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遗传性神经病的遗传谱,发病于一岁以内。

Genetic spectrum of hereditary neuropathies with onset in the first year of life.

机构信息

Neurogenetics Group, VIB Department of Molecular Genetics, University of Antwerp, Universiteitsplein 1, B-2610 Antwerpen, Belgium.

出版信息

Brain. 2011 Sep;134(Pt 9):2664-76. doi: 10.1093/brain/awr184. Epub 2011 Aug 11.

Abstract

Early onset hereditary motor and sensory neuropathies are rare disorders encompassing congenital hypomyelinating neuropathy with disease onset in the direct post-natal period and Dejerine-Sottas neuropathy starting in infancy. The clinical spectrum, however, reaches beyond the boundaries of these two historically defined disease entities. De novo dominant mutations in PMP22, MPZ and EGR2 are known to be a typical cause of very early onset hereditary neuropathies. In addition, mutations in several other dominant and recessive genes for Charcot-Marie-Tooth disease may lead to similar phenotypes. To estimate mutation frequencies and to gain detailed insights into the genetic and phenotypic heterogeneity of early onset hereditary neuropathies, we selected a heterogeneous cohort of 77 unrelated patients who presented with symptoms of peripheral neuropathy within the first year of life. The majority of these patients were isolated in their family. We performed systematic mutation screening by means of direct sequencing of the coding regions of 11 genes: MFN2, PMP22, MPZ, EGR2, GDAP1, NEFL, FGD4, MTMR2, PRX, SBF2 and SH3TC2. In addition, screening for the Charcot-Marie-Tooth type 1A duplication on chromosome 17p11.2-12 was performed. In 35 patients (45%), mutations were identified. Mutations in MPZ, PMP22 and EGR2 were found most frequently in patients presenting with early hypotonia and breathing difficulties. The recessive genes FGD4, PRX, MTMR2, SBF2, SH3TC2 and GDAP1 were mutated in patients presenting with early foot deformities and variable delay in motor milestones after an uneventful neonatal period. Several patients displaying congenital foot deformities but an otherwise normal early development carried the Charcot-Marie-Tooth type 1A duplication. This study clearly illustrates the genetic heterogeneity underlying hereditary neuropathies with infantile onset.

摘要

早发性遗传性运动感觉神经病是罕见的疾病,包括先天性轴索性神经病,其在出生后直接发病,还有 Dejerine-Sottas 神经病,其在婴儿期发病。然而,其临床谱超出了这两种历史上定义的疾病实体的范围。已知 PMP22、MPZ 和 EGR2 的新生显性突变是非常早发性遗传性神经病的典型原因。此外,几种其他显性和隐性遗传性运动感觉神经病基因的突变也可能导致类似的表型。为了估计突变频率并深入了解早发性遗传性神经病的遗传和表型异质性,我们选择了一个异质的 77 名无关患者队列,这些患者在出生后的第一年就出现了周围神经病的症状。这些患者中的大多数在他们的家族中是孤立的。我们通过直接测序 11 个基因的编码区进行了系统的突变筛查:MFN2、PMP22、MPZ、EGR2、GDAP1、NEFL、FGD4、MTMR2、PRX、SBF2 和 SH3TC2。此外,还对 17p11.2-12 染色体上的 Charcot-Marie-Tooth 1A 型重复进行了筛查。在 35 名患者(45%)中发现了突变。在早期出现低张力和呼吸困难的患者中,最常发现 MPZ、PMP22 和 EGR2 的突变。在早期出现足部畸形和运动里程碑后出现可变延迟的新生儿期无事件发生的患者中,发现了隐性基因 FGD4、PRX、MTMR2、SBF2、SH3TC2 和 GDAP1 的突变。几个表现为先天性足部畸形但其他方面早期发育正常的患者携带 Charcot-Marie-Tooth 1A 型重复。这项研究清楚地说明了婴儿期发病的遗传性神经病的遗传异质性。

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