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uric acid/crise épileptique
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Molecular diagnosis and clinical characterization of pseudohypoparathyroidism type-Ib in a patient with mild Albright's hereditary osteodystrophy-like features, epileptic seizures, and defective renal handling of uric acid.
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We describe a patient who presented with epileptic seizures unresponsive to anticonvulsive treatment. Laboratory investigations demonstrated epileptiform seizure activity in the brain but also revealed severe hypocalcemia, hyperphosphatemia, and elevated serum parathyroid hormone. In addition, the
Elevated Serum Uric Acid in Benign Convulsions with Mild Gastroenteritis in Children.
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Acute Uric Acid Nephropathy following Epileptic Seizures: Case Report and Review.
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Acute hyperuricemia most commonly occurs in patients who experience tumor lysis syndrome. Hyperuricemia along with other electrolyte abnormalities like hyperkalemia, hypocalcemia, and hyperphosphatemia leads to acute kidney injury (AKI) due to acute uric acid nephropathy which is associated with
Kainic acid causes redox changes in cerebral cortex extracellular fluid: NMDA receptor activity increases ascorbic acid whereas seizure activity increases uric acid.
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Kainic acid (KA) causes seizures and extensive brain damage in rats. To study the effects of KA on the redox state in cerebral cortex extracellular fluid (ECF), ascorbic and uric acid concentrations were measured in intracerebral microdialysis samples before and after systemic KA administration
Uric acid is released in the brain during seizure activity and increases severity of seizures in a mouse model for acute limbic seizures.
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Recent evidence points at an important role of endogenous cell-damage induced pro-inflammatory molecules in the generation of epileptic seizures. Uric acid, under the form of monosodium urate crystals, has shown to have pro-inflammatory properties in the body, but less is known about its role in
Elevation of serum uric acid levels in patients with seizures.
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Reddish-orange discoloration of urine due to uric acid crystalluria after recurrent seizures.
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Changes in urinary uric acid-creatinine ratio after electrically induced convulsions in man.
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Erratum to: Elevated Serum Uric Acid in Benign Convulsions with Mild Gastroenteritis in Children.
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This corrects the article on p. 496 in vol. 15, PMID: 31591838.
Serum Uric Acid Is Highly Associated with Epilepsy Secondary to Cerebral Infarction.
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In this study, we examined the association between serum uric acid levels and epilepsy secondary to cerebral infarction. Clinical data including age, gender, epileptic seizure type, imaging, and serum uric acid levels before and after seizures in patients with cerebral infarction that were collected
[Analysis of the blood and serum biochemistry findings in patients demonstrating convulsion with mild gastroenteritis].
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We analyzed the blood cell count and serum biochemistry findings in patients demonstrating convulsion with mild gastroenteritis (CwG). As a control group, age matched patients presenting with only gastroenteritis during the same period were compared. The results showed significant differences
Uric acid is a useful marker to differentiate between responsive and refractory status epilepticus.
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Allopurinol does not affect the anticonvulsant activity of carbamazepine and valproate in maximal electroshock-induced convulsions in mice.
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Allopurinol, an inhibitor of xanthine oxidase, is indicated in the management of patients with elevated serum and urinary uric acid levels. It was also reported to be beneficial in patients with epilepsy when added to traditional antiepileptic drug. Here, we investigated the effect of allopurinol
Concentration of purine compounds in the cerebrospinal fluid of infants suffering from sepsis, convulsions and hydrocephalus.
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Catabolites of purine nucleotides were measured in the cerebrospinal fluid (CSF) of newborn infants with sepsis, seizures and hydrocephalus using isocratic reversed-phase HPLC. The inosine levels in the CSF of the infants with any of the illnesses were significantly higher when compared with the
Increased nucleotide catabolism after cerebral convulsions.
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Cardiazol induced seizures in rabbits showed that the highest oxypurine concentrations can be detected in the CSF 1 hour after the convulsions. There is a sharp decline continuing until the third hour. After that the CSF values remain nearly constant until the 24th hour being about ten times higher
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