Case Report

Carlson, Teri; Reynolds, C. A.; Caplan, Rochelle

doi:10.1097/chi.0b013e31802ed8b2

Cited by 28 publications

(12 citation statements)

References 23 publications

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“…Because the 17 different antipsychotics prescribed are quite different in physicochemical and pharmacological properties, we undertook a multivariate analysis to determine if any of them independently influenced the blood ammonia level (Table 5). We found that concomitant administration of risperidone or blonanserin was associated with a reduced blood concentration of ammonia, which somewhat conflicts with the results reported by previous studies [11–13], our data will need to be confirmed in a study with a larger number of patients: the number of patients receiving blonanserin with VPA was small ( n = 3) in the present study.…”

Section: Discussioncontrasting

confidence: 99%

“…Previous studies have suggested that the concomitant use of VPA with an antipsychotic, risperidone, may be a risk factor for hyperammonemia through competition for drug protein binding [11–13]. However, it remains to be clarified whether or not the combination of certain antipsychotics reduces CPS1 activity.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have reported that the administration of therapeutic doses of VPA to patients with epilepsy or bipolar disorder can cause hyperammonemia and alter serum carnitine and amino acid concentrations [11–14], whereas no attempts have been made to determine if VPA causes hyperammonemia when administered to patients with schizophrenia. Here, we report the relationships between blood ammonia concentration and the concentrations of free carnitine, acyl-carnitine, and amino acids, including glutamate and citrulline, in a cohort of schizophrenic patients receiving VPA.…”

Section: Introductionmentioning

confidence: 99%

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Association between the blood concentrations of ammonia and carnitine/amino acid of schizophrenic patients treated with valproic acid

Ando

Amayasu

Itai

et al. 2017

BioPsychoSocial Med

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BackgroundAdministration of valproic acid (VPA) is complicated with approximately 0.9% of patients developing hyperammonemia, but the pathogenesis of this adverse effect remains to be clarified. The aim of the present study was to search for mechanisms associated with VPA-induced hyperammonemia in the light of changes in serum amino acids concentrations associated with the urea cycle of schizophrenic patients.MethodBlood samples (10 mL) were obtained from 37 schizophrenic patients receiving VPA for the prevention of violent behaviors in the morning after overnight fast. Blood concentrations of ammonia, VPA, free carnitine, acyl-carnitine, and 40 amino acids including glutamate and citrulline were measured for each patient. Univariate and multivariate regression analyses were performed to identify amino acids or concomitantly administered drugs that were associated with variability in the blood concentrations of ammonia.ResultThe blood ammonia level was positively correlated with the serum glutamate concentration (r = 0.44, p < 0.01) but negatively correlated with glutamine (r = −0.41, p = 0.01), citrulline (r = −0.42, p = 0.01), and glycine concentrations (r = −0.54, p < 0.01). It was also revealed that the concomitant administration of the mood stabilizers (p = 0.04) risperidone (p = 0.03) and blonanserin (p < 0.01) was positively associated with the elevation of the blood ammonia level.ConclusionWe hypothisized that VPA would elevate the blood ammonia level of schizophrenic patients. The observed changes in serum amino acids are compatible with urea cycle dysfunction, possibly due to reduced carbamoyl-phosphate synthase 1 (CPS1) activity. We conclude that VPA should be prudently prescribed to schizophrenic patients, particularly those receiving mood stabilizers or certain antipsychotics.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Association between the blood concentrations of ammonia and carnitine/amino acid of schizophrenic patients treated with valproic acid

Ando

Amayasu

Itai

et al. 2017

BioPsychoSocial Med

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“…Hyperammonemic encephalopathy has also been described in children and adults who received a combination of valproate and risperidone. Competition for protein binding sites leading to increase in free valproate levels was considered as a possible mechanism 14,15 . An interaction between valproate and lorazepam was implicated in another case of hyperammonemic encephalopathy 16 .…”

Section: Discussionmentioning

confidence: 99%

Valproate-Induced Hyperammonemic Encephalopathy in a patient with Ischemic Stroke

Solomon

Singaravelu

2016

Klinik Psikofarmakoloji Bülteni-Bulletin of Clinical Psychophar

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Valproate-induced hyperammonemic encephalopathy in a patient with ischemic stroke Hyperammonemic encephalopathy is a rare, life threatening complication of valproate therapy. We describe an adult male with manic disorder and alcohol dependence who developed encephalopathy within two weeks of therapy with valproate. Risperidone and lorazepam were the concomitant medications. His serum ammonia was found to be elevated. There was complete resolution of symptoms after valproate was stopped. The patient's clinical picture was further complicated by imaging findings of ischemic changes and infarcts in the brain. Our report highlights the importance of considering hyperammonemic encephalopathy in any patients who develops acute changes in mental state while receiving valproate.

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“…Due to limited literature reports of valproic acid-induced abnormal behavior, the severity and psychopathological nature of behavioral disturbances induced by valproic acid remains obscure. [15]…”

Section: Discussionmentioning

confidence: 99%

Valproic acid-induced abnormal behavior

Nagalakshmi

Ramesh

Parthasarathi

et al. 2010

Indian J Psychiatry

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A 12-year-old female was admitted to hospital with complaints of abnormal behavior. She was on valproic acid 200mg twice daily and clobazam 5mg at night for the past 13 weeks for her complex partial seizures with secondary generalized seizures. On day 60 of the treatment with valproic acid she developed behavioral disturbances and initiated treatment with tablet chlorpromazine, olanzapine and risperidone. During the present hospitalization, as there was no improvement in abnormal behavior, antipsychotics were discontinued and she was on observation for five days. On day 6, valproic acid was replaced with carbamazepine. Patient started recovering gradually from the abnormal behavior three days after the withdrawal of valproic acid and completely recovered after three months. Causality of valproic acid-induced abnormal behavior was ‘possible’. Behavioral disturbances associated with valproic acid are rare and is reversible upon discontinuation of the drug. There is a need for vigilance on abnormal behavioral effects in patients receiving valproic acid.

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Case Report

Cited by 28 publications

References 23 publications

Association between the blood concentrations of ammonia and carnitine/amino acid of schizophrenic patients treated with valproic acid

Association between the blood concentrations of ammonia and carnitine/amino acid of schizophrenic patients treated with valproic acid

Valproate-Induced Hyperammonemic Encephalopathy in a patient with Ischemic Stroke

Valproic acid-induced abnormal behavior

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