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中华妇幼临床医学杂志(电子版) ›› 2020, Vol. 16 ›› Issue (04) : 398 -408. doi: 10.3877/cma.j.issn.1673-5250.2020.04.005

所属专题： 文献；

论著

RANBP2基因突变致家族性急性坏死性脑病患儿的诊治并文献复习
罗泽民1, 李久伟2,†(), 刘星宇1, 蒋琼1, 朱书瑶1, 谢丹凤1   
  1. 1. 四川省妇幼保健院儿童神经科，成都　610045
    2. 首都医科大学附属北京儿童医院神经内科　100045
  • 收稿日期:2019-09-19 修回日期:2020-05-21 出版日期:2020-08-01
  • 通信作者: 李久伟

Diagnosis and treatment of children with familial acute necrotizing encephalopathy caused by RANBP2 gene mutation and literature review

Zemin Luo1, Jiuwei Li2,†(), Xingyu Liu1, Qiong Jiang1, Shuyao Zhu1, Danfeng Xie1   

  1. 1. Department of Pediatric Neurology, Sichuan Provincial Hospital for Women and Children, Chengdu 610045, Sichuan Province, China
    2. Department of Neurology, Beijing Children′s Hospital Affiliated to Capital Medical University, Beijing 100045, China
  • Received:2019-09-19 Revised:2020-05-21 Published:2020-08-01
  • Corresponding author: Jiuwei Li
  • About author:
    Corresponding author: Li Jiuwei, Email:
  • Supported by:
    Scientific Research Project of Health Commission of Sichuan Province(19PJ256)
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引用本文：

罗泽民, 李久伟, 刘星宇, 蒋琼, 朱书瑶, 谢丹凤. RANBP2基因突变致家族性急性坏死性脑病患儿的诊治并文献复习[J]. 中华妇幼临床医学杂志(电子版), 2020, 16(04): 398-408.

Zemin Luo, Jiuwei Li, Xingyu Liu, Qiong Jiang, Shuyao Zhu, Danfeng Xie. Diagnosis and treatment of children with familial acute necrotizing encephalopathy caused by RANBP2 gene mutation and literature review[J]. Chinese Journal of Obstetrics & Gynecology and Pediatrics(Electronic Edition), 2020, 16(04): 398-408.

目的

探讨RANBP2基因突变致家族性急性坏死性脑病(ANE1)的临床特征、诊治及预后。

方法

选择2018年1月及2019年3月，于北京儿童医院(患儿1)及四川省妇幼保健院(患儿2)确诊的2例RANBP2基因突变所致ANE1患儿为研究对象。回顾性分析其临床病例资料，包括临床表现、实验室检查结果、头颅MRI特征、治疗及随访结果等。同时，检索国内外数据库中RANBP2基因突变所致ANE1患者相关文献进行复习。本研究遵循的程序符合2013年修订的《世界医学协会赫尔辛基宣言》要求。

结果

①临床病例资料：患儿1系发热后头痛、嗜睡、精神反应差、表情淡漠、直线行走不稳、近期记忆力下降；患儿2系甲型流感病毒感染后，出现发热、头痛、呕吐、进行性意识障碍伴面瘫。2例患儿头颅MRI检查均提示丘脑、岛叶、脑桥、外囊等多部位对称性损害，部分囊性改变。基因检测结果显示，2例患儿均为RANBP2基因第12外显子c.1754 C>T(p.Thr585Met)杂合错义突变；经丙种球蛋白、糖皮质激素调节免疫功能治疗，以及"线粒体鸡尾酒疗法"修复线粒体功能等治疗后，患儿颅内病灶均好转，精神及运动能力均恢复。②文献复习：总结文献报道的74例及本组2例RANBP2基因突变所致ANE1患者临床特征如下。其发病年龄为5个月至40岁，首发年龄中位数为3.5岁，男女患者比例为35∶41。其主要临床表现中，发热为82.5%(47/57)，癫痫发作为81.1%(43/53)，局灶性神经功能障碍(FND)为28.6%(8/28)，脑病为93.4%(71/76)；脑脊液蛋白升高(EP)为90.3%(56/62)，脑脊液细胞数增多(Pl)为28.6%(8/28)。患儿头颅MRI/CT检查提示的病变部位，主要位于丘脑(83.1%，49/59)，脑干(72.9%，43/59)，颞叶(71.2%，42/59)，小脑(26.3%，5/19)，脊髓(13.8%，4/29)，基底节(8.5%，5/59)。

结论

RANBP2基因突变所致ANE1，具有典型临床症状和特征性头颅MRI表现，临床对发热性疾病伴丘脑等部位对称性损害患者，应注意本病可能。对疑似该病的患者，应尽早进行RANBP2基因检测，将有助于明确本病诊断、进行合理治疗并改善患者预后。

关键词: 急性发热性脑病, 家族性, Ran结合蛋白2, 磁共振成像, 遗传学, 突变，误义, 丘脑, 儿童
Objective

To investigate clinical characteristics, diagnosis, treatment and prognosis of familial acute necrotizing encephalopathy (ANE1) caused by RANBP2 gene mutation.

Methods

A total of 2 children with ANE1 caused by RANBP2 gene mutation who were confirmed in Beijing Children′s Hospital in January 2018 (case 1) and in Sichuan Provincial Hospital for Women and Children in March 2019 (case 2), were chosen as research subjects. We retrospectively analyzed their clinical case data, including clinical manifestations, laboratory examination results, head MRI features, treatment and follow-up data. Meanwhile, literature related to ANE1 caused by RANBP2 gene mutation were searched in mainstream databases for literature review. And the procedure followed in the whole study were in accordance with World Medical Association Declaration of Helsinki revised in 2013.

Results

① Clinical case data: clinical manifestation of case 1 was presented with headache after fever, drowsiness, poor mental response, indifferent expression, unstable walking in a straight line, and recent memory decline; and of case 2 with fever, headache, vomiting, progressive disturbance of consciousness and facial paralysis after infection of influenza A virus. Their head MRI examinations revealed symmetrical damage to multiple parts of thalamus, insula, pons and external capsule, with some cystic changes. Their gene detection results showed that heterozygosity mutation of RANBP2 gene on exon 12: c. 1754 C>T (p.Thr585Met), a missense mutation. After treatment with gamma globulin, glucocorticoids to regulate immunity, and " mitochondrial cocktail therapy" to repair mitochondrial function, their intracranial lesions improved, and mental and athletic abilities were restored. ② Clinical features of ANE1 caused by RANBP2 gene mutation of 74 cases by literature review and 2 cases in this study were summarized. Their clinical features were as follows: their age of onset ranged from 5 months to 40 years old, median age of first onset was 3.5 years old, the ratio of male to female patients was 35∶41. Among main clinical manifestations, ratio of fever was 82.5% (47/57), epilepsy was 81.1% (41/53), focal neurological deficit (FND) was 28.6% (8/28), encephalopathy was 93.4% (71/76), elevated CSF protein (EP) was 90.3% (56/62), pleocytosis in CSF (Pl) was 28.6% (8/28). Head MRI/CT showed that main lesions of patients were located in thalami (83.1%, 49/59), brainstem (72.9%, 43/59), temporal lobe (71.2%, 42/59), cerebellum (26.3%, 5/19), spinal cord (13.8%, 4/29), basal ganglia (8.5%, 5/59).

Conclusions

ANE1 caused by RANBP2 gene mutation has typical clinical features and characteristic head MRI findings. Febrile disease with symmetrical lesions in thalamus and other brain parts should be a vigilant signal to ANE1 patients. For patients suspected of ANE1, early detection of RANBP2 gene will be helpful to clarify diagnosis, rational treatment and improve their prognosis.

Key words: Acute febrile encephalopathy, Familial, Ran-binding protein 2, Magnetic resonance imaging, Genetics, Mutation, missense, Thalamus, Child
图1 患儿2(男性，6岁5个月)入院时头颅MRI检查结果(图1A～1G：双侧岛叶、边缘间脑结构，双侧颞叶深部局部、脑桥、中脑可见斑片状异常信号，与基底节分界清，累及外囊，内囊未见受累。其中，图1A～1C示病变区T1WI呈低信号，图1D～1G示T2WI及T2WI-FLAIR呈高信号。图1H：DWI外囊及背侧丘脑部分呈高信号)
图2 患儿2(男性，6岁5个月)入院后及随访期头颅MRI与MRS检查结果[图2A～2C：入院7 d时头颅MRS结果示，双侧大脑病变区NAA峰减低，胆碱峰升高，NAA/胆碱、NAA/肌酸降低，左侧大脑病变重，未见确切乳酸峰；图2D～2K：入院7 d时复查头颅MRI结果示，双侧岛叶、边缘间脑结构，双侧颞叶深部局部、脑桥、中脑可见斑点、斑片状异常信号，与基底节分界清，累及外囊，病变区T1WI呈低信号，T2WI高信号，并且双侧岛叶病变中可见串珠样高亮信号(图2F、2J红色箭头所示)，病变区T2WI-FLAIR呈高信号；图2L～2M：入院19 d时复查头颅MRI结果示，双侧边缘系统及丘脑、间脑、外囊系统多灶性病变异常信号，与入院7 d的头颅MRI结果比较，病灶范围缩小，双侧外囊软化灶形成(红色箭头所示)；图2N～2O：出院15 d时复查头颅MRI结果示，左侧大脑脚及脑桥左侧斑点状异常信号，与入院19 d的头颅MRI结果比较，双侧外囊、左侧大脑脚及脑桥左侧异常信号灶范围缩小，双侧外囊软化灶形成(红色箭头所示)]
图4 患儿2(男性，6岁5个月)及父母Sanger法测序图[图4A：患儿RANBP2基因第12外显子c.1754 C>T(p.Thr585Met)杂合突变，为错义突变(红色箭头所示)；图4B：患儿父亲RANBP2基因第12外显子c.1754 C>T(p.Thr585Met)杂合突变(红色箭头所示)；图4C：患儿母亲RANBP2基因相应位点未见异常(绿色箭头所示)]
表1 76例RANBP2基因突变所致ANE1患者的主要临床表现
文献(第1作者，文献发表年) 例数 发病年龄 男性∶女性 发热[%(n/n′)] 癫痫发作[%(n/n′)] FND[%(n/n′)] 脑病[%(n/n′)]
Singh[7]，2014 59 5个月龄至36岁 28∶31 75.0(30/40) 91.9(34/37) 16.7(2/12) 91.5(54/59)
McSwiney[17]，2014 1 3岁 1∶0 100.0(1/1) 0(0/1) 100.0(1/1) 100.0(1/1)
Bloch[18]，2015 2 10、40岁 1∶1 100.0(2/2) 50.0(1/2) 0(0/2) 100.0(2/2)
Anand[19]，2015 1 28个月龄 1∶0 100.0(1/1) 0(0/1) 0(0/1) 100.0(1/1)
朱金兰[5]，2015 1 8个月龄首次、18个月龄再次、25个月龄第3次发作 0∶1 100.0(1/1) 100.0(1/1) 0(0/1) 100.0(1/1)
Sell[20]，2016 2 10、19个月龄 0∶2 100.0(2/2) 100.0(2/2) 50.0(1/2) 100.0(2/2)
Sondhi[21]，2016 1 3.5岁 1∶0 100.0(1/1) 0(0/1) 0(0/1) 100.0(1/1)
Lee[22]，2017 2 12个月龄、2岁 0∶2 100.0(2/2) 100.0(2/2) 0(0/2) 100.0(2/2)
Soriano-Ramos[23]，2018 1 7个月龄首次、10岁再次发作 0∶1 100.0(1/1) 未提及 未提及 100.0(1/1)
Howard[24]，2018 2 17个月龄、5岁 1∶1 100.0(2/2) 100.0(2/2) 0(0/2) 100.0(2/2)
Is?kay[25]，2018 1 12岁首次、14岁再次发作 0∶1 100.0(1/1) 100.0(1/1) 0(0/1) 100.0(1/1)
Kelly[26]，2019 1 15个月龄首次、22岁再次发作 1∶0 100.0(1/1) 0(0/1) 100.0(1/1) 100.0(1/1)
罗泽民，2020 2 6岁5个月龄、10岁4个月龄 1∶1 100.0(2/2) 0(0/2) 50.0(1/2) 100.0(2/2)
文献(第1作者，文献发表年) 脑脊液检查结果[%(n/n′)] 头颅MRI/CT检查病变部位[%(n/n′)]
Singh[7]，2014 EP：93.6(44/47)；Pl：16.7(2/12) 双侧丘脑：78.6(33/42)；基底节：2.4(1/42)；颞叶：78.6(33/42)；脑干：76.2(32/42)；小脑：13.3(2/15)；脊髓：14.8(4/27)
McSwiney[17]，2014 Pl：100.0(1/1) 累及双侧丘脑、海马、脑干、内囊、下丘脑及小脑
Bloch[18]，2015 EP：100.0(2/2)；Pl：50.0(1/2) 100.0(2/2)累及双侧丘脑、脑干及海马
Anand[19]，2015 EP：100.0(1/1)；Pl：100.0(1/1) 累及双侧丘脑及基底节
朱金兰[5]，2015 EP：100.0(1/1)；Pl：100.0(1/1) 累及双侧丘脑、脑干、基底节、胼胝体、颞叶、顶叶及小脑
Sell[20]，2016 EP：50.0(1/2)；Pl：100.0(2/2) 双侧丘脑及脑干：100.0(2/2)；外囊及颞叶：50.0(1/2)
Sondhi[21]，2016 EP：100.0(1/1)；Pl：0(0/1) 累及双侧丘脑、脑干、小脑及颞叶
Lee[22]，2017 EP：100.0(2/2)；Pl：0(0/2) 双侧丘脑：100.0(2/2)；外囊、脑干、基底节及小脑：50.0(1/2)
Soriano-Ramos[23]，2018 EP：100.0(1/1)；Pl：0(0/1) 累及双侧丘脑、颞叶、枕叶、外囊及脑干
Howard[24]，2018 EP：0(0/1)；Pl：0(0/1) 外囊：100.0(2/2)；颞叶：100.0(1/1)；双侧丘脑、脑干及顶叶：50.0(1/2)
Is?kay[25]，2018 EP：0(0/1)；Pl：0(0/1) 累及双侧丘脑、岛叶及基底节
Kelly[26]，2019 EP：100.0(1/1)；Pl：0(0/1) 累及双侧丘脑、脑干及海马
罗泽民，2020 EP：100.0(2/2)；Pl：0(0/2) 双侧丘脑、岛叶、脑干及外囊：100.0(2/2)；基底节及颞叶：50.0(1/2)；脊髓：0(0/2)
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