Affiliations 

  • 1 Department of Human Genetics, Graduate School of Medicine, Yokohama City University, Yokohama, Japan
  • 2 Department of Genetics, Hospital Kuala Lumpur, Jalan Pahang, Malaysia
  • 3 Child Neurology Service, Hospital de Puerto Montt, Puerto Montt, Chile
  • 4 Child Neurology Service, Hospital San Borja Arriarán, Universidad de Chile, Santiago, Chile
  • 5 Department of Radiology, Clínica Alemana de Santiago, Santiago, Chile
  • 6 Osaka Women's and Children's Hospital, Osaka, Japan
  • 7 Department of Human Genetics, Graduate School of Medicine, Yokohama City University, Yokohama, Japan. nmiyake@yokohama-cu.ac.jp
  • 8 Department of Human Genetics, Graduate School of Medicine, Yokohama City University, Yokohama, Japan. naomat@yokohama-cu.ac.jp
J Hum Genet, 2020 Sep;65(9):751-757.
PMID: 32405030 DOI: 10.1038/s10038-020-0765-3

Abstract

Inborn errors of metabolism can cause epileptic encephalopathies. Biallelic loss-of-function variants in the ITPA gene, encoding inosine triphosphate pyrophosphatase (ITPase), have been reported in epileptic encephalopathies with lack of myelination of the posterior limb of the internal capsule, brainstem tracts, and tracts to the primary visual and motor cortices (MIM:616647). ITPase plays an important role in purine metabolism. In this study, we identified two novel homozygous ITPA variants, c.264-1 G > A and c.489-1 G > A, in two unrelated consanguineous families. The probands had epilepsy, microcephaly with characteristic magnetic resonance imaging findings (T2 hyperintensity signals in the pyramidal tracts of the internal capsule, delayed myelination, and thin corpus callosum), hypotonia, and developmental delay; both died in early infancy. Our report expands the knowledge of clinical consequences of biallelic ITPA variants.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.