Results 131 to 140 of about 9,393 (183)
Biochemical, Clinical, and Functional Characterization of a Rare c.-106C>A Promoter Region Variant in Late-Onset Ornithine Transcarbamylase Deficiency: A Multifamily Case Series. [PDF]
JIMD RepTholl SQ +9 more
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Identification of Primary Hyperoxaluria Type III by Gas Chromatography/Mass Spectrometry-Based Urine Metabolomics. [PDF]
MetabolitesKuhara T +4 more
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Chest, 2007
Patients experiencing acute elevations of ammonia present to the ICU with encephalopathy, which may progress quickly to cerebral herniation. Patient survival requires immediate treatment of intracerebral hypertension and the reduction of ammonia levels.
Alison S Clay, Bryan E Hainline
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Patients experiencing acute elevations of ammonia present to the ICU with encephalopathy, which may progress quickly to cerebral herniation. Patient survival requires immediate treatment of intracerebral hypertension and the reduction of ammonia levels.
Alison S Clay, Bryan E Hainline
exaly +3 more sources
American Journal of Therapeutics, 2016
Hyperammonemia is most commonly associated with liver disease. Nonhepatic causes of hyperammonemia are uncommon. We present a case of nonhepatic hyperammonemia that turned fatal within a short period of time and discuss the possible treatment modalities for the same.
Ranjita, Pallavi, Beata, Matejak-Popis
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Hyperammonemia is most commonly associated with liver disease. Nonhepatic causes of hyperammonemia are uncommon. We present a case of nonhepatic hyperammonemia that turned fatal within a short period of time and discuss the possible treatment modalities for the same.
Ranjita, Pallavi, Beata, Matejak-Popis
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Archives of Pediatrics & Adolescent Medicine, 1967
AN UNDERSTANDING of the nature of the underlying biochemical disorder in hyperammonemia is essential to a rational approach to therapy of this condition. Three types of hereditary enzyme defect in the biosynthesis of urea have been characterized in recent years (Table 1): arginosuccinic aciduria (reaction 4), citrullinuria (reaction 3), and ...
B, Levin, A, Russell
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AN UNDERSTANDING of the nature of the underlying biochemical disorder in hyperammonemia is essential to a rational approach to therapy of this condition. Three types of hereditary enzyme defect in the biosynthesis of urea have been characterized in recent years (Table 1): arginosuccinic aciduria (reaction 4), citrullinuria (reaction 3), and ...
B, Levin, A, Russell
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Pharmacotherapy for hyperammonemia
Expert Opinion on Pharmacotherapy, 2014Hepatic encephalopathy (HE) is a serious neuropsychiatric complication that is seen in patients with liver failure. The pathogenesis of HE is not entirely understood, but several hypotheses have emerged and persisted during the years. Despite the many prevalent hypotheses, most of the existing evidence point to ammonia as the main culprit behind ...
Anna, Hadjihambi +2 more
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MONATSSCHRIFT KINDERHEILKUNDE, 2014
Eine Erhöhung des Ammoniakgehalts des Bluts über die Referenzgrenzen hinaus wird als Hyperammonämie bezeichnet. Ein solcher Zustand kann akut oder chronisch sein. Eine akute Hyperammonämie äußert sich aufgrund eines begleitenden Hirnödems mit Symptomen im Sinne eines veränderten Bewusstseins.
Gregory M. Enns, Tina M. Cowan
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Eine Erhöhung des Ammoniakgehalts des Bluts über die Referenzgrenzen hinaus wird als Hyperammonämie bezeichnet. Ein solcher Zustand kann akut oder chronisch sein. Eine akute Hyperammonämie äußert sich aufgrund eines begleitenden Hirnödems mit Symptomen im Sinne eines veränderten Bewusstseins.
Gregory M. Enns, Tina M. Cowan
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Current Problems in Pediatrics, 1984
A symptomatic elevation in plasma ammonium concentration, termed hyperammonemia, is associated with numerous congenital and acquired conditions (Table 11). In some cases, such as urea cycle disorders, ammonia is the principal toxin. In other instances, such as portal systemic encephalopathy, it is but one of a number of metabolic disturbances, However,
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A symptomatic elevation in plasma ammonium concentration, termed hyperammonemia, is associated with numerous congenital and acquired conditions (Table 11). In some cases, such as urea cycle disorders, ammonia is the principal toxin. In other instances, such as portal systemic encephalopathy, it is but one of a number of metabolic disturbances, However,
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Clinical Chemistry and Laboratory Medicine, 2002
Hyperammonemia is mainly found in hepatic encephalopathy and in genetic defects of the urea cycle or other pathways of the intermediary metabolism. Clinically a difference has to be made between chronic moderate hyperammonemia and acutely increased concentrations. Pathogenetic mechanisms of ammonia toxicity to the brain are partly unraveled.
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Hyperammonemia is mainly found in hepatic encephalopathy and in genetic defects of the urea cycle or other pathways of the intermediary metabolism. Clinically a difference has to be made between chronic moderate hyperammonemia and acutely increased concentrations. Pathogenetic mechanisms of ammonia toxicity to the brain are partly unraveled.
openaire +3 more sources