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(sodium phenylacetate sodium benzoate)
69 results
  • Acute pediatric hyperammonemia: current diagnosis and management strategies. [Review]
    Hepat Med 2018; 10:105-115Savy N, Brossier D, … Jouvet P
  • Acute hyperammonemia may induce a neurologic impairment leading to an acute life-threatening condition. Coma duration, ammonia peak level, and hyperammonemia duration are the main risk factors of hyperammonemia-related neurologic deficits and death. In children, hyperammonemia is mainly caused by severe liver failure and inborn errors of metabolism. In an acute setting, obtaining reliable plasma …
  • GeneReviews®: Lysinuric Protein Intolerance [BOOK]
    University of Washington, Seattle: Seattle (WA)Adam MP, Ardinger HH, … Amemiya ANunes V, Niinikoski HBOOK
  • Lysinuric protein intolerance (LPI) typically presents after an infant is weaned from breast milk or formula; variable findings include recurrent vomiting and episodes of diarrhea, episodes of stupor and coma after a protein-rich meal, poor feeding, aversion to protein-rich food, failure to thrive, hepatosplenomegaly, and muscular hypotonia. Over time, findings include: poor growth, osteoporosis,…
  • Prenatal treatment of ornithine transcarbamylase deficiency. [Case Reports]
    Mol Genet Metab 2018; 123(3):297-300Wilnai Y, Blumenfeld YJ, … Enns GM
  • CONCLUSIONS: Prenatal treatment of mothers who harbor severe OTCD mutations and carry affected male fetuses with intravenous Ammonul and arginine, followed by immediate institution of maintenance infusions after delivery, results in therapeutic levels of benzoate and phenylacetate in the newborn at delivery and, in conjunction with high-caloric enteral nutrition, prevents acute hyperammonemia and neurological decompensation. Following initial medical management, early liver transplantation may improve developmental outcome.
  • Saline is as effective as nitrogen scavengers for treatment of hyperammonemia. [Journal Article]
    Sci Rep 2017; 7(1):13112van Straten G, de Sain-van der Velden MGM, … Verhoeven-Duif NM
  • Urea cycle enzyme deficiency (UCED) patients with hyperammonemia are treated with sodium benzoate (SB) and sodium phenylacetate (SPA) to induce alternative pathways of nitrogen excretion. The suggested guidelines supporting their use in the management of hyperammonemia are primarily based on non-analytic studies such as case reports and case series. Canine congenital portosystemic shunting (CPSS)…
  • A Patient with MSUD: Acute Management with Sodium Phenylacetate/Sodium Benzoate and Sodium Phenylbutyrate. [Case Reports]
    Case Rep Pediatr 2017; 2017:1045031Köse M, Canda E, … Çoker M
  • In treatment of metabolic imbalances caused by maple syrup urine disease (MSUD), peritoneal dialysis, and hemofiltration, pharmacological treatments for elimination of toxic metabolites can be used in addition to basic dietary modifications. Therapy with sodium phenylacetate/benzoate or sodium phenylbutyrate (NaPB) in urea-cycle disorder cases has been associated with a reduction in branched-chai…
  • Brain MRS glutamine as a biomarker to guide therapy of hyperammonemic coma. [Case Reports]
    Mol Genet Metab 2017; 121(1):9-15O'Donnell-Luria AH, Lin AP, … Frank NY
  • Acute idiopathic hyperammonemia in an adult patient is a life-threatening condition often resulting in a rapid progression to irreversible cerebral edema and death. While ammonia-scavenging therapies lower blood ammonia levels, in comparison, clearance of waste nitrogen from the brain may be delayed. Therefore, we used magnetic resonance spectroscopy (MRS) to monitor cerebral glutamine levels, th…
  • Management and long-term evolution of a patient with 3-hydroxy-3-methylglutaryl-coenzyme A lyase deficiency. [Case Reports]
    Ital J Pediatr 2017; 43(1):12Muñoz-Bonet JI, Ortega-Sánchez MD, León Guijarro JL
  • CONCLUSIONS: The alcohol consumption must be avoided in patients with HMG-CoA lyase deficiency. In our patient hyperamoniemia was effectively treated with sodium phenylacetate and sodium benzoate. Magnetic resonance imaging showed and quantified the cytotoxic brain edema. Belatedly, a cerebral vasospasm was an additional mechanism of cerebral injury. None of these observations has been previously reported.
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