Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Valproic acid has been widely used for the treatment of epilepsy. Although it is usually well tolerated, it has been associated with some side effects. A poor studied side effect is the hyperammonemia, which independs from the drug hepatotoxic action. The hyperammonemia may occurs just after the beginning or during the treatment and is characterized by vomiting, progressive impairment of consciousness, focal neurologic signs and increased seizure frequency. We report boy a 6 year-old boy who presented with hyperammonemia during the use of valproic acid within the therapeutic range. Complementary investigation was negative for aminoacidopathy, organic acidemia and urea cycle disorders. The hypothesis of secondary effect to the valproic acid was reinforced by the normalization of ammonia levels after drug withdrawal. The pathogenesis of valproate-induced hyperammonemia have been discussed. We conclude that routine monitoring of ammonia blood concentration are strongly recommended in patients under valproic acid treatment.
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PMID:[Hyperammonemia secondary to the use of valproic acid: case report]. 1610 Sep 94

Valproate-induced hyperammonemic encephalopathy (VHE) is an unusual complication characterized by a decreasing level of consciousness, focal neurological deficits, cognitive slowing, vomiting, drowsiness, and lethargy. We have thoroughly reviewed the predisposing factors and their screening, the biochemical and physiopathological mechanisms involved, the different treatments described, and those that are being investigated. Etiopathogenesis is not completely understood, although hyperammonemia has been postulated as the main cause of the clinical syndrome. The increase in serum ammonium level is due to several mechanisms, the most important one appearing to be the inhibition of carbamoylphosphate synthetase-I, the enzyme that begins the urea cycle. Polytherapy with several drugs, such as phenobarbital and topiramate, seems to contribute to hyperammonemia. Hyperammonemia leads to an increase in the glutamine level in the brain, which produces astrocyte swelling and cerebral edema. There are several studies that suggest that treatment with supplements of carnitine can lead to an early favorable clinical response due to the probable carnitine deficiency induced by a valproate (VPA) treatment. Development of the progressive confusional syndrome, associated with an increase in seizure frequency after VPA treatment onset, obliges us to rule out VHE by screening for blood ammonium levels and the existence of urea cycle enzyme deficiency, such as ornithine carbamoyltransferase deficiency. Electroencephalography (EEG) is characterized by signs of severe encephalopathy with continuous generalized slowing, a predominance of theta and delta activity, occasional bursts of frontal intermittent rhythmic delta activity, and triphasic waves. These EEG findings, as well as clinical manifestations and hyperammonemia, tend to normalize after VPA withdrawal.
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PMID:Valproate-induced hyperammonemic encephalopathy. 1677 19

This trial sought to evaluate our experience using the antimigraine prophylactic drug, use of valproate for the prophylactic management of cyclic vomiting syndrome (CVS) in children. Thirteen children diagnosed with severe CVS were enrolled. Prophylactic therapy consisted of valproate administered at a dose of 10-40 mg/kg/day. Upon enrollment in the study, all patients underwent diagnostic tests to rule out organic causes of their symptoms. Vomiting was severe enough in all patients to cause dehydration requiring hospitalization for intravenous rehydration. Nine of 13 patients did not respond to numerous previous medical therapies like propranolol, amitriptyline, cyproheptadine, phenobarbital, phenytoin, and carbamazepine. Three of 13 patients required combination therapy with valproate and phenobarbital. Of the 13 patients, two showed complete resolution of their symptoms, nine had marked improvement in their symptoms, as evidenced by infrequent attacks of reduced severity, and two failed to respond to valproate therapy. Four patients experienced relapse with a decreased dosage of valproate. Side effects associated with long-term valproate administration were not observed. Valproate appears to be effective for the prophylactic management of severe CVS, with 85% of all patients achieving at least a reduction in the frequency of attacks.
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PMID:Effective prophylactic therapy for cyclic vomiting syndrome in children using valproate. 1875 10

Valproate-induced hyperammonemic encephalopathy is an unusual but serious complication that may occur in people with normal liver-associated enzyme levels, despite normal therapeutic doses and serum levels of valproate. Here, we describe an adolescent girl who had absence seizure and complained about progressive dizziness and general malaise several days after restarting valproate. Then, she presented vomiting and decreased consciousness three weeks after valproate use. Notably, her serum ammonia level was five times the upper limit of normal (184 micrommol/L), with normal liver-associated enzyme and supra-therapeutic valproate level. EEG showed continuous generalized slowing. The tandem mass analysis revealed carnitine deficiency. Consciousness improved after emergent hemodialysis. Ammonia level and EEG also returned to normal. Possible mechanisms, risk factors and the treatments of valproate-induced hyperammonemic encephalopathy are described. Physicians should consider this possibility when consciousness disturbance occurs in patients treated with valproate.
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PMID:Valproate-induced hyperammonemic encephalopathy treated by hemodialysis. 1879 59

Valproate-induced hyperammonemic encephalopathy is an unusual but serious complication that can occur in people with normal liver-associated enzyme levels, and despite normal therapeutic doses and serum levels of valproate. Here, we describe an adolescent girl suffering from absence seizures, who complained of progressive dizziness and general malaise several days after restarting valproate. She developed vomiting and decreased consciousness after 3 weeks of valproate use. She had a serum ammonia level five times higher than the upper normal limit, normal liver-associated enzymes, and a supra-therapeutic valproate level. Electroencephalography (EEG) showed continuous generalized slowing. Tandem mass spectrometry analysis revealed carnitine deficiency. Her consciousness improved after emergent hemodialysis. Her ammonia level and EEG also became normal. Possible mechanisms, risk factors and treatments of valproate-induced hyperammonemic encephalopathy are described. Physicians should consider this possibility when consciousness disturbance occurs in patients treated with valproate.
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PMID:Valproate-induced hyperammonemic encephalopathy. 1913 74

Divalproex (DVP) delayed release and DVP extended release (DVP ER) are approved by the Food and Drug Administration for bipolar disorder, epilepsy, and migraine prophylaxis. Divalproex ER is given once daily, improving compliance and reducing adverse events. Overnight switch to DVP ER is advised in the package insert but could produce more adverse events in this susceptible population. In this pilot study, we compared tolerability of overnight versus gradual switching to DVP ER in 16 adults with intellectual and developmental disabilities receiving DVP, in 9 for epilepsy and in all 16 for comorbid bipolar disorder. The study design was open with parallel groups. Sixteen subjects with intellectual and developmental disabilities were randomized to overnight or gradual conversion for 4 to 6 days. A blinded rater completed the Multidimensional Observation Scale for Elderly Subjects on days +1, +4, and +8 after the switch began. We found no major differences between the 2 groups at each time point. Neither group of subjects, except for 1 subject in the overnight group, manifested sedation, seizures, worsening of tremor, or gastrointestinal adverse events. One subject in the overnight group manifested acute diarrhea and vomiting, followed by a very brief tonic leg seizure 6 days later. Larger studies are warranted.
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PMID:Overnight versus progressive conversion of multiple daily-dose divalproex to once-daily divalproex extended release: which strategy is better tolerated by adults with intellectual disabilities? 1974 51

Delirium may present with hyperactive, hypoactive or mixed clinical pictures. The signs of hypoactive delirium are lethargy, confusion, apathy, hypersomnia, muttering, difficulty in maintaining attention, and difficulty in understanding and performing commands. Valproate is commonly used for the treatment of epilepsy and bipolar disorders. It is also used for the management of alcohol withdrawal delirium and agitative-aggressive deliriums. However, few reports are available about the valproate-induced delirium. In this report, we present a 46 years-old woman with bipolar disorder for 14 years. During her last two hospital admissions, she had been diagnosed with manic episode with psychotic features and she had received valproate. She experienced three hypoactive delirium episodes lasting 2-3 days throughout the treatment period of first week. The patient predominantly had the following signs; vomiting, hypersalivation, confusion, drowsiness, dysphasia, and hypoactivity. At the first day of delirium episode, serum valproate level was found to be within the therapeutic range (98.4, 117.1, and 65.6 mug/ml; respectively). In addition, she had normal results of cranial MRI, complete blood count, urine analysis, electrocardiogram, ALT, AST, albumin, bilirubin, BUN, creatinine and electrolytes. The serum ammonia level of the patient could not been measured due to limitations of laboratory facilities. The patient's consciousness improved dramatically 2-3 days after cessation of valproate. In conclusion, valproate can induce delirium at therapeutic blood levels in some patients via various mechanisms and this side effect has to be considered during valproate use.
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PMID:[Valproate induced hypoactive delirium in a bipolar disorder patient with psychotic features]. 2020 7

A 36-years-old man on phenytoin, levetiracetam, and sodium valproate presented with acute confusion. Routine investigations including serum valproate and phenytoin concentration were normal. His serum ammonia concentration was raised. His valproate was held and 2 days later he recovered with concordant normalisation of serum ammonia concentration. Urea acid cycle disorder was ruled out, and a diagnosis of valproate induced hyperammonemic encephalopathy (VHE) was made. Asymptomatic hyperammonemia occurs in 15-50% of valproate-treated patients, and while the true incidence of VHE is not known, it is a recognized complication of sodium valproate treatment. VHE typically presents acutely with impaired consciousness, lethargy, and vomiting. Valproate concentrations may be in the therapeutic range, and liver function tests are typically "normal." Treatment for VHE consists of ceasing valproate and providing supportive care. Some have advocated carnitine replacement.
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PMID:A case of valproate induced hyperammonemic encephalopathy. 2162 19

Valproate-induced hyperammonemic encephalopathy is a rare event clinically characterized by impaired sensorium, vomiting, headache, seizures and focal neurological deficits. The pathogenesis of this dreadful complication is not well understood, although hyperammonemia has been implicated in causation of encephalopathy. In this submission, we have highlighted a case of valproate-induced encephalopathy who presented mainly with bilateral cerebellar features and generalized slowing on electroencephalogram. High index of suspicion of valproate-induced hyperammonemic encephalopathy is required if diffuse ataxia is present as it is a potentially reversible clinical disorder.
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PMID:Valproate-induced encephalopathy with predominant pancerebellar syndrome. 2234 88

Valproate is one of the most used anti-epileptic drugs. Its common side effects are nausea, vomiting, weight gain, hair loss, tremor, changes in behavior, slowed thinking and impaired liver function. Blood dyscrasias are also relatively frequent and a few studies reported changes in serum immunoglobulin concentrations with valproate treatment. We describe a case of panhypogammaglobulinemia with transient pancytopenia due to valproate. Pancytopenia was recovered after discontinuation of valproate but panhypogammaglobulinemia has been persisting. Intravenous immunoglobulin is being administrated monthly. Previous reports describe that other sodium channel blockers, such as phenytoin and carbamazepine, have been associated with hypogammaglobulinemia. This report also suggests that immunodeficiencies can be caused by valproate.
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PMID:Valproate-induced panhypogammaglobulinemia. 2279 22


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