| Literature DB >> 22772462 |
Hye Won Park1, Yonghee Lee, Gu-Hwan Kim, Byong Sop Lee, Ki Soo Kim, Han-Wook Yoo, Ellen Ai-Rhan Kim.
Abstract
Gaucher's disease is caused by a deficiency of glucocerebrosidase (GBA) and results in the accumulation of glucocerebroside within macrophages. We report on a 33(+2) gestational week premature infant whose family history was significant for a previously undiagnosed premature sibling with similar clinical features, including severe hydrops fetalis, hepatosplenomegaly, skin lesions at birth followed by death. The diagnosis of Gaucher's disease type 2 in the present case was based on postmortem pathological findings and a subsequent gene analysis that indicated a heterozygous condition for the novel deletion mutation at GBA cDNA nucleotide position 630 resulting in the frameshift (Pro171fsX21) in exon 6 and a G→A transition mutation at GBA cDNA nucleotide position 887 (Arg257Gln) in exon 7.Entities:
Mesh:
Substances:
Year: 2012 PMID: 22772462 DOI: 10.1016/j.gene.2012.06.090
Source DB: PubMed Journal: Gene ISSN: 0378-1119 Impact factor: 3.688