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由IgM头孢菌素依赖性抗体介导的“免疫复合物”型血管内溶血。

'Immune complex' mediated intravascular hemolysis due to IgM cephalosporin-dependent antibody.

作者信息

Salama A, Göttsche B, Schleiffer T, Mueller-Eckhardt C

机构信息

Institute of Clinical Immunology and Blood Transfusion, Justus Liebig University, Giessen, FRG.

出版信息

Transfusion. 1987 Nov-Dec;27(6):460-3. doi: 10.1046/j.1537-2995.1987.27688071694.x.

DOI:10.1046/j.1537-2995.1987.27688071694.x
PMID:3500531
Abstract

Immune hemolytic anemia (IHA) related to cephalosporins is rare and generally considered to be the result of a drug-adsorption mechanism. In previously reported cases, the hemolysis was usually extravascular and the causative antibodies were IgG, incapable of activating complement, and demonstrable by the direct or indirect antiglobulin test using red cells (RBCs) pretreated in vitro with cephalosporin. The authors report a patient in whom acute intravascular hemolysis developed while she was receiving cefotaxime (a cephalosporin as yet not reported to cause IHA). The patient's RBCs were coated only with complement fragments (C3d), even at the peak of the hemolytic episode. Her serum and eluates repeatedly yielded negative results when tested against normal or cephalosporin-coated RBCs. However, strong hemagglutination and C5b-9-mediated hemolysis were observed if the patient's serum was tested against RBCs in the presence of the drug, its ex vivo antigen and, to a lesser degree, cephalothin and ceftriaxon, but not in the presence of penicillin and other related cephalosporins. The positive reactions were not changed by preincubating the serum with different amounts of the drugs. All of these findings reflect the typical picture of drug-induced IHA by the so-called "immune complex" mechanism and not by the drug-adsorption mechanism. The authors conclude that cephalosporin can cause immune hemolysis in two ways: the drug-adsorption mechanism and, as described here, the "immune complex" mechanism.

摘要

与头孢菌素相关的免疫性溶血性贫血(IHA)较为罕见,通常被认为是药物吸附机制的结果。在先前报道的病例中,溶血通常为血管外溶血,致病抗体为IgG,不能激活补体,可通过使用体外经头孢菌素预处理的红细胞(RBC)进行直接或间接抗球蛋白试验来证实。作者报告了一名患者,她在接受头孢噻肟(一种尚未报道可引起IHA的头孢菌素)治疗时发生了急性血管内溶血。即使在溶血发作高峰期,该患者的红细胞也仅被补体片段(C3d)包被。当用正常或头孢菌素包被的红细胞进行检测时,她的血清和洗脱液反复产生阴性结果。然而,如果在药物、其体外抗原以及程度较轻的头孢噻吩和头孢曲松存在的情况下,用该患者的血清检测红细胞,则会观察到强烈的血凝反应和C5b - 9介导的溶血,但在青霉素和其他相关头孢菌素存在的情况下则不会。血清与不同量的药物预孵育后,阳性反应没有改变。所有这些发现都反映了所谓“免疫复合物”机制而非药物吸附机制导致的药物性IHA的典型表现。作者得出结论,头孢菌素可通过两种方式引起免疫溶血:药物吸附机制以及此处所述的“免疫复合物”机制。

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引用本文的文献

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BMJ Case Rep. 2018 Mar 27;2018:bcr-2017-223209. doi: 10.1136/bcr-2017-223209.
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