Disease relevance of VALPROIC ACID

• Acute hepatic failure associated with the use of sodium valproate [1].
• The anticonvulsants ethosuximide, sodium valproate, and trimethadione that are specific for petit mal epilepsy abolished in rats the electrical seizure activity and behavioral abnormalities produced by leucine enkephalin, whereas phenobarbital and phenytoin had no effect [2].
• Pure red cell aplasia associated with sodium valproate therapy [3].
• Sodium valproate, pregnancy, and infantile fatal liver failure [4].
• Acute liver disease associated with sodium valproate [5].

Psychiatry related information on VALPROIC ACID

• Nocturnal enuresis associated with sodium valproate [6].
• Sodium valproate in Huntington's disease [7].
• Three patients with organic and affective symptoms related to multiple sclerosis or systemic lupus erythematosus responded dramatically to sodium valproate after other treatments had failed [8].
• Treatment of bulimia and rapid-cycling bipolar disorder with sodium valproate: a case report [9].
• Sodium valproate may be of use in a range of affective disorders [10].

High impact information on VALPROIC ACID

• All the patients had epilepsy that had previously been untreated, and had been randomly assigned to receive carbamazepine, phenytoin, or sodium valproate [11].
• Cutaneous vasculitis induced by sodium valproate [12].
• Hepatitis A in three patients taking sodium valproate [13].
• Sodium valproate and heterogeneity of pituitary dependent Cushing's syndrome [14].
• Sodium valproate and platelet-count [15].

Chemical compound and disease context of VALPROIC ACID

• Additional features were: absence of prior major diseases; normal results of neurological and neuroradiological examinations; excellent response to anticonvulsant treatment with sodium valproate and/or phenobarbital; frequent family history of epileptic seizures (25% of patients); and association with generalized seizures (57.2% of patients) [16].
• Lumbar CSF HVA, MHPG, 5HIAA, cAMP, and cGMP were measured in 12 chronic schizophrenics with tardive dyskinesia before and 3 weeks after sodium valproate (VPA) or cyproheptadine treatment [17].
• To determine the role of gamma-aminobutyric acid (GABA) in islet tissue, sodium valproate (1600 mg/day) was administered for 6 days to 10 normal subjects and 1 patient with a somatostatinoma [18].
• METHODS: This study tested if the antidepressant imipramine or the mood stabilizers lithium and sodium valproate regulated pathophysiological serine-dephosphorylation of GSK3 caused by hypoxia in mouse brain in vivo [19].
• Fasting blood glucose levels decreased in the somatostatinoma patient during sodium valproate administration [18].

Biological context of VALPROIC ACID

• Sodium valproate: pharmacokinetics and effectivensss in treating intractable seizures [20].
• Pharmacokinetics and bioavailability of sodium valproate [21].
• Effect of single doses of sodium valproate on serum phenytoin levels and protein binding in epileptic patients [22].
• The effect of sodium valproate (400 mg three times daily) on the disposition kinetics of intravenous phenytoin (250 mg) was investigated in seven normal subjects [23].
• Inhibitory effects of sodium valproate on oxidative phosphorylation [24].

Anatomical context of VALPROIC ACID

• By microarray studies, we found evidence that treatment of human hepatocellular carcinoma cells with the histone deacetylase inhibitor (HDAC-I) sodium valproate (VPA) mediates recognition of cancer cells by cytotoxic lymphocytes via NKG2D [25].
• Bone marrow suppression developed in a patient while she was on a regimen of sodium valproate [26].
• Naloxone reverses the inhibition by sodium valproate of GABA transport across the Deiters' neuronal plasma membrane [27].
• Human brain, plasma, and cerebrospinal fluid concentration of sodium valproate after 72 hours of therapy [28].
• Sodium valproate (VP) inhibited oxidative phosphorylation in isolated rat liver mitochondria [24].

Associations of VALPROIC ACID with other chemical compounds

• OBJECTIVE: The authors explored the relationship of adherence to treatment with mood stabilizers (lithium, carbamazepine, and sodium valproate) and plasma levels of these drugs to future psychiatric hospitalizations [29].
• The cell membrane-disordering potencies of sodium valproate, the sodium salts of other short-chain fatty acids, and ethanol were compared using fluorescence polarization with the probe 1,6-diphenyl-1,3,5-hexatriene [30].
• Poor correlation between single-dose data and steady-state kinetics for phenobarbitone, primidone, carbamazepine and sodium valproate in children during monotherapy. Possible reasons for the lack of correlation [31].
• Of 88 patients with intractable epilepsy, 60 have been treated with clonazepam for up to three years and 60 have been treated with sodium valproate for up to 18 months [32].
• Up-regulation of hippocampal glutamate transport during chronic treatment with sodium valproate [33].

Gene context of VALPROIC ACID

• Thus combination of an agonistic TRAIL-R1 Ab and an HDACi, such as the anticonvulsant sodium valproate, could be of value in treating CLL [34].
• Cholinergic stimulation of early growth response-1 DNA binding activity requires protein kinase C and mitogen-activated protein kinase kinase activation and is inhibited by sodium valproate in SH-SY5Y cells [35].
• Sodium valproate, a mood stabilizer, when chronically administered to rats (200 mg/kg i.p. daily for 30 days) significantly reduced the brain protein levels of cyclooxygenase (COX)-1 and COX-2, without altering the mRNA levels of these enzymes [36].
• The inhibitory effects due to overexpressed GSK3 beta were reversed by treatment with lithium and with another GSK 3beta inhibitor, sodium valproate [37].
• In the presence of sodium valproate, GH and PRL levels rose 3- and 1.5-fold, respectively, in response to exercise [38].

Analytical, diagnostic and therapeutic context of VALPROIC ACID

• Five patients, four of them children, had acute liver disease after treatment with sodium valproate [5].
• Lowered erythrocyte-sedimentation rate with sodium valproate [39].
• Sodium valproate: serial monitoring of EEG and serum levels [40].
• We included 43 patients with migraine without aura in a triple-blind, placebo- and dose-controlled, crossover study of the prophylactic effect of slow-release sodium valproate; 34 patients completed the trial [41].
• Rectal administration of sodium valproate in status epilepticus [42].

References