| Literature DB >> 32405030 |
Masamune Sakamoto1,2, Den Kouhei1, Muzhirah Haniffa3, Sebastián Silva4, Mónica Troncoso5, Paola Santander5, Valeria Schonstedt6, Ximena Stecher6,7, Nobuhiko Okamoto8, Kohei Hamanaka1, Takeshi Mizuguchi1, Satomi Mitsuhashi1, Noriko Miyake9, Naomichi Matsumoto10.
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.Entities:
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Year: 2020 PMID: 32405030 DOI: 10.1038/s10038-020-0765-3
Source DB: PubMed Journal: J Hum Genet ISSN: 1434-5161 Impact factor: 3.172