Pyruvate carboxylase deficiency--insights from liver transplantation

Mol Genet Metab. 2002 Sep-Oct;77(1-2):143-9. doi: 10.1016/s1096-7192(02)00123-3.

Abstract

Pyruvate carboxylase deficiency, complex form, presents in early infancy with lethal metabolic acidosis, resulting from ketoacidosis and lactic acidemia. Renal tubular acidosis, hyperammonemia, and citrullinemia complete the picture. In an infant with this disease, large amounts of glucose ameliorated the ketoacidosis, but worsened the lactic acidosis. Orthotopic hepatic transplantation completely reversed the ketoacidosis and the renal tubular abnormality and ameliorated the lactic acidemia. Concentrations of glutamine in cerebrospinal fluid were low and did not improve with liver transplantation.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acidosis, Renal Tubular / etiology
  • Citrullinemia / etiology
  • Glucose / administration & dosage
  • Glutamine / cerebrospinal fluid
  • Humans
  • Hyperammonemia / etiology
  • Infant
  • Lactic Acid / blood
  • Liver Transplantation*
  • Male
  • Pyruvate Carboxylase Deficiency Disease / complications
  • Pyruvate Carboxylase Deficiency Disease / drug therapy
  • Pyruvate Carboxylase Deficiency Disease / metabolism*
  • Pyruvate Carboxylase Deficiency Disease / surgery*

Substances

  • Glutamine
  • Lactic Acid
  • Glucose