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5q35.2-q35.3 处 1.07Mb 微缺失导致 NSD1 杂合性缺失及 Sotos 综合征的产前诊断及分子细胞遗传学特征

Prenatal diagnosis and molecular cytogenetic characterization of a 1.07-Mb microdeletion at 5q35.2-q35.3 associated with NSD1 haploinsufficiency and Sotos syndrome.

机构信息

Department of Obstetrics and Gynecology, Mackay Memorial Hospital, Taipei, Taiwan; Department of Medical Research, Mackay Memorial Hospital, Taipei, Taiwan; Department of Biotechnology, Asia University, Taichung, Taiwan; School of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung, Taiwan; Institute of Clinical and Community Health Nursing, National Yang-Ming University, Taipei, Taiwan; Department of Obstetrics and Gynecology, School of Medicine, National Yang-Ming University, Taipei, Taiwan.

Department of Obstetrics and Gynecology, Mackay Memorial Hospital, Taipei, Taiwan; Department of Medicine, Mackay Medical College, New Taipei City, Taiwan.

出版信息

Taiwan J Obstet Gynecol. 2014 Dec;53(4):583-7. doi: 10.1016/j.tjog.2014.10.002.

Abstract

OBJECTIVE

To present prenatal diagnosis and molecular cytogenetic characterization of a de novo 5q35 microdeletion associated with Sotos syndrome.

METHODS

This was the first pregnancy of a 29-year-old woman. The pregnancy was uneventful until 27 weeks of gestation when left ventriculomegaly was first noted. At 31 weeks of gestation, polyhydramnios, macrocephaly, and ventriculomegaly were prominent on ultrasound, and left pyelectasis and bilateral ventriculomegaly were diagnosed on magnetic resonance imaging. The woman underwent amniocentesis and cordocentesis at 32 weeks of gestation. Conventional cytogenetic analysis was performed using cultured amniocytes and cord blood lymphocytes. Array comparative genomic hybridization (aCGH) was performed on uncultured amniocytes and parental blood. Metaphase fluorescence in situ hybridization (FISH) was performed on cultured lymphocytes.

RESULTS

Conventional cytogenetics revealed a karyotype of 46,XX. aCGH on uncultured amniocytes revealed a de novo 1.07-Mb microdeletion at 5q35.2-q35.3 encompassing NSD1. Metaphase FISH analysis on the cord blood lymphocytes confirmed the deletion at 5q35.2. The postnatal phenotype was consistent with Sotos syndrome.

CONCLUSION

Fetuses with Sotos syndrome may present macrocephaly, polyhydramnios, ventriculomegaly, and pyelectasis in the third trimester. aCGH and metaphase FISH are useful for rapid diagnosis of 5q35 microdeletion associated with Sotos syndrome.

摘要

目的

介绍一例与 Sotos 综合征相关的新发 5q35 微缺失的产前诊断和分子细胞遗传学特征。

方法

这是一位 29 岁女性的首次妊娠。妊娠过程无特殊,直到 27 孕周时首次发现左心室肥大。31 孕周时,超声检查发现羊水过多、大头畸形和左肾盂扩张,磁共振成像(MRI)诊断为双侧脑室扩大。孕妇在 32 孕周时接受了羊膜穿刺术和脐带血穿刺术。使用培养的羊水细胞和脐带血淋巴细胞进行常规细胞遗传学分析。对未培养的羊水细胞和父母血样进行微阵列比较基因组杂交(aCGH)。对培养的淋巴细胞进行中期荧光原位杂交(FISH)。

结果

常规细胞遗传学显示核型为 46,XX。未培养的羊水细胞 aCGH 显示 5q35.2-q35.3 处存在一个 1.07Mb 的新发微缺失,包括 NSD1。脐带血淋巴细胞的中期 FISH 分析证实了 5q35.2 处的缺失。新生儿的表型与 Sotos 综合征一致。

结论

Sotos 综合征胎儿在妊娠晚期可能表现为大头畸形、羊水过多、脑室扩大和肾盂扩张。aCGH 和中期 FISH 可用于快速诊断与 Sotos 综合征相关的 5q35 微缺失。

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