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遗传性球形红细胞增多症患儿的基因型-表型相关性

Genotype-phenotype correlation in children with hereditary spherocytosis.

作者信息

Tole Soumitra, Dhir Priya, Pugi Jakob, Drury Luke J, Butchart Sheila, Fantauzzi Michelle, Langer Jacob C, Baker Jillian M, Blanchette Victor S, Kirby-Allen Melanie, Carcao Manuel D

机构信息

Department of Paediatrics, Division of Haematology/Oncology, Hospital for Sick Children, Toronto, Ontario, Canada.

Department of Paediatrics, Division of Haematology/Oncology, Children's Hospital, London Health Sciences Centre, London, Ontario, Canada.

出版信息

Br J Haematol. 2020 Nov;191(3):486-496. doi: 10.1111/bjh.16750. Epub 2020 May 20.

Abstract

Hereditary spherocytosis (HS) is a common inherited haemolytic anaemia attributed to disturbances in five different red cell membrane proteins. We performed a retrospective study of 166 children with HS and describe the clinical phenotype according to the genotype. In 160/166 (97%) children with HS a disease-causing mutation was identified. Pathogenic variants in ANK1, SPTB, SLC4A1 and SPTA1 were found in 49%, 33%, 13% and 5% of patients. Children with SLC4A1-HS had the mildest phenotype, showing the highest haemoglobin (P < 0·001), lowest reticulocyte counts (P < 0·001) and lowest unconjugated bilirubin levels (P = 0·006), and none required splenectomy in childhood (P < 0·001). Conversely, children with autosomal recessive SPTA1-HS had the most severe clinical phenotype, with almost all patients undergoing splenectomy in early childhood. Patients with ANK1 and SPTB variants showed a similar clinical phenotype. Within each gene, variant type or location did not predict disease severity or likelihood of splenectomy. Among patients with a genetic diagnosis, 47 (29%) underwent splenectomy (23 partial; 24 total) while 57 (36%) underwent cholecystectomy. Total splenectomy led to greater improvements in haemoglobin (P = 0·02). Select use of genetic testing (especially in patients without a family history) may help predict clinical phenotype in childhood and guide family counselling.

摘要

遗传性球形红细胞增多症(HS)是一种常见的遗传性溶血性贫血,归因于五种不同红细胞膜蛋白的紊乱。我们对166例HS患儿进行了一项回顾性研究,并根据基因型描述了临床表型。在166例HS患儿中,有160例(97%)鉴定出致病突变。ANK1、SPTB、SLC4A1和SPTA1的致病变异分别在49%、33%、13%和5%的患者中发现。SLC4A1-HS患儿的表型最轻微,血红蛋白水平最高(P<0.001),网织红细胞计数最低(P<0.001),未结合胆红素水平最低(P=0.006),且儿童期均无需行脾切除术(P<0.001)。相反,常染色体隐性SPTA1-HS患儿的临床表型最严重,几乎所有患者在幼儿期均接受了脾切除术。ANK1和SPTB变异的患者表现出相似的临床表型。在每个基因中,变异类型或位置均不能预测疾病严重程度或脾切除术的可能性。在进行基因诊断的患者中,47例(29%)接受了脾切除术(23例部分切除;24例全切除),57例(36%)接受了胆囊切除术。全脾切除术使血红蛋白有更大改善(P=0.02)。选择性使用基因检测(尤其是在无家族史的患者中)可能有助于预测儿童期的临床表型并指导家庭咨询。

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