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无脑回畸形的颅外表现:非染色体、非综合征型。

Extracephalic manifestations of nonchromosomal, nonsyndromic holoprosencephaly.

机构信息

Medical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland.

出版信息

Am J Med Genet C Semin Med Genet. 2018 Jun;178(2):246-257. doi: 10.1002/ajmg.c.31616. Epub 2018 May 15.

DOI:10.1002/ajmg.c.31616
PMID:29761634
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6125181/
Abstract

Nonchromosomal, nonsyndromic holoprosencephaly (NCNS-HPE) has traditionally been considered as a condition of brain and craniofacial maldevelopment. In this review, we present the results of a comprehensive literature search supporting a wide spectrum of extracephalic manifestations identified in patients with NCNS-HPE. These manifestations have been described in case reports and in large cohorts of patients with "single-gene" mutations, suggesting that the NCNS-HPE phenotype can be more complex than traditionally thought. Likely, a complex network of interacting genetic variants and environmental factors is responsible for these systemic abnormalities that deviate from the usual brain and craniofacial findings in NCNS-HPE. In addition to the systemic consequences of pituitary dysfunction (as a direct result of brain midline defects), here we describe a number of extracephalic findings of NCNS-HPE affecting various organ systems. It is our goal to provide a guide of extracephalic features for clinicians given the important clinical implications of these manifestations for the management and care of patients with HPE and their mutation-positive relatives. The health risks associated with some manifestations (e.g., fatty liver disease) may have historically been neglected in affected families.

摘要

非染色体性、非综合征性全前脑畸形(NCNS-HPE)传统上被认为是一种脑和颅面发育不良的疾病。在这篇综述中,我们展示了全面文献检索的结果,这些结果支持了在 NCNS-HPE 患者中发现的广泛的颅外表现。这些表现已经在病例报告和“单基因”突变的大量患者队列中被描述过,这表明 NCNS-HPE 的表型可能比传统观念更复杂。很可能,一个相互作用的遗传变异和环境因素的复杂网络导致了这些偏离 NCNS-HPE 中常见的脑和颅面发现的系统性异常。除了由于脑中线缺陷导致的垂体功能障碍的系统后果(作为直接结果)之外,我们在这里还描述了一些影响各种器官系统的 NCNS-HPE 的颅外表现。我们的目标是为临床医生提供颅外特征指南,因为这些表现对 HPE 患者及其突变阳性亲属的管理和护理具有重要的临床意义。一些表现(如脂肪肝疾病)相关的健康风险在受影响的家庭中可能在历史上被忽视了。

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本文引用的文献

1
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J Hepatol. 2018 Mar;68(3):550-562. doi: 10.1016/j.jhep.2017.10.017. Epub 2017 Oct 26.
2
BOC is a modifier gene in holoprosencephaly.BOC 是前脑无裂畸形的修饰基因。
Hum Mutat. 2017 Nov;38(11):1464-1470. doi: 10.1002/humu.23286. Epub 2017 Jul 21.
3
Human germline hedgehog pathway mutations predispose to fatty liver.人类种系 hedgehog 信号通路突变易导致脂肪肝。
J Hepatol. 2017 Oct;67(4):809-817. doi: 10.1016/j.jhep.2017.06.008. Epub 2017 Jun 21.
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In-depth investigations of adolescents and adults with holoprosencephaly identify unique characteristics.对患有前脑无裂畸形的青少年和成年人进行深入调查可识别出独特的特征。
Genet Med. 2018 Jan;20(1):14-23. doi: 10.1038/gim.2017.68. Epub 2017 Jun 22.
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Conserved signaling mechanisms in Drosophila heart development.果蝇心脏发育中的保守信号传导机制。
Dev Dyn. 2017 Sep;246(9):641-656. doi: 10.1002/dvdy.24530. Epub 2017 Jul 12.
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Sonic hedgehog signaling pathway mediates development of hepatocellular carcinoma.音猬因子信号通路介导肝细胞癌的发展。
Tumour Biol. 2016 Dec;37:16199–16205. doi: 10.1007/s13277-016-5463-6. Epub 2016 Oct 15.
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Gli2 gene-environment interactions contribute to the etiological complexity of holoprosencephaly: evidence from a mouse model.Gli2基因与环境的相互作用导致了前脑无裂畸形病因的复杂性:来自小鼠模型的证据。
Dis Model Mech. 2016 Nov 1;9(11):1307-1315. doi: 10.1242/dmm.026328. Epub 2016 Sep 1.
8
Zic2 mutation causes holoprosencephaly via disruption of NODAL signalling.Zic2突变通过破坏NODAL信号传导导致前脑无裂畸形。
Hum Mol Genet. 2016 Sep 15;25(18):3946-3959. doi: 10.1093/hmg/ddw235. Epub 2016 Jul 27.
9
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