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)

The authors report on the case of a 12.5 and year-old epileptic boy with severe acute pancreatitis which appeared 39 months after starting treatment with sodium valproate (VAP) at a daily dosage of 26.6 mg/kg. Twelve days after hospitalization, a pseudocyst of the pancreas developed, leading to cystoduodenostomy 3 months later. Following VPA suppression, no recurrence of pancreatic symptomatology was observed. The pathophysiological mechanism of this adverse side-effect of VPA treatment remains unclear. The appearance of a painful epigastric syndrome and/or vomiting in a patient subjected to a VPA treatment indicates the possibility or acute pancreatitis, to be confirmed by blood and urinary determination of amylases and abdominal tomodensitometric examination. Finally, the fact that this side-effect may be severe even lethal, brings into question the prescription of this drug in the management of epilepsy.
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PMID:[Acute pancreatitis caused by sodium valproate. Review of the literature apropos of a case in a child]. 166 40

Valproic acid represents a new class of anticonvulsants that are widely employed in the management of many types of seizure disorders. Compared with other anticonvulsants, it has been considered relatively free of adverse effects. Recently, acute hepatic failure has been ascribed to valproic acid. Now experience is accumulating that implicates this agent in causing pancreatitis. Contributing to this evidence, the patient described herein had well-documented, recurrent pancreatitis while he was taking valproic acid. Nonspecific vomiting and abdominal pain frequently occur with valproic acid; however, pancreatitis must be considered whenever these symptoms are severe or protracted.
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PMID:Recurrent pancreatitis induced by valproic acid. A case report and review of the literature. 616 6

Valproic acid, used alone or in combination with other anticonvulsants in 100 children with epilepsy, improved seizure control in all age groups. Mean improvement in seizure control was 82%. Petit mal seizures responded best, but other types of seizures, even with associated mental and physical handicaps, also responded well. A substantial improvement in alertness and behavior often occurred. Leukopenia (27%) and an elevated SGOT value (44%) were frequent but transient. Other side effects included alopecia (1), gastrointestinal distress with vomiting (7), pancreatitis (1), thrombocytopenia (1), edema (2), and coma (2). Three severely retarded children with frequent seizures died while receiving valproic acid, but it is not clear that death was caused by valproic acid. Children must be monitored carefully for potential toxic effects, and drug interactions with other anticonvulsants may cause problems in treatment.
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PMID:Valproic acid therapy in childhood epilepsy. 677 26

Valproic acid is a branched-chained fatty acid, structurally unrelated to any other antiepileptic drug. Since publication of the original review in the Journal in 1977, several clinical trials have documented its efficacy and safety in adults and children for the treatment of generalised seizures (absence, tonic-clonic, myoclonic), partial seizures (simple, complex, secondarily generalised) and compound/combination seizures (including those refractory to treatment with other antiepileptic drugs). Valproic acid monotherapy has demonstrated efficacy equivalent to that of carbamazepine, phenytoin, and phenobarbital in the treatment of both generalised and partial seizures and ethosuximide in the treatment of absence seizures. Adverse effects associated with the drug are primarily gastrointestinal (nausea, vomiting, dyspepsia) in nature, although the use of enteric-coated formulations has reduced the incidence of abdominal discomfort. Weight gain, tremor and transient hair loss are commonly reported. Importantly, valproic acid has minimal neurological adverse effects (sedation, ataxia, impairment of cognitive function) compared with other antiepileptic drugs, a finding that may be of particular relevance in many patients with epilepsy. The incidence of rare, fatal liver failure has been greatly reduced by identifying and avoiding administration of valproic acid to high risk patient populations. An estimated risk of 1 to 2% for neural tube defects, predominantly spina bifida aperta, with maternal use of valproic acid therapy has been reported. Valproic acid inhibits hepatic drug metabolism and displaces other highly bound drugs from their plasma protein binding sites. Therefore, coadministered drugs which are highly protein bound or hepatically metabolised may require dosage adjustment. Enzyme-inducing antiepileptic drugs may increase valproic acid metabolism and necessitate increasing its dosage. Thus, comparative trials and extensive clinical experience have demonstrated the efficacy and tolerability of valproic acid and support its role as a valuable and well established first-line treatment for patients with a broad range of seizure types.
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PMID:Valproic acid. A reappraisal of its pharmacological properties and clinical efficacy in epilepsy. 751 5

Ornithine transcarbamylase deficiency is an X linked disorder and the most common inherited cause of hyperammonaemia. Fluctuating concentrations of ammonia, glutamine, and other excitotoxic amino acids result in a chronic or episodically recurring encephalopathy. A heterozygous female patient first presented with protein intolerance, attacks of vomiting, and signs of mental retardation in early childhood. At the age of 16 complex partial seizures occurred which were treated with sodium valproate. Seven days after initiation of valproate therapy, she developed severe hyperammonaemic encephalopathy with deep somnolence. The maximum concentration of ammonia was 480 micromol/l. After withdrawal of valproate, three cycles of plasma dialysis, and initiation of a specific therapy for the inborn metabolic disease, ammonia concentrations fell to normal values. The patient remitted, returning to her premorbid state. Valproate can cause high concentrations of ammonia in serum in patients with normal urea cycle enzymes and may worsen a pre-existing hyperammonaemia caused by an enzymatic defect of the urea cycle. Sufficient diagnostic tests for the detection of metabolic disorders must be performed before prescribing valproate for patients with a history of encephalopathy.
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PMID:Hyperammonaemic encephalopathy after initiation of valproate therapy in unrecognised ornithine transcarbamylase deficiency. 959 92

We report the first case of the syndrome of periodic adrenocorticotropin (ACTH) and vasopressin (ADH) discharge associated with focal glomerulosclerosis. Approximately 30 cases of this syndrome have so far been reported in Japan, but no cases associated with renal dysfunction have yet been reported. The patient, a 10-year-old Japanese boy, was referred to our hospital because of recurrent attacks of vomiting. He was diagnosed as having this syndrome from clinical and laboratory findings. While various drugs were tried to manage his vomiting attacks, only valproic acid appeared to be effective in reducing the frequency of the attacks. Chronic nephritis was manifested when the patient was 12 years old, which required treatment with continuous ambulatory peritoneal dialysis. Valproic acid was proved to be effective in reducing the number of attacks over 4 months.
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PMID:Periodic discharge of adrenocorticotropin and vasopressin associated with focal glomerulosclerosis. 989 98

This randomized, double-blind trial was designed to evaluate the efficacy of a transdermal system of piribedil on the motor symptoms of Parkinson's disease during 3 weeks of treatment administered to three different groups: placebo, one piribedil patch (1 PP), and two (2 PP) piribedil patches. Twenty-seven patients with idiopathic Parkinson's disease, treated with L-dopa but not sufficiently controlled, were included in this trial. The test treatment did not demonstrate any clinical efficacy on either the main end point (Unified Parkinson's Disease Rating Scale motor score) or the secondary end points (rigidity, bradykinesia, postural, and resting tremor scores). The main adverse events were nausea (11%), vomiting (7.4%), and malaise (7.4%) mainly observed in the placebo group (four of seven patients). The local acceptability of the transdermal system was good. Plasma piribedil concentrations at the end of treatment were 6.74+/-1.10 and 9.31+/-3.33 ng/mL in the 1 PP and 2 PP groups, respectively. These plasma levels could account for the lack of clinical efficacy, because a previous pharmacokinetics-PD study conducted in parkinsonian patients and treated with the intravenous route demonstrated that the critical limits of activity on tremor were between 10 and 30 ng/mL.
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PMID:A randomized, double-blind study of a skin patch of a dopaminergic agonist, piribedil, in Parkinson's disease. 1009 30

Among the idiosyncratic reactions related to VPA, pancreatitis is the most rare and less remembered even though its potentially fatal course. We report the case of a 5 year-old boy with epilepsy treated with VPA 40 mg/kg/day associated with CBZ 20 mg/kg/day and PB 3 mg/kg/day, admitted for vomiting, abdominal pain, low grade fever, abdominal tension and amylasis of 288 UI. On evolution presented upper digestive hemorrhage, shock and amylasis of 564 UI. The patient was submitted to exploratory laparotomy with findings of hemorrhagic ascitis, retroperitoneal hematoma, increased volume of pancreas with edema and hemorrhage leading to diagnosis of necro-hemorrhagic pancreatitis and a fatal course. Pancreatic complications are well known complications related to VPA treatment and may vary between asymptomatic hyperamilasemy to fatal acute pancreatitis. The characteristics of our patient correlates with the data on literature: we found 7 similar cases reported, 4 of which died.
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PMID:[Fatal necro-hemorrhagic pancreatitis related to sodium valproate: case report]. 1159 93

Valproic acid is a widely used drug in the treatment of epilepsy and, compared to other anticonvulsant drugs, is considered safe. The most common side effects of valproic acid ingestion or therapy are transient nausea, vomiting, abdominal cramps, and diarrhea. Most of these complaints are mild. However, more serious adverse reactions can occur such as hepatotoxicity and pancreatitis. It has been proposed that, whenever possible, valproic acid not be used in the younger child, the child with a severe seizure disorder or other neurological disorders, mental retardation, developmental delay, organic brain disease, congenital abnormalities, or the child who is taking multiple anticonvulsant drugs, as these factors may increase the likelihood of hepatotoxicity and/or pancreatitis. In the present report, we describe a fatal case of acute hemorrhagic pancreatitis in a four and a half-year-old Hispanic female child who was receiving valproic acid in combination with another anticonvulsant drug for control of focal seizures. The patient also received the macrolide antibiotic azithromycin. For pediatricians and forensic pathologists valproic acid-induced pancreatitis can be a challenging diagnosis which must not be mistaken for abdominal trauma. We discuss the workup of the patient and differential diagnosis.
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PMID:Pathological case of the month: sudden death in a child as a result of pancreatitis during valproic acid therapy. 1239 3

There is currently little evidence available concerning the risks of foetal exposure to new anti-epileptic drugs such as lamotrigine, vigabatrin, gabapentine, topiramate. A small number of malformations without organ specificity have been described and are not easy to interpret because of the existence of concomitant treatments. We have reported a series of 12 pregnancies with exposure to recent anti-epilepticdrugs and that were reported to the Post-marketing Surveillance office in Tours, France. Five concerned Lamictal of which 2 related to monotherapy, one concerned Epitomax used in monotherapy and there were 6 cases of polytherapy including Sabril. Associated drug therapies were Depakine, Tegretol, Rivotril and Urbanyl. Six of the patients were on folic acid supplements. The average age of the women was 26.5 years. In each case, treatment had been initiated before conception and was continued for at least 3 months. Of the 12 babies born, only one presented with a malformation (aplasia of the muscle of the left lower lip and asymmetrical abduction of the hips) following exposure to Lamictal and Depakine. Four infants, two of whom were premature, showed signs of neonatal stress: transient respiratory distress and difficulty in taking feeding-bottles following exposure throughout the pregnancy to Epitomax; suction disorders, hypotonia and vomiting were observed after exposure to Sabril, Tegretol and Rivotril throughout the pregnancy; respiratory distress and apnoea--bradycardia were observed after exposure throughout the pregnancy to Lamictal and Urbanyl; respiratory distress and thrombocytopaenia were observed after exposure throughout the pregnancy to Lamictal". This small series confirms that the current data concerning the teratogenicity of new anti-epileptic drugs are as yet insufficient to exclude any teratogenic risk. Consequently, strict adherence to current recommendations relating to drug use during pregnancy is essential. The treatment of all patients wishing to become pregnant should be discussed.
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PMID:[New antiepileptic drugs in pregnancy: outcome of 12 exposed pregnancies]. 1242 60


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