N-acetylglutamate synthetase deficiency: clinical and laboratory observations

J Inherit Metab Dis. 1991;14(5):685-90. doi: 10.1007/BF01799936.

Abstract

Two male siblings presented in the first 6 weeks of life with emesis, diarrhoea, metabolic acidosis and lethargy. A male sibling had previously died at 14 months of age from liver failure of unknown aetiology. Both of the current cases had mild hyperammonaemia with normal orotic acid, organic acid and argininosuccinic acid levels. Citrulline and arginine levels were normal or mildly decreased. One of the brothers was biopsied and had no detectable N-acetylglutamate synthetase activity and normal values for other enzymes of the urea cycle in liver. Treatment with a low-protein diet and sodium benzoate/sodium phenylacetate resulted in near normal blood ammonia levels, except during viral illness. Subsequent neurological development has been normal to mildly delayed. These patients differ from those previously described with N-acetylglutamate synthetase deficiency in that their presentation and subsequent course were relatively benign.

Publication types

  • Case Reports

MeSH terms

  • Acetyltransferases / deficiency*
  • Amino-Acid N-Acetyltransferase
  • Ammonia / blood
  • Arginine / blood
  • Benzoates / therapeutic use
  • Benzoic Acid
  • Citrulline / blood
  • Dietary Proteins / administration & dosage
  • Humans
  • Infant
  • Infant, Newborn
  • Liver / enzymology
  • Male
  • Phenylacetates / therapeutic use

Substances

  • Benzoates
  • Dietary Proteins
  • Phenylacetates
  • Citrulline
  • Ammonia
  • Benzoic Acid
  • Arginine
  • Acetyltransferases
  • Amino-Acid N-Acetyltransferase
  • NAGS protein, human
  • phenylacetic acid