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uracil/crise épileptique
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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
Elevated urine, blood and cerebrospinal fluid levels of uracil and thymine in a child with dihydrothymine dehydrogenase deficiency.
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In the urine of a child with unexplained convulsions large amounts of uracil and thymine were detected by gas chromatography. Identification was performed by coupled gas chromatography-mass spectrometry. Quantitation of the urinary excretion by means of a sensitive high-performance liquid
General pharmacological properties of UFT, a new type of anti-cancer agent consisting of 1-(2-tetrahydrofuryl)-5-fluorouracil (FT) and uracil. I: Pharmacological analysis of the combined effect of FT and uracil.
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The pharmacological properties of a new type of anti-cancer agent, 1-(2-tetrahydrofuryl)-5-fluorouracil (FT) and uracil (U), in a molar ratio of 1:4, were investigated and compared with those of FT, 5-fluorouracil (5-FU) and uracil. UFT at doses larger than 874.8 (FT: 270.0) mg/kg p.o. produced
Expression and function of the metabotropic purinergic P2Y receptor family in experimental seizure models and patients with drug-refractory epilepsy.
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ATP is released into the extracellular space during pathologic processes including increased neuronal firing. Once released, ATP acts on P2 receptors including ionotropic P2X and metabotropic P2Y receptors, resulting in changes to glial function and neuronal network excitability. Evidence suggests
An incidental case of dihydropyrimidine dehydrogenase deficiency: One case, multiple challenges.
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Dihydropyrimidine dehydrogenase (DPD) deficiency is an autosomal recessive disorder that shows large phenotypical variability, ranging from no symptoms to intellectual disability, motor retardation, and convulsions. In addition, homozygous and heterozygous mutation carriers can develop severe
[Clinical characteristics and analysis of mass spectrometric data in patients with ornithine transcarbamylase deficiency].
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OBJECTIVE
To explore the clinical manifestations and biochemical characteristics of patients with ornithine transcarbamylase deficiency (OTCD) so as to increase the clinician awareness for this disease.
METHODS
The clinical manifestations, blood ammonia levels, citrulline levels, urinary orotic acid
Dihydropyrimidine Dehydrogenase Deficiency: Metabolic Disease or Biochemical Phenotype?
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Dihydropyrimidine dehydrogenase (DPD) deficiency is an autosomal recessive disorder of pyrimidine metabolism that impairs the first step of uracil und thymine degradation. The spectrum of clinical presentations in subjects with the full biochemical phenotype of DPD deficiency ranges from
A neonate with recurrent vomiting and generalized hypotonia diagnosed with a deficiency of dihydropyrimidine dehydrogenase.
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Deficiency of dihydropyrimidine dehydrogenase (DPD) is a rare inborn error of pyrimidine metabolism. To date, only about 50 patients are known worldwide. The clinical picture is varied and is not yet fully described. Most patients are diagnosed at the age of 1-3 years. We present a patient diagnosed
[A Case with Solitary Brain Metastatic Tumor from Colon Cancer].
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We report a rare long-surviving case of solitary brain metastasis from colon cancer. The patient was a 64-year-old female. She had undergone laparoscopic right hemicolectomy for ascending colon cancer in October 2012(pStage III b). She was discharged from the hospitalin a satisfactory state, but 26
[Fatal acute encephalopathy due to 5-fluorouracil treatment].
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BACKGROUND
Encephalopathies from 5 fluorouracil (5FU) are rare and generally resolve favorably.
METHODS
Six days after her first course of chemotherapy combining 5FU and cisplatin, a 45-year-old woman developed acute encephalopathy with altered consciousness and convulsions. MRI showed hyperintense
Neurotoxic effects of alpha-fluoro-beta-alanine (FBAL) and fluoroacetic acid (FA) on dogs.
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In order to clarify the mechanism of the neurotoxicity of 5-FU and/or its masked compounds, we studied the effects of alpha-fluoro-beta-alanine (FBAL) and fluoroacetic acid (FA) on the formation of vacuolar changes in the dog cerebrum, using the dosage of 3.0 mg/kg/day of FBAL-HCl (FBAL x HCl) and
Dihydropyrimidine dehydrogenase deficiency caused by a novel genomic deletion c.505_513del of DPYD.
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Dihydropyrimidine dehydrogenase (DPD) deficiency is an autosomal recessive disorder of the pyrimidine degradation pathway. In a patient presenting with convulsions, psychomotor retardation and Reye like syndrome, strongly elevated levels of uracil and thymine were detected in urine. No DPD activity
5-FU-induced neurotoxicity in cancer patients with profound DPD deficiency syndrome: a report of two cases.
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OBJECTIVE
5-Fluorouracil (5-FU) is a mainstay for treating various solid tumours in adults, including digestive and head and neck cancers. 5-FU-related toxicities usually include haematological, digestive and cutaneous features. Additionally, 5-FU has been described as being potentially neurotoxic
Dihydropyrimidine dehydrogenase deficiency in two malaysian siblings with abnormal MRI findings.
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Dihydropyrimidine dehydrogenase (DPD) deficiency is an autosomal recessive disorder of the pyrimidine metabolism. Deficiency of this enzyme leads to an accumulation of thymine and uracil and a deficiency of metabolites distal to the catabolic enzyme. The disorder presents with a wide clinical
Comprehensive analysis of pyrimidine metabolism in 450 children with unspecific neurological symptoms using high-pressure liquid chromatography-electrospray ionization tandem mass spectrometry.
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To evaluate the significance of inborn metabolic disorders of the pyrimidine degradation pathway, 450 children with unspecific neurological symptoms were comprehensively studied; 200 healthy children were recruited as controls. Uracil and thymine as well as their degradation products in urine were
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