Felderhoff-Mueser Ursula, Uhl Johannes, Penzel Roland, Van Landeghem Frank, Vogel Martin, Obladen Michael, Kopitz Jürgen
Department of Neonatology, Charité, Campus Virchow Klinikum, Berlin, Germany.
Am J Med Genet A. 2004 Jul 15;128A(2):138-43. doi: 10.1002/ajmg.a.20445.
A subset of patients with type 2 Gaucher disease is characterized by intrauterine onset of rapidly progressive neuropathic disease, arthrogryposis, hydrops fetalis and in some cases restrictive dermopathy. beta-Glucocerebrosidase (beta-glucosidase) activity is usually low or undetectable. In most cases death ensues either in-utero or within hours or days after birth. We report on an infant born to non-consanguineous parents of Caucasian origin presenting at birth with hydrops, arthrogryposis, severe respiratory distress, hepatosplenomegaly, and liver failure. Death occurred within several hours after delivery and autopsy revealed typical Gaucher cells in multiple organs in combination with severe apoptotic neurodegeneration throughout the brain. beta-Glucocerebrosidase activity was 1% of the norm in fibroblasts and a novel heterozygous insertion c.1515_1516insAGTGAGGGCAAT was identified by genomic sequencing and an insertion-specific seminested PCR. In addition, molecular studies revealed a previously described in type 1 Gaucher disease missense mutation c.476G --> A which results in a heterozygous substitution of R120Q. Our observations confirm considerable genotypic heterogeneity in patients with type 2 Gaucher disease. The transheterozygous combination of a mutation, previously described in type 1 Gaucher disease, together with a newly identified insertion may result in this severe phenotype.
2型戈谢病患者的一个亚组具有以下特征:宫内发病的快速进展性神经病变、关节挛缩、胎儿水肿,在某些情况下还有限制性皮肤病变。β-葡萄糖脑苷脂酶(β-葡糖苷酶)活性通常较低或无法检测到。在大多数情况下,患者会在宫内或出生后数小时或数天内死亡。我们报告了一名白人非近亲父母所生的婴儿,出生时出现水肿、关节挛缩、严重呼吸窘迫、肝脾肿大和肝功能衰竭。婴儿在分娩后数小时内死亡,尸检显示多个器官中有典型的戈谢细胞,同时整个大脑存在严重的凋亡性神经变性。成纤维细胞中的β-葡萄糖脑苷脂酶活性为正常水平的1%,通过基因组测序和插入特异性半巢式PCR鉴定出一个新的杂合插入c.1515_1516insAGTGAGGGCAAT。此外,分子研究还发现了1型戈谢病中先前描述的一个错义突变c.476G→A,该突变导致R120Q的杂合替代。我们的观察结果证实了2型戈谢病患者存在相当大的基因异质性。先前在1型戈谢病中描述的一个突变与新发现的插入的反式杂合组合可能导致了这种严重的表型。