Eblan Michael J, Goker-Alpan Ozlem, Sidransky Ellen
Section on Molecular Neurogenetics, National Institute of Mental Health and Medical Genetics Branch, National Human Genome Research Institute, NIH, Bethesda, MD 20892, USA.
Fetal Pediatr Pathol. 2005 Jul-Oct;24(4-5):205-22. doi: 10.1080/15227950500405296.
Gaucher disease, the inherited deficiency of glucocerebrosidase, is characterized by significant genetic and phenotypic heterogeneity. At the extreme end of the phenotypic continuum is the perinatal lethal variant, typically presenting in utero or during the neonatal period as hydrops and/orcongenital ichthyosis, with severe and progressive neurological involvement. Insights from the null-allele Gaucher mouse model contributed to the identification of this distinct phenotype, which has unique epidermal involvement. While multiple mutations are encountered, many affected infants are homozygous for recombinant alleles. The diagnosis is often missed due to the early lethality and the failure to recognize the association between lysosomal disorders and hydrops fetalis. The incidence of severe perinatal Gaucher disease may prove more common than currently appreciated with greater physician awareness of the disorder.
戈谢病是一种因葡萄糖脑苷脂酶遗传性缺乏所致的疾病,其特点是具有显著的遗传和表型异质性。在表型连续谱的极端情况是围产期致死型变异,通常在子宫内或新生儿期表现为水肿和/或先天性鱼鳞病,并伴有严重且进行性的神经受累。来自无效等位基因戈谢病小鼠模型的见解有助于识别这种具有独特表皮受累情况的独特表型。虽然会遇到多种突变,但许多受影响的婴儿是重组等位基因的纯合子。由于早期致死性以及未能认识到溶酶体疾病与胎儿水肿之间的关联,诊断常常被漏诊。随着医生对该疾病的认识提高,严重围产期戈谢病的发病率可能比目前所认为的更为常见。