Withdrawal Of Carbamazepine Research Articles

Treatment-related transient splenial lesion of the Corpus Callosum in patients with neuropsychiatric disorders: a literature overview with a case report

ABSTRACTIntroduction: Transient-localized lesions of the splenium of the corpus callosum (SCC) have been described in various clinical conditions, some of them being attributed to the withdrawal of psychotropic drugs. The pathophysiology of the lesion reflects cytotoxic edema and reversible demyelination.Areas covered: The present article aimed at reviewing cases of transient SCC lesion exclusively related to changes in pharmacotherapy. It also reports the original case of a patient receiving a complex psychopharmacological therapy who developed a transient SCC lesion investigated by magnetic resonance imaging (MRI), magnetic resonance spectroscopy (MRS), and pharmacogenetic profiling.Expert opinion: To date, only one review on the subject has been published, analyzing 22 cases of transient SCC lesion arising in epileptic patients on antiepileptic therapy. It hypothesized that the nature of the lesion is a cytotoxic edema and the cases described in the subsequent 14 years seem to support this hypothesis. The authors reported the case of an Italian-Egyptian patient who developed a transient SCC lesion after the rapid withdrawal of Carbamazepine and Lurasidone. The lesion completely disappeared from the MRI performed after 1 month. Patient’s ethnic group and its pharmacogenetic profile were considered as possible causes of altered drug metabolism and, likely, of the SCC lesion.

Drug rash with eosinophilia and systemic symptoms syndrome in an adolescent - efficiency of immunoglobulin G in a corticosteroid resistant case

Introduction. Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome (sy) to carbamazepine has a heterogeneous clinical presentation. The aim of this report is to indicate the efficacy of immunoglobulin G in the treatment of corticosteroidresistant DRESS sy. Case outline. An adolescent suffering from epilepsy treated with carbamazepine and Na-valproate was hospitalized for fever, elevated transaminases, lymphadenopathy, splenomegaly. There was an eruption of skin efflorescence daily. On the sixth day of hospitalization, the number of eosinophils increased to 24% (780/ml absolute number). There was no desired response to methylprednisolone during the first eight days of treatment or to prednisolone during further treatment, with concomitant administration of antihistamines from day one of hospitalization, to Na-valproate, metformin hydrochloride, elimination diets, and carbamazepine withdrawal. Significant clinical, hematologic, and biochemical improvement occurred the day after the first dose of intravenous immunoglobulin G (IVIG). Conclusion. We point out the need to change the DRESS sy treatment recommendations in favor of the IVIG (as soon as the third or fourth day of treatment) in patients in whom the treatment with corticosteroids has no effect. Until new cases of the proven role of IVIG in the treatment of DRESS sy are published, corticosteroids remain the first therapeutic choice.

Carbamazepine-induced toxic epidermal necrolysis

Toxic epidermal necrolysis (TEN) is an uncommon; however, life-threatening dermatological condition which occurs most frequently by the use of drugs. Some group of medications, such as antiepileptics, antibiotics as well as antivirals, can induce such adverse drug reaction (ADR). Among the antiepileptics, carbamazepine is widely prescribed in case of epilepsy and trigeminal neuralgia. Here, we report a case of 22-year-old male with seizure disorder with a history of carbamazepine-induced skin lesions. Patient along with caregiver had approached local physician for increased seizure episodes but did not mention about the allergic history, and he was restarted on carbamazepine. As a result, the patient again developed skin lesions for which he consulted the dermatology outpatient department of the hospital. After outpatient department consultation, he was admitted to the ward for further clinical management. On hospitalization, the patient was diagnosed with carbamazepine-induced TEN (body surface area >40%). The management included immediate withdrawal of carbamazepine and supportive therapy with corticosteroids, antibiotics, antiepileptics, and antiallergic medications. After 15 days of rigorous treatment and hospitalization, the patient was discharged, as erosions healed with reepithelization. Based on this case, it can be concluded that reinitiation of a medication with a history of known allergy can result in TEN which is a serious life-threatening ADR. For the prevention of such ADR, thorough patient medical history should be obtained on each consultation. In addition, the patient and caregiver have to be informed about the clinical condition and the drugs which can provoke such adverse reaction.

Intravenous carbamazepine: a new formulation of a familiar drug

ABSTRACTIntroduction: Oral carbamazepine (CBZ), a broad-spectrum antiseizure drug (ASD) widely used for over 50 years, remains an important treatment choice for focal (partial) epilepsy. Although CBZ is a known inducer of cytochrome P450 (CYP) isoenzymes, many prescribers fail to recognize the potential issues with CBZ induction and are therefore unaware of the risk of drug toxicity upon CBZ withdrawal.Areas covered: Managing concomitant medications in CBZ-treated patients can be difficult. Abruptly stopping CBZ treatment, as may occur when patients are unable to take oral medication, can affect plasma concentrations of other medications. An intravenous (IV) formulation of CBZ has been recently approved by the US FDA for short-term replacement therapy in patients with focal and generalized seizures. Use of IV CBZ allows maintenance of stable plasma concentrations in circumstances when oral administration is temporarily impractical.Expert commentary: CBZ remains a frequently used treatment for focal seizures. With knowledge of the potential issues related to de-induction upon CBZ withdrawal, continuity of care with IV CBZ is an important step in improving the overall care of CBZ-treated patients.

Cutaneous adverse reaction during lithium treatment: a case report and updated systematic review with meta-analysis

ObjectivesTo present a new case of adverse cutaneous reaction during lithium treatment and to update the systematic review and meta-analysis of the incidence of this adverse reaction.MethodsWe conducted a systematic search (performed in September 2016) for peer-reviewed articles in English indexed in Medline (2011-present). Meta-analytical estimates were obtained using the “Metafor” package.Case presentationMs. H., a 31-year-old Caucasian woman with BD1, was admitted to the inpatient unit for a full-blown psychotic episode and treated with carbamazepine 400 mg q.d., lithium carbonate 450 mg q.d., and risperidone 4 mg q.d. with clinical improvement. After 12 days from the start of psychopharmacological treatment, she manifested a cutaneous reaction that motivated the stop of carbamazepine treatment, as well as the increase in lithium carbonate dose (750 mg q.d.). Risperidone dose remained unvaried. Since the skin lesion persisted after 8 days from withdrawal of carbamazepine, the private practitioner stopped also lithium carbonate treatment (de-challenge), maintaining risperidone treatment. The cutaneous reaction resolved spontaneously after six days from withdrawal of lithium carbonate. Subsequently, the worsening of psychopathological conditions motivated a new admission during which lithium carbonate was reintroduced (16 days after its suspension) (re-challenge). On the following day, we observed an itching erythematous maculopapular rash involving the trunk, the four limbs, and the oral mucosa.ConclusionsOur case of an erythematous maculopapular rash during lithium treatment was the first to present a challenge–de-challenge–re-challenge sequence that suggests causality. Although meta-analysis does not point to an increased rate of adverse skin reaction during lithium treatment, clinicians should not neglect to monitor cutaneous symptoms during lithium treatment.

Carbamazepine withdrawal

Carbamazepine withdrawal

Carbamazepine withdrawal

Carbamazepine withdrawal

"Late" Withdrawal Syndrome after Carbamazepine In Utero Exposure in a CYP2C9 Slow Metabolizer Newborn.

We report a case of carbamazepine withdrawal syndrome following in utero exposure to carbamazepine related to a pharmacogenetic predisposition factor. The infant was born at 37 1/7 weeks’ gestation by cesarean section to a mother treated for epilepsy with carbamazepine. One hour and thirty minutes after birth, the infant presented a respiratory distress with severe oxygen desaturation requiring intubation 5 h after birth. On the third day of life the infant developed clinical signs of a withdrawal syndrome which resolved progressively after 16 days and symptomatic treatment. The infant genotype analysis showed two low activity CYP2C9 allelic variants (∗2/∗3 heterozygote) predicting a CYP2C9 slow metabolizer phenotype which could explain reduced carbamazepine elimination and a late and long-lasting withdrawal symptoms observed 3 days after birth. The association of a withdrawal syndrome with carbamazepine exposure has not been previously reported and pharmacogenetic tests might therefore be useful in identifying patients at risk.

Carbamazepine versus phenytoin monotherapy for epilepsy: an individual participant data review.

Carbamazepine versus phenytoin monotherapy for epilepsy: an individual participant data review.

Síndrome DRESS inducido por carbamazepina

Drug reaction with eosinophilia and systemic symptoms (DRESS) is a rare clinical condition. It is presented a case of carbamazepine-induced DRESS syndrome in an alcoholic patient who presented with skin rash and lab tests compatible with hepatitis that improved with steroids and carbamazepine withdrawal.

Transient Splenial Lesion Following Abrupt Withdrawal of Carbamazepine.

Transient Splenial Lesion Following Abrupt Withdrawal of Carbamazepine.

Carbamazepine versus phenobarbitone monotherapy for epilepsy: an individual participant data review.

Carbamazepine versus phenobarbitone monotherapy for epilepsy: an individual participant data review.

Favorable change of lipid profile after carbamazepine withdrawal.

Patients treated with carbamazepine (CBZ) have increased serum levels of total cholesterol (TC), high-density lipoproteins (HDL), and low-density lipoproteins (LDL). We aimed to investigate whether these changes of serum lipids are reversible after CBZ withdrawal. We used a prospective, randomized double-blinded design. A total of 160 patients who had been seizure free on anti-epileptic drug monotherapy for more than 2years were included and randomized to withdrawal or not. The intervention was completed by 150 (80 females, 53%) patients. Serum samples from before and 4months after completed withdrawal or no withdrawal were obtained from 130 patients (63 females, 48%). Of these, 84 were treated with CBZ, 28 with valproate, nine with phenytoin, four with phenobarbital, and five with lamotrigine. Of the patients who had been treated with CBZ, 47 were randomized to the withdrawal group, and 37 were randomized to the non-withdrawal group. Among the CBZ-treated patients, a significant decrease in serum levels of TC, LDL, and apolipoprotein B (ApoB) were found in the withdrawal group compared with the non-withdrawal group. Mean differences in change were as follows: TC 0.68mmol/l (P=0.005, CL - 1.15 to -0.21); LDL - 0.67mmol/l (P=0.001, CL - 1.03 to -0.29); ApoB - 0.13g/l (P=0.02, CL - 0.23 to -0.03). No significant changes in HDL, apolipoprotein A, and C-reactive protein were detected. Our results indicate that CBZ may have unfavorable effects on serum levels of TC, LDL, and ApoB. However, these changes seem to be reversible even after years of treatment.

Carbamazepine Withdrawal-induced Hyperalgesia in Chronic Neuropathic Pain

Combined pharmacological treatments are the most used approach for neuropathic pain. Carbamazepine, an antiepileptic agent, is generally used as a third-line treatment for neuropathic pain and can be considered an option only when patients have not responded to the first- and second-line medications. In the case presented herein, a patient with neuropathic pain was treated using a combined pharmacological regimen. The patient’s pain deteriorated, despite increasing the doses of opioids, when carbamazepine was discontinued, potentially because carbamazepine withdrawal disrupted the balance that was achieved by the multifaceted pharmacological regimen, thus inducing hyperalgesia. Interestingly, when carbamazepine was prescribed again, the patient’s pain was successfully managed. Animal research has reported that carbamazepine can potentiate the analgesic effectiveness of morphine in rodent models of neuropathic pain and postoperative pain. This clinical case demonstrates that carbamazepine may have a synergistic effect on the analgesic effectiveness of morphine and may inhibit or postpone opioid-induced hyperalgesia. We postulate that a probable mechanism of action of carbamazepine may involve -aminobutyric acid-ergic potentiation and the interruption of glutamatergic function via N-methyl-D-aspartate receptors. Further research is warranted to clarify the analgesic action of carbamazepine and its potential use for the prevention of opioidinduced hyperalgesia in chronic neuropathic pain patients. Key words: Analgesia, hyperalgesia, carbamazepine, opioids, neuropathic pain, pharmacologic treatment

Carbamazepine withdrawal

Carbamazepine withdrawal

Carbamazepine and oxcarbazepine in adult patients with Dravet syndrome: Friend or foe?

PurposeIn newly diagnosed patients with Dravet syndrome sodium channel blockers are usually avoided. However, in many adult patients the diagnosis was made long after the initiation of therapy. The purpose of our study was to acquire information concerning the potential risks and benefits of (ox)carba(ma)zepine withdrawal in adult patients with genetically confirmed Dravet syndrome. MethodWe identified 16 adults with Dravet syndrome, living in a tertiary care facility for people with epilepsy and an intellectual disability. We reviewed clinical history, genetic findings, the type and duration of sodium channels blockers that were used, seizure types and frequency, and the effect of a change in these medications. ResultsThe study population consisted of 9 men and 7 women. Median age was 35 years (range 20–61 years).An attempt to withdraw carbamazepine (CBZ) was made in 9 patients. In 3 of these patients an increase in tonic-clonic seizures was observed. An attempt to withdraw oxcarbazepine (OXC) was made in 3 patients, leading to a complete stop in 2 patients.3 of the 4 deaths in the withdrawal-group were related to epilepsy. ConclusionIn adult patients with Dravet syndrome withdrawal of CBZ or OXC is not without risks. We suggest that (ox)carba(ma)zepine withdrawal should be considered in these patients but only if there is a good reason to do so and only if they are closely monitored.

Carbamazepine withdrawal

Carbamazepine withdrawal

Reversible Splenial Lesion Following Rapid Withdrawal of Carbamazepine

A 19-year-old man with paroxysmal kinesigenic dyskinesia (PKD) taking 200mg carbamazepine per day for six years was admitted to our hospital because of a medical certificate for soldiers. The dyskinesias were usually precipitated by sudden movements and these attacks occurred several times a day and had a brief duration (less than one minute). The drug was abruptly withdrawn seven days before the brain imaging and video-electroencephalography monitoring. Magnetic resonance imaging showed cytotoxic edema in the splenium, which were completely resolved three months later (Figure).

Tapered withdrawal of phenytoin removes protective effect in EAE without inflammatory rebound and mortality

Axon degeneration has been identified as a major contributor to non-remitting neurological deficits in patients with multiple sclerosis (MS), which has elicited substantial interest in the development of neuroprotective therapies. Sodium channel blockers, including phenytoin, carbamazepine, flecainide and lamotrigine, have been shown to protect axons from degeneration, attenuate immune cell infiltrates and slow the acquisition of neurological deficits in mice with experimental autoimmune encephalomyelitis (EAE), a model of MS. However, the sudden withdrawal of sodium channel blockers, phenytoin and carbamazepine, is associated with severe exacerbation of EAE characterized by massive inflammatory infiltrates and high mortality. In the present study, we asked whether a slow, tapered withdrawal of phenytoin treatment from mice with EAE produced sudden worsening similar to that of sudden withdrawal. Our results demonstrate that gradual withdrawal of phenytoin treatment from mice with EAE is associated with worsening of clinical scores which approach non-treated levels, but was not associated with increased immune cell infiltrates or deaths as have been observed with abrupt withdrawal. These observations support sodium channel blockers as a potential therapeutic agent in the treatment of MS, but indicate caution if treatment is ceased.

Carbamazepine withdrawal

Carbamazepine withdrawal