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红细胞膜骨架磷酸化诱导凝胶化缺失:遗传性球形红细胞增多症的一种诊断工具。

Absence of phosphorylation-induced gelation of erythrocyte membrane skeletons: a diagnostic tool for hereditary spherocytosis.

作者信息

Armbrust R, Eber S W, Schröter W

机构信息

Department of Pediatrics, University of Göttingen, Federal Republic of Germany.

出版信息

Ann Hematol. 1992 Feb;64(2):93-6. doi: 10.1007/BF01715352.

Abstract

As yet there is no single test specific for the diagnosis of hereditary spherocytosis. In the search for a specific test, a method described by Pinder et al. [14] using a cAMP-independent protein kinase extracted from normal erythrocyte membranes was used. Membrane skeletons were prepared from erythrocyte ghosts by extraction with a non-ionic detergent, i.e., Triton X-100. Upon phosphorylation with c-AMP-independent protein kinase the suspension of normal membrane skeletons set to a gelatinous mass. Membrane skeletons from patients with spherocytosis failed to show this phenomenon. In order to clarify whether this phenomenological difference can be used as a diagnostic tool for hereditary spherocytosis, a semiquantitative method of observing the gelation process was used under definite shear stress conditions. We investigated 33 patients with different hemolytic anemias (spherocytosis, hereditary elliptocytosis, hereditary stomatocytosis, homozygous beta-thalassemia and enzymopenic hemolytic anemias). With the exception of spherocytosis, all preparations of membrane skeletons showed gelation after 30-50 min. Spherocytosis membrane skeletons did not show a significant gelation even after 12 h of incubation. Thus, the failing gelation is specific for the diagnosis of hereditary spherocytosis. The "gelation assay" might be a valuable method for defining patients with hemolytic anemias due to erythrocyte membrane defects. Its molecular basis and the possible importance for the pathogenesis of spherocytosis require further investigations.

摘要

目前尚无单一的特异性检测方法用于诊断遗传性球形红细胞增多症。在寻找特异性检测方法的过程中,采用了Pinder等人[14]描述的一种方法,即使用从正常红细胞膜中提取的一种不依赖环磷酸腺苷(cAMP)的蛋白激酶。通过用非离子去污剂(即Triton X-100)提取,从红细胞影体制备膜骨架。用不依赖cAMP的蛋白激酶进行磷酸化后,正常膜骨架的悬浮液会变成凝胶状物质。球形红细胞增多症患者的膜骨架未出现这种现象。为了阐明这种现象学差异是否可作为遗传性球形红细胞增多症的诊断工具,在确定的剪切应力条件下采用了一种半定量观察凝胶化过程的方法。我们研究了33例不同类型的溶血性贫血患者(球形红细胞增多症、遗传性椭圆形红细胞增多症、遗传性口形红细胞增多症、纯合子β地中海贫血和酶缺乏性溶血性贫血)。除球形红细胞增多症外,所有膜骨架制剂在30 - 50分钟后均出现凝胶化。即使孵育12小时后,球形红细胞增多症的膜骨架也未显示出明显的凝胶化。因此,凝胶化失败是遗传性球形红细胞增多症诊断的特异性表现。“凝胶化测定”可能是一种用于鉴别因红细胞膜缺陷导致溶血性贫血患者的有价值方法。其分子基础以及对球形红细胞增多症发病机制的可能重要性需要进一步研究。

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