Valproate Metabolites and Hyperammonemia
نویسندگان
چکیده
منابع مشابه
Valproate-induced hyperammonemia in juvenile ceroid lipofuscinosis (Batten disease)
PURPOSE Valproate-induced hyperammonemia (VHA) and hyperammonemic encephalopathy (VHE) are well-known complications of valproate (VPA) treatment. Currently recognised risk factors for VHE include a high VPA dosage, the need for polytherapy and long duration of treatment. Despite the severe nature of the epilepsy, presence of concomitant psychiatric manifestations, and frequent need for poly-pha...
متن کاملSudden valproate-induced hyperammonemia managed with L-carnitine in a medically healthy bipolar patient
RATIONALE Valproic Acid is a commonly used psychiatric drug primarily used as a mood stabilizer. Mild hyperammonemia is a Valproic Acid common adverse effect. This report presents an example of treated hyperammonemia on Valproic acid therapy managed with L-carnitine administration in BD patients characterized by sudden vulnerability. PATIENT CONCERNS We report the case of a 29-year-old man su...
متن کاملTherapy of hyperammonemia
Recently, Ghallab and colleagues have identified a novel strategy to reduce hyper-ammonemia in mice (Ghallab et al., 2015). The authors reduced blood ammonia concentrations by infusing a cocktail of glutamate dehydrogenase and its cofactors alpha-ketoglutarate and NADPH. This approach may be clinically relevant, because therapy of hyperammonemia is challenging (Levesque et al., 1999; Enns et al...
متن کاملHyperammonemia in the ICU.
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. When hyperammonemia is not thought to be the result of liver failure, treatment for an occult disorder of metabolism must begin prior to the co...
متن کاملHyperammonemia with citrullinemia.
Two cases of hyperammonemia with elevated citrulline are reported, one resulting from a deficiency of pyruvate carboxylase and the other from a partial deficiency of argininosuccinate synthetase. Diagnosis was based on clinical, biochemical and amino acid profiles. The utility of amino acid determinations in hyperammonemia suspected to underlie an inborn error of metabolism is emphasized.
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ژورنال
عنوان ژورنال: Pediatric Neurology Briefs
سال: 1992
ISSN: 2166-6482,1043-3155
DOI: 10.15844/pedneurbriefs-6-7-7