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一种新的 PLS3 突变导致极为罕见的 X 连锁型成骨不全症。

A novel mutation in PLS3 causes extremely rare X-linked osteogenesis imperfecta.

机构信息

Department of Endocrinology, National Health Commission Key Laboratory of Endocrinology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Department of Endocrinology, Beijing Friendship Hospital, Capital Medical University, Beijing, China.

出版信息

Mol Genet Genomic Med. 2020 Dec;8(12):e1525. doi: 10.1002/mgg3.1525. Epub 2020 Nov 9.

Abstract

BACKGROUND

Osteogenesis imperfecta (OI) is a phenotypically and genetically heterogeneous bone disease characterized by bone fragility and recurrent fractures. X-linked inherited OI with mutation in PLS3 is so rare that its genotype-phenotype characteristics are not available.

METHODS

We designed a novel targeted next-generation sequencing (NGS) panel with the candidate genes of OI to detect pathogenic mutations and confirmed them by Sanger sequencing. The phenotypes of the patients were also investigated.

RESULTS

The proband, a 12-year-old boy from a nonconsanguineous family, experienced multiple fractures of long bones and vertebrae and had low bone mineral density (BMD Z-score of -3.2 to -2.0). His younger brother also had extremity fractures. A novel frameshift mutation (c.1106_1107insGAAA; p.Phe369Leufs*5) in exon 10 of PLS3 was identified in the two patients, which was inherited from their mother who had normal BMD. Blue sclerae were the only extraskeletal symptom in all affected individuals. Zoledronic acid was beneficial for increasing BMD and reshaping the compressed vertebral bodies of the proband.

CONCLUSION

We first identify a novel mutation in PLS3 that led to rare X-linked OI and provide practical information for the diagnosis and treatment of this disease.

摘要

背景

成骨不全症(OI)是一种表型和遗传异质性的骨骼疾病,其特征是骨骼脆弱和反复骨折。X 连锁遗传性 OI 伴 PLS3 基因突变极为罕见,其基因型-表型特征尚不清楚。

方法

我们设计了一个新的靶向下一代测序(NGS)面板,包含 OI 的候选基因,以检测致病突变,并通过 Sanger 测序进行确认。还对患者的表型进行了调查。

结果

先证者是一个来自非近亲家庭的 12 岁男孩,经历了多次长骨和椎体骨折,且骨密度(BMD Z 评分-3.2 至-2.0)较低。他的弟弟也有四肢骨折。在这两名患者中发现了 PLS3 外显子 10 中的一个新的移码突变(c.1106_1107insGAAA;p.Phe369Leufs*5),该突变来自其 BMD 正常的母亲。所有受累个体仅存在蓝巩膜这一骨骼外症状。唑来膦酸有利于增加 BMD 和重塑先证者受压的椎体。

结论

我们首次在 PLS3 中发现了一个导致罕见 X 连锁 OI 的新突变,为该疾病的诊断和治疗提供了实用信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd82/7767536/76444ffe509c/MGG3-8-e1525-g001.jpg

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