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通过靶向下一代测序鉴定 SPTB 基因拷贝数变异引起的遗传性血影细胞增多症。

Hereditary spherocytosis caused by copy number variation in SPTB gene identified through targeted next-generation sequencing.

机构信息

Department of Laboratory Medicine, College of Medicine, Seoul St. Mary's Hospital, The Catholic University of Korea, Seoul, Republic of Korea.

Catholic Genetic Laboratory Center, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.

出版信息

Int J Hematol. 2019 Aug;110(2):250-254. doi: 10.1007/s12185-019-02630-0. Epub 2019 Mar 21.

Abstract

Hereditary spherocytosis (HS) is a heterogeneous genetic disorder characterized by spherocytosis on peripheral blood smear with hemolytic anemia, accompanied by signs of hemolysis. Herein, we report a 5-month-old Korean girl with HS resulting from a de novo 271 Kb microdeletion of 14q23.3. She presented with hemolytic anemia and mild splenomegaly. Spherocytosis was seen on examination of peripheral blood. Eosin-5'-maleimide (EMA) test and flow cytometric osmotic fragility test were positive. She had no relevant family history of spherocytosis. No pathogenic single nucleotide variants or small insertions/deletions were detected in HS-associated genes. Array comparative genomic hybridization analysis revealed a 271 Kb deletion at chromosome 14q23.3, encompassing the SPTB, CHURC1, GPX2, RAB15, FNTB, and MAX genes. We found a deletion affecting 5' UTR, exon 1, and part of intron 1 of the SPTB gene using targeted next-generation sequencing (NGS) analysis, suggesting that NGS may be able to identify disease-causing copy number variations (CNVs), as well as small point mutations in HS patients. In addition, chromosomal microarray may be useful in defining combined deleted genes. Additional evaluations should thus be considered in the diagnosis of HS, especially when CNV is revealed as disease-causing abnormality.

摘要

遗传性球形红细胞增多症(HS)是一种异质性遗传疾病,其特征是外周血涂片出现球形红细胞,伴有溶血性贫血,并伴有溶血迹象。在此,我们报告了一例由 14q23.3 上的从头发生的 271kb 微缺失引起的 5 月龄韩国女孩 HS。她表现为溶血性贫血和轻度脾肿大。外周血检查可见球形红细胞。伊文思蓝 5'-马来酰亚胺(EMA)试验和流式细胞术渗透脆性试验阳性。她没有球形红细胞增多症的相关家族史。HS 相关基因中未发现致病性单核苷酸变异或小插入/缺失。阵列比较基因组杂交分析显示染色体 14q23.3 上有 271kb 的缺失,包括 SPTB、CHURC1、GPX2、RAB15、FNTB 和 MAX 基因。我们通过靶向下一代测序(NGS)分析发现了一个影响 SPTB 基因 5'UTR、外显子 1 和部分内含子 1 的缺失,提示 NGS 可能能够识别致病拷贝数变异(CNVs),以及 HS 患者的小点突变。此外,染色体微阵列可能有助于定义联合缺失基因。因此,在诊断 HS 时应考虑额外的评估,特别是当 CNV 被揭示为致病异常时。

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