Short-chain L-3-hydroxyacyl-CoA dehydrogenase deficiency in muscle: a new cause for recurrent myoglobinuria and encephalopathy

Ann Neurol. 1991 Sep;30(3):415-9. doi: 10.1002/ana.410300315.

Abstract

We report on a 16-year-old girl with short-chain L-3-hydroxyacyl-coenzyme A (CoA) dehydrogenase deficiency resulting in juvenile-onset recurrent myoglobinuria, hypoketotic hypoglycemic encephalopathy, and hypertrophic/dilatative cardiomyopathy. Urinary organic acids showed traces of 3-hydroxy-dodecanedioic acids and small amounts of suberic, sebacic, and adipic acids. There was a marked decrease in L-3-hydroxyacyl-CoA dehydrogenase activity in muscle with acetoacetyl-CoA as substrate (2.48 mumol/min/gm; normal = 6.90 +/- 1.80 mumol/min/gm of tissue; n = 11), contrasting with normal L-3-hydroxyacyl-CoA dehydrogenase activity with 3-ketooctanoyl-CoA and 3-ketopalmitoyl-CoA as substrates. Short-chain L-3-hydroxyacyl-CoA dehydrogenase activity was normal in fibroblasts, suggesting a tissue-specific defect.

Publication types

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

MeSH terms

  • 3-Hydroxyacyl CoA Dehydrogenases / deficiency*
  • Adolescent
  • Brain Diseases / etiology*
  • Cardiomegaly / etiology
  • Female
  • Humans
  • Muscles / enzymology*
  • Myoglobinuria / etiology*
  • Recurrence

Substances

  • 3-Hydroxyacyl CoA Dehydrogenases