Radhakrishnan Periyasamy, Moirangthem Amita, Nayak Shalini S, Shukla Anju, Mathew Mary, Girisha Katta M
Departments of Medical Genetics.
Pathology, Kasturba Medical College, Manipal Academy of Higher Education, Manipal, India.
Clin Dysmorphol. 2019 Jan;28(1):17-21. doi: 10.1097/MCD.0000000000000248.
Glycogen storage disease IV (GSD IV), caused by a defect in GBE1, is a clinically heterogeneous disorder. A classical hepatic form and a neuromuscular form have been described. The severe neuromuscular form presents as a fetal akinesia deformation sequence or a congenital subtype. We ascertained three unrelated families with fetuses/neonates who presented with fetal akinesia deformation sequence to our clinic for genetic counseling. We performed a detailed clinical evaluation, exome sequencing, and histopathology examination of two fetuses and two neonates from three unrelated families presenting with these perinatally lethal neuromuscular forms of GSD IV. Exome sequencing in the affected fetuses/neonates identified four novel pathogenic variants (c.1459G>T, c.144-1G>A, c.1680C>G, and c.1843G>C) in GBE1 (NM_000158). Histopathology examination of tissues from the affected fetuses/neonate was consistent with the diagnosis. Here, we add three more families with the severe perinatally lethal neuromuscular forms of GSD IV to the GBE1 mutation spectrum.
糖原贮积病IV型(GSD IV)由GBE1缺陷引起,是一种临床异质性疾病。已描述了经典的肝脏型和神经肌肉型。严重的神经肌肉型表现为胎儿运动不能变形序列或先天性亚型。我们确定了三个不相关的家庭,其胎儿/新生儿因胎儿运动不能变形序列前来我们诊所进行遗传咨询。我们对来自三个不相关家庭的两名胎儿和两名新生儿进行了详细的临床评估、外显子组测序和组织病理学检查,这些胎儿和新生儿患有这些围产期致死性神经肌肉型GSD IV。对受影响的胎儿/新生儿进行外显子组测序,在GBE1(NM_000158)中鉴定出四个新的致病变异(c.1459G>T、c.144-1G>A、c.1680C>G和c.1843G>C)。对受影响的胎儿/新生儿组织进行的组织病理学检查与诊断一致。在此,我们将另外三个患有严重围产期致死性神经肌肉型GSD IV的家庭添加到GBE1突变谱中。