UNASSIGNED: Malignant hypertension is the most severe form of hypertension that may cause life-threatening manifestations. Carbamazepine is an antiepileptic drug primarily used for seizure disorders and trigeminal neuralgia. One of the rarely triggered adverse side effects of carbamazepine is drug-induced malignant hypertension. Here, we intend to present the first case report of carbamazepine-induced malignant hypertension from Nepal.
UNASSIGNED: Here, we aim to present a case report of a 26-year-old female with a history of generalized tonic-clonic seizure who had developed de-novo hypertension after initiation of carbamazepine with no decrease in blood pressure to normal levels despite several antihypertensive administrations which eventually resolved on the discontinuation of drug carbamazepine. The patient was subsequently managed at our institution, where levetiracetam was used as an alternative. The patient was in close follow-up monitoring blood pressure charting.
UNASSIGNED: Although rare, a variety of cardiovascular side effects, including hypertension led by the drug carbamazepine, have been reported. Carbamazepine acts by inducing cytochrome P450, which facilitates an early metabolism and clearance of several antihypertensive medications, causing a decrease in their role in hypertension. The exact etiology is still debatable. However, the removal of the drug carbamazepine may result in a remission of hypertension, as illustrated in several literatures.
UNASSIGNED: Malignant hypertension is caused in rare cases to the use of the drug carbamazepine. The hypertension can undergo remission by subsequent discontinuation of the carbamazepine therapy. Regular blood pressure monitoring and charting are crucial in such cases.

BACKGROUND: Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but life-threatening skin lesion triggered by hypersensitive drug reaction. They are characterized by extensive epidermal necrosis and skin exfoliation. Fulminant type 1 diabetes mellitus (FT1DM) is featured by a rapid-onset of hyperglycemia with ketoacidosis due to severely destroyed β-cell function. Fulminant type 1 diabetes mellitus as a sequela of SJS/TEN has rarely been reported.
METHODS: We present a 73-year-old female patient who developed SJS/TEN skin allergic reaction after taking carbamazepine and phenytoin for 35 days. Then, hyperglycemia and diabetic ketoacidosis occurred 20 days after discontinuation of antiepileptic drugs. A very low serum C-peptide level (8.79 pmol/l) and a near-normal glycosylated hemoglobin level met the diagnostic criteria for fulminant T1DM. Intravenous immunoglobulin (IVIG) and insulin were promptly administered, and the patient recovered finally.
CONCLUSIONS: This rare case indicates that monitoring blood glucose is necessary in SJS/TEN drug reaction, and comprehensive therapy with rehydration, insulin, antibiotics, and IVIG may improve the prognosis.

Carbamazepine is utilized for various indications. Due to its pharmacokinetic profile and drug properties, toxicity can be delayed and persistent despite supportive care. We report a severe case of intentional carbamazepine toxicity in a carbamazepine naive individual mimicking brain death that was not diagnosed until three days after consumption of carbamazepine when the patient was comatose. Symptoms of overdose persisted for several days despite attempted treatment with activated charcoal and whole bowel irrigation, hemodialysis, and plasmapheresis. Symptoms only began to improve with bowel evacuation as a result of administration of neostigmine intravenously plus hemodialysis and plasmapheresis additionally. Despite previous literature that reported success with hemodialysis and/or plasmapheresis we did not find either to be overly effective in our case possibly due to lack of ability to perform multidose activated charcoal and whole bowel irrigation. To our knowledge this is one of the few cases of carbamazepine overdose utilizing both hemodialysis and plasmapheresis but without activated charcoal and the only case report in which neostigmine was administered as an attempt to remove drug via the gastrointestinal tract with success.

We report three sisters with self-limited familial infantile epilepsy, caused by a mutation in proline-rich transmembrane protein2. Self-limited familial infantile epilepsy has been established as a distinct epileptic syndrome characterized by focal seizures in clusters of infantile-onset. The seizure types of our cases were focal with or without secondary generalization. The seizures manifested at 3-5 months of age, and each lasted 1-2 min. All three sisters fulfilled the criteria for self-limited familial infantile epilepsy, except in one case who showed interictal spikes in the right central area. The seizures were controlled with carbamazepine. When carbamazepine treatment was started, one case developed a rash, and her treatment was switched to valproic acid. However, the seizures persisted in this case such that carbamazepine was restarted. The rash did not recur. Electroencephalography showed spikes in only one case on interictal electroencephalography. All three sisters were developmentally normal, and no dyskinesia was observed during follow-up. All three sisters and their father, but not their mother, had the following pathogenic variant in proline-rich transmembrane protein2: NM_001256442.2(PRRT2): c.649dup[p.(Arg217Profs*8)]. This mutation has been identified in the majority of families with self-limited familial infantile epilepsy, paroxysmal kinesigenic dyskinesia, and/or infantile convulsion and choreoathetosis. Their father had no history of either self-limited familial infantile epilepsy or paroxysmal kinesigenic dyskinesia. The lack of a clear genotype-phenotype correlation was demonstrated in our cases with this proline-rich transmembrane protein2 mutation.

UNASSIGNED: Palilalia is a type of speech characterized by compulsive repetition of words, phrases, or syllables. Several reports have noted that palilalia can occur in response to external verbal stimuli. Here, we report, for the first time, a patient with palilalia induced by gait, which we call \"movement-related palilalia.\"
UNASSIGNED: Eleven months after the onset of cerebral infarction sparing the right precentral gyrus and its adjacent subcortical regions, a 63-year-old, left-handed Japanese man was referred for psychiatric consultation because of a complaint of irritability caused by the stress of compulsive repetition of a single meaningless word, \"wai.\" The repetition of a word, palilalia, in this case, was characterized by its predominant occurrence during walking and by its melodic tones. The palilalia during walking disappeared almost completely after 5 months of treatment with carbamazepine 600 mg.
UNASSIGNED: Palilalia induced by gait can occur in patients with a history of cerebral infarction. This palilalia during walking may be due to the reorganization of networks in areas nearby or surrounding cerebral infarcts.

BACKGROUND: Treating refractory status epilepticus (RSE) remains a challenge. Thiamylal can be used as a second- or third-line treatment; however, its potential to induce cytochrome P450 (CYP) activity may reduce the concentration of antiepileptic drugs (AEDs) administered prior to thiamylal. This report details a case of RSE patient treated with thiamylal, with monitored concentrations of thiamylal and other AEDs.
METHODS: A 72-year-old healthy man developed RSE. Despite the administration of various AEDs, his seizures were not resolved. Thiamylal was then administered at an initial bolus dose of 2.1 mg/kg, followed by a continuous infusion of 4.2-5.2 mg/kg/h. The initial thiamylal concentration was observed at 7.8 μg/mL, increasing to 35.2 μg/mL before decreasing after dose reduction and cessation. Concurrently, the concentration of concomitant carbamazepine decreased from 5.59 μg/mL to 2.1 μg/mL and recovered as thiamylal concentration decreased. Lesser impacts were noted for other AEDs.
CONCLUSIONS: This case report underscored the efficacy of thiamylal in treating RSE. However, it also highlighted the need for clinicians to closely monitor the concentrations of concurrent AEDs, especially carbamazepine, during thiamylal therapy.

A case of Kloos syndrome is presented, a rare psychopathological manifestation in psychiatry characterized by the experience of \"time paralysis\" related to an epileptic focus in the left temporoparietal areas. This syndrome was identified through a detailed psychopathological analysis and detected by an electroencephalographic record. The patient\'s symptoms disappeared after receiving antiepileptic treatment with Carbamazepine. In this case report we highlight the detailed phenomenological and clinical analysis, as well as the importance of carrying out complementary tests when we are faced with unusual or sudden-onset symptoms without any trigger, as took place in the case exposed.

This case report examines the possible correlation between the clozapine/norclozapine ratio and the occurrence of constipation and paralytic ileus. We present the case of a 42-year-old patient diagnosed with schizoaffective disorder undergoing clozapine therapy. Despite intensive treatment with clozapine, haloperidol, valproic acid and biweekly electroconvulsive therapy sessions for over a year, florid psychotic symptoms and fluctuating mood swings persisted. Therefore, valproic acid was replaced by carbamazepine, a potent inducer of several CYP450-enzymes. To maintain clozapine plasma levels, fluvoxamine, a CYP1A2-inhibitor, was introduced at a dose of 25 mg before this switch. After addition of carbamazepine, there was a significant decline in clozapine levels, necessitating an increase in fluvoxamine dosage to 50 mg. Five weeks later the patient was admitted to a general hospital with a diagnosis of paralytic ileus. Treatment with enemas proved effective. Drug concentration analysis revealed a 2.5-fold increase in norclozapine levels in the weeks preceding hospital admission, resulting in an inverted clozapine/norclozapine ratio. Treatment with clozapine, carbamazepine and fluvoxamine was continued as the patient demonstrated clinical improvement on carbamazepine. Concurrently, an intensive laxative regimen was initiated. Two weeks later, the patient was readmitted to the general hospital due to suspected paralytic ileus and faecal vomiting, once again displaying an inverted clozapine/norclozapine ratio. We discuss potential mechanisms contributing to the occurrence of the paralytic ileus in this patient, including the antagonism of muscarinic M3 receptors by both clozapine and norclozapine, as well as the agonism of delta-opioid receptors by norclozapine. This case highlights the potential significance of both the clozapine/norclozapine ratio and absolute norclozapine levels as risk factors for constipation and paralytic ileus in patients on clozapine therapy.

BACKGROUND: Carbamazepine (CBZ) is an antiseizure medication known to induce the expression of cytochrome P4503A metabolic enzymes. Here, we describe a man living with HIV who underwent several changes in the daily dose of CBZ, which resulted in different induction effects on darunavir trough concentrations.
METHODS: A 59-year-old man with HIV, successfully undergoing maintenance antiretroviral treatment with darunavir/cobicistat once daily (combined with raltegravir), was prescribed CBZ for recurrent trigeminal neuralgia. Over subsequent months, the patient underwent various changes in the doses (from 200 to 800 mg/d) and trough concentrations (from 3.6 to 18.0 mg/L) of CBZ, guided by clinical response to trigeminal neuralgia.
RESULTS: A highly significant inverse association was observed between darunavir trough concentration and both CBZ dose or trough concentration (coefficient of determination >0.75, P < 0.0001). Ultimately, the darunavir dose was increased to 600 mg twice daily with ritonavir and dolutegravir to ensure optimal antiretroviral coverage, anticipating potential further uptitration of CBZ doses.
CONCLUSIONS: The impact of CBZ on boosted darunavir exposure seemed to be dose- and concentration-dependent. The management of such drug-drug interactions in daily practice was facilitated through therapeutic drug monitoring. This case underscores the importance of a multidisciplinary approach that incorporates both antiretroviral and nonantiretroviral comedications contributing to the optimal management of polypharmacy in individuals living with HIV.

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