Abstract
Seizures resistant to phenobarbital were controlled in four of six neonates by valproic acid (VPA) monotherapy and in one with polytherapy at the Moses H Cone Memorial Hospital, Greensboro, NC.
Highlights
Animal experiments show that valproic acid (VPA)-induced hyperammonemia is caused primarily by impairment of hepatic intramitochondrial citrullinogenesis, and the renal contribution to systemic hyperammonemia is small
One patient with meningitis whose seizures were unresponsive to VPA died shortly after the drug was discontinued; a serum ammonia elevation to 900 umol/1 after 5 days of treatment returned to normal with 24-48 hrs after discontinuing the drug
VPA toxicity, hepatotoxicity, in infants and young children may be reduced in frequency by elimination of concurrent anticonvulsants, but serum ammonia must be closely monitored even with monotherapy
Summary
Animal experiments show that VPA-induced hyperammonemia is caused primarily by impairment of hepatic intramitochondrial citrullinogenesis, and the renal contribution to systemic hyperammonemia is small Seizures resistant to phenobarbital were controlled in four of six neonates by valproic acid (VPA) monotherapy and in one with polytherapy at the Moses H Cone Memorial Hospital, Greensboro, NC. A loading dose of 20 mg/kg followed by a maintenance dose of 10 mgAg every 12 hrs was recommended until VPA clearance and serum levels are determined.
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