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部分丙酮酸激酶缺乏症加重遗传性球形红细胞增多症一家系中 3 带缺乏的表型表达。

Partial pyruvate kinase deficiency aggravates the phenotypic expression of band 3 deficiency in a family with hereditary spherocytosis.

机构信息

Laboratory of Red Blood Cell Diagnostics, Department of Blood Cell Research, Sanquin Blood Supply Foundation, Amsterdam, The Netherlands.

出版信息

Am J Hematol. 2015 Mar;90(3):E35-9. doi: 10.1002/ajh.23899. Epub 2014 Nov 24.

DOI:10.1002/ajh.23899
PMID:25388786
Abstract

In a family with mild dominant spherocytosis, affected members showed partial band 3 deficiency. The index patient showed more severe clinical symptoms than his relatives, and his red blood cells displayed concomitant low pyruvate kinase activity. We investigated the contribution of partial PK deficiency to the phenotypic expression of mutant band 3 in this family. Pyruvate kinase deficiency and band 3 deficiency were characterized by DNA analysis. Results of red cell osmotic fragility testing, the results of cell deformability obtained by the Automated Rheoscope and Cell Analyzer and the results obtained by Osmotic Gradient Ektacytometry, which is a combination of these tests, were related to the red cell ATP content. Spherocytosis in this family was due to a novel heterozygous mutation in SLC4A1, the gene for band 3. Reduced PK activity of the index patient was attributed to a novel mutation in PKLR inherited from his mother, who was without clinical symptoms. Partial PK deficiency was associated with decreased red cell ATP content and markedly increased osmotic fragility. This suggests an aggravating effect of low ATP levels on the phenotypic expression of band 3 deficiency.

摘要

在一个轻度显性球形体贫血的家族中,受影响的成员表现出部分 3 带缺陷。该患者的临床表现比其亲属更为严重,且其红细胞同时存在丙酮酸激酶活性降低。我们研究了部分 PK 缺陷对该家族突变 3 带表型表达的影响。通过 DNA 分析来确定丙酮酸激酶缺乏和 3 带缺陷。红细胞渗透脆性试验、自动流变仪和细胞分析仪测定的细胞变形性结果以及这些试验结合的渗透梯度 ektacytometry 结果与红细胞 ATP 含量相关。该家族的球形红细胞症是由于 SLC4A1 基因(即 3 带基因)的一种新型杂合突变所致。该患者的 PK 活性降低归因于其母亲遗传的 PKLR 中的一个新突变,而其母亲无临床症状。部分 PK 缺陷与红细胞 ATP 含量降低和明显增加的渗透脆性有关。这表明低 ATP 水平对 3 带缺陷表型表达有加重作用。

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