[Mutation analysis of a family with 2-Methyl-3-hydroxybutyryl-CoA dehydrogenase deficiency]

Zhonghua Er Ke Za Zhi. 2013 Oct;51(10):783-6.
[Article in Chinese]

Abstract

Objective: The aim of this study was to explore the genetic features of a family with 2-methyl-3-hydroxybutyryl-CoA dehydrogenase deficiency (MHBDD) which may provide the basis for the diagnosis and genetic counseling.

Method: Clinical data of the proband was collected, total RNA and genomic DNA were extracted from the peripheral blood. The whole coding region of the ACAT1 gene was amplified by RT-PCR. 5' noncoding region of the ACAT1 gene and all 6 exons and flanking intron regions of the HADH2 gene were amplified by PCR. All amplification products were directly sequenced and compared with the reference sequence.

Result: (1) The patient was a one-year-old boy who presented with psychomotor retardation and astasia when he was admitted to the hospital. Biochemical test revealed slight hyperlactatemia (3.19 mmol/L) and magnetic resonance imaging showed delayed myelination. 2-Methylacetoacetyl-CoA thiolase deficiency was suggested by gas chromatography-mass spectrometry. (2) There was no mutation in the ACAT1 gene and a hemizygous missense mutation c.388C > T was found in the 4 exon of the HADH2 gene which resulted in p. R130C. Proband's mother was the heterozygote and the father was normal.

Conclusion: This is the first report on MHBDD patient and HADH2 mutation in China. p.R130C is responsible for the pathogenesis of the disease in the infant.

Publication types

  • Case Reports

MeSH terms

  • 3-Hydroxyacyl CoA Dehydrogenases / genetics
  • Acetyl-CoA C-Acetyltransferase / deficiency*
  • Acetyl-CoA C-Acetyltransferase / genetics
  • Acyl Coenzyme A / genetics
  • Acyl Coenzyme A / metabolism
  • Base Sequence
  • DNA Mutational Analysis
  • Dyskinesias
  • Heterozygote
  • Humans
  • Infant
  • Intellectual Disability / enzymology
  • Intellectual Disability / genetics*
  • Intellectual Disability / pathology
  • Lipid Metabolism, Inborn Errors / genetics*
  • Lipid Metabolism, Inborn Errors / pathology
  • Male
  • Mutation, Missense*
  • Pedigree
  • Reverse Transcriptase Polymerase Chain Reaction
  • X-Linked Intellectual Disability

Substances

  • Acyl Coenzyme A
  • 2-methylacetoacetyl-coenzyme A
  • 3-Hydroxyacyl CoA Dehydrogenases
  • HSD17B10 protein, human
  • Acetyl-CoA C-Acetyltransferase

Supplementary concepts

  • Mental Retardation, X-Linked, Syndromic 10