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神经氨酸酶诱导的溶血性贫血。实验与临床观察(作者译)

[Neuraminidase induced hemolytic anemia. Experimental and clinical observations (author's transl)].

作者信息

Poschmann A, Fischer K, Grundmann A, Vongjirad A

出版信息

Monatsschr Kinderheilkd (1902). 1976 Jan;124(1):15-24.

PMID:1246237
Abstract

Recently, increasing attention has been focussed on the in vivo action of neuraminidase as possible pathogenetical factor of hemolytic anemia and even hemolytic-uremic syndrome. Neuraminidase action in red cell membranes results in the release of neuraminic acid, and thereby the uncovering of previously hidden receptors, socalled cryptantigens. With special reference to the phythemagglutinin Anti-TAh from the peanut (Arachis hypogae) and the agglutinin Anti-AHP from the albumin gland of the small Helix pomatia we describe some new methods for the detection of these cryptantigens. In addition to the screebubg genagglutination test with Anti-TAh we developed an "Anti-T-consumption test" for quantitative detection of neuraminidase action on red cells. With the purified reagents we developed an indirect fluorescnet antibody method on blood smears for the detection of cryptantigens on single cells. By animal experiments we could show that not only the membranes of red cells but the intima of renal capillaries as well are damaged by neuraminidase. With these new methods we observed 14 patients suffering from hemolytic anemia due to bacterial or viral neuraminidase. Some of these patients developed a hemolytic-uremic syndrome. We believe that the positive reaction with Anti-T Ah should lead to prophylactic heparinization to prevent dissiminated intravascular coagulation. Neuraminidase is the first identified toxin which directly acts on the membranes of red cells and the intima of renal capillaries as well, and thereby in some patients may induce hemolytic-uremic syndrome. Possibly, these results may stimulate the development of further testsystems for the detection of still unknown toxins which are not tested with our reagents, but may equally be involved in the damage of cell membranes.

摘要

最近,神经氨酸酶的体内作用作为溶血性贫血甚至溶血尿毒综合征可能的致病因素受到了越来越多的关注。神经氨酸酶作用于红细胞膜会导致唾液酸释放,从而使先前隐藏的受体,即所谓的隐蔽抗原暴露出来。特别参考来自花生(落花生)的植物血凝素抗TAh和来自小田螺白蛋白腺的凝集素抗AHP,我们描述了一些检测这些隐蔽抗原的新方法。除了用抗TAh进行筛查性凝集试验外,我们还开发了一种“抗T消耗试验”,用于定量检测神经氨酸酶对红细胞的作用。利用纯化的试剂,我们开发了一种基于血涂片的间接荧光抗体法,用于检测单个细胞上的隐蔽抗原。通过动物实验我们可以证明,不仅红细胞膜,而且肾毛细血管内膜也会受到神经氨酸酶的损伤。通过这些新方法,我们观察了14例因细菌或病毒神经氨酸酶导致溶血性贫血的患者。其中一些患者发展为溶血尿毒综合征。我们认为,抗TAh的阳性反应应导致预防性肝素化,以防止弥散性血管内凝血。神经氨酸酶是第一种被确定的毒素,它直接作用于红细胞膜和肾毛细血管内膜,从而在一些患者中可能诱发溶血尿毒综合征。这些结果可能会刺激进一步检测系统的开发,以检测尚未用我们的试剂进行检测,但可能同样参与细胞膜损伤的未知毒素。

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