl Martin; Rosenow, Felix; Strzelczyk, Adam

doi:10.1016/j.seizure.2017.02.019

Cited by 7 publications

(4 citation statements)

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“…Of note is one patient who developed an allergic reaction with hypotension upon first infusion of BRV, and one adolescent (16 years) who developed a hyperpigmentation of both upper limbs following treatment with BRV for >6 months. In another patient, skin rash was probably due to carbamazepine exposure in the presence of a HLA‐A*31:01 haplotype . We observed two pregnancies, with exposure to BRV of 2 days in one case and approximately 6 weeks in a second case, during the first term.…”

Section: Resultsmentioning

confidence: 69%

“…In another patient, skin rash was probably due to carbamazepine exposure in the presence of a HLA-A*31:01 haplotype. 23 We observed two pregnancies, with exposure to BRV of 2 days in one case and approximately 6 weeks in a second case, during the first term. In both patients, BRV treatment was stopped and they were immediately switched to LEV.…”

Section: Treatment-emergent Adverse Effectsmentioning

confidence: 73%

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Postmarketing experience with brivaracetam in the treatment of epilepsies: A multicenter cohort study from Germany

et al. 2017

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BRV in broad clinical postmarketing use is a well-tolerated anticonvulsant drug with 50% responder rates, similar to those observed in the regulatory trials, even though 90% of the patients included had previously been exposed to LEV. An immediate switch from LEV to BRV at a ratio of 10:1 to 15:1 is feasible. The only independent significant predictor of efficacy was the start of BRV in patients not currently taking LEV. The occurrence of BAE during previous LEV exposure predicted poor psychobehavioral tolerability of BRV treatment. A switch to BRV can be considered in patients with LEV-induced BAE.

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Section: Resultsmentioning

confidence: 69%

Section: Treatment-emergent Adverse Effectsmentioning

confidence: 73%

Postmarketing experience with brivaracetam in the treatment of epilepsies: A multicenter cohort study from Germany

et al. 2017

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“…184,185 Eslicarbazepine is contraindicated in patients with hypersensitivity reactions to CBZ (European Medicines Agency, London, UK), but some studies have suggested that severe skin reactions occur less frequently with eslicarbazepine compared to other anticonvulsants, leading to treatment discontinuation in only 0.1% of the cases. 186 As data are scarce and contradictory, [187][188][189] further studies are clearly needed before definitive conclusions may be drawn. Eslicarbazepine has been shown to interact selectively with the inactive state of VGSCs through altered slow inactivation, as opposed to the effects on fast inactivation associated with CBZ and OXC.…”

Section: Additional Pharmacological Perspectivesmentioning

confidence: 99%

Trigeminal neuralgia: An overview from pathophysiology to pharmacological treatments

2020

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The trigeminal nerve (V) is the fifth and largest of all cranial nerves, and it is responsible for detecting sensory stimuli that arise from the craniofacial area. The nerve is divided into three branches: ophthalmic (V1), maxillary (V2), and mandibular (V3); their cell bodies are located in the trigeminal ganglia and they make connections with second-order neurons in the trigeminal brainstem sensory nuclear complex. Ascending projections via the trigeminothalamic tract transmit information to the thalamus and other brain regions responsible for interpreting sensory information. One of the most common forms of craniofacial pain is trigeminal neuralgia. Trigeminal neuralgia is characterized by sudden, brief, and excruciating facial pain attacks in one or more of the V branches, leading to a severe reduction in the quality of life of affected patients. Trigeminal neuralgia etiology can be classified into idiopathic, classic, and secondary. Classic trigeminal neuralgia is associated with neurovascular compression in the trigeminal root entry zone, which can lead to demyelination and a dysregulation of voltage-gated sodium channel expression in the membrane. These alterations may be responsible for pain attacks in trigeminal neuralgia patients. The antiepileptic drugs carbamazepine and oxcarbazepine are the first-line pharmacological treatment for trigeminal neuralgia. Their mechanism of action is a modulation of voltage-gated sodium channels, leading to a decrease in neuronal activity. Although carbamazepine and oxcarbazepine are the first-line treatment, other drugs may be useful for pain control in trigeminal neuralgia. Among them, the anticonvulsants gabapentin, pregabalin, lamotrigine and phenytoin, baclofen, and botulinum toxin type A can be coadministered with carbamazepine or oxcarbazepine for a synergistic approach. New pharmacological alternatives are being explored such as the active metabolite of oxcarbazepine, eslicarbazepine, and the new Nav1.7 blocker vixotrigine. The pharmacological profiles of these drugs are addressed in this review.

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“… 43 In this respect, the official summary of product characteristics contraindicates ESL in patients with hypersensitivity reactions to CBZ. 9 A recent report described the case of a patient with the HLA-A*31:01 haplotype who, after the development of a severe cutaneous reaction following CBZ administration, was successfully prescribed ESL without experiencing any adverse event, 44 and it suggested that ESL may be considered if the benefits are thought to exceed the risks. The safety of ESL in subjects with HLA-B*15:02 or HLA-A*31:01 haplotypes and a history of CBZ- or OXC-induced hypersensitivity reactions remain, however, to be fully addressed in larger studies before drawing definitive conclusions.…”

Section: Introductionmentioning

confidence: 99%

Eslicarbazepine acetate in the treatment of adults with partial-onset epilepsy: an evidence-based review of efficacy, safety and place in therapy

Lattanzi¹,

Brigo²,

Cagnetti³

et al. 2018

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IntroductionUp to 30% of the patients diagnosed with epilepsy will continue suffering from seizures despite treatment with antiepileptic drugs, either in monotherapy or polytherapy. Hence, there remains the need to develop new effective and well-tolerated therapies.AimThe objective of this article was to review the evidence for the efficacy and safety of eslicarbazepine acetate (ESL) as adjunctive treatment in adult patients with focal onset seizures.Evidence reviewESL is the newest, third-generation, single enantiomer member of the dibenzazepine family. Following oral administration, ESL is rapidly and extensively metabolized by hepatic first-pass hydrolysis to the active metabolite eslicarbazepine, which has linear, dose-proportional pharmacokinetics and low potential for drug-drug interactions. Eslicarbazepine works as a competitive blocker of the voltage gated sodium channels; unlike carbamazepine (CBZ) and oxcarbazepine (OXC), it has a lower affinity for the resting state of the channels, and reduces their availability by selectively enhancing slow inactivation. Efficacy and safety of ESL have been assessed in four randomized, Phase III clinical trials: the median relative reduction in standardized seizure frequency was 33.4% and 37.8% in the ESL 800 and 1,200 mg daily dose groups, and the responder rates were 33.8% and 43.1%, respectively. The incidence of treatment-emergent adverse events (TEAEs) increased with raising the dosage (ESL 400 mg: 63.8%, ESL 800 mg: 67.0%, ESL 1,200 mg: 73.1%). The TEAEs were generally mild to moderate in intensity, and the most common were dizziness, somnolence, headache and nausea. Open-label studies confirmed the findings from the pivotal trials and demonstrated sustained therapeutic effect of ESL over time and improvement of tolerability profile in patients switching from OXC/CBZ. No unexpected safety signals emerged over >5 years of follow-up.ConclusionOnce-daily adjunctive ESL at the doses of 800 and 1,200 mg was effective to reduce the seizure frequency and was fairly well tolerated in adults with focal onset epilepsy. Starting treatment at 400 mg/day, followed by 400 mg increments every 7–14 days, could provide the optimal balance of efficacy and tolerability.

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Eslicarbazepine acetate as a therapeutic option in a patient with carbamazepine-induced rash and HLA-A*31:01

Cited by 7 publications

References 5 publications

Postmarketing experience with brivaracetam in the treatment of epilepsies: A multicenter cohort study from Germany

Postmarketing experience with brivaracetam in the treatment of epilepsies: A multicenter cohort study from Germany

Trigeminal neuralgia: An overview from pathophysiology to pharmacological treatments

Eslicarbazepine acetate in the treatment of adults with partial-onset epilepsy: an evidence-based review of efficacy, safety and place in therapy

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