Pulmonary infiltrates associated with leukoagglutinin transfusion reactions.
01 Nov 1970-Annals of Internal Medicine (American College of Physicians)-Vol. 73, Iss: 5, pp 689-694
TL;DR: During the past 3 years four patients have been observed with "noncardiac pulmonary edema" that occurred as a complication of blood transfusion, and typical reactions were characterized by the typical reactions.
Abstract: During the past 3 years four patients have been observed with "noncardiac pulmonary edema" that occurred as a complication of blood transfusion. Typical reactions were characterized by the...
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TL;DR: Blood banks need to identify donors whose plasma causes these reactions in order to prevent their recurrence, and HLA‐specific antibodies were identified in donor serums in 65 percent of cases evaluated.
782 citations
TL;DR: Clinicians can diagnose and report TRALI cases to the blood bank and researchers can use this definition to determine incidence, pathophysiology, and strategies to prevent this leading cause of transfusion-associated mortality.
Abstract: Background:Transfusion-related acute lung injury (TRALI) is now the leading cause of transfusion-associated mortality, even though it is probably still underdiagnosed and underreported.National Heart, Lung, and Blood Institute Action:The National Heart, Lung, and Blood Institute convened a working g
668 citations
Cites background from "Pulmonary infiltrates associated wi..."
...Other early reports of patients with what now would be called TRALI were described in a variety of terms: pulmonary hypersensitivity reaction to transfusion (5), pulmonary infiltrates associated with leukoagglutinin in transfusion reactions (6), pulmonary “hypersensitivity” reactions induced by transfusion of non-human leukocyte antigen (HLA) leukoagglutinins (7), pulmonary edema in the course of a blood transfusion without overloading the circulation (8), transfusion reactions with pulmonary infiltration associated with HLA-specific leukocyte antibodies (9), and fulminating noncardiogenic pulmonary edema—a newly recognized hazard during cardiac operations (10)....
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TL;DR: TRALI may be more frequent than previously recognized and that patient susceptibility, product age, and increased levels of bioactive lipids in components may predispose patients to TRALI.
597 citations
TL;DR: A prospective cooperative study of 1629 patients in 24 centers demonstrated that antibodies foretold subsequent failures after a follow‐up period of 6 months (p’= 0.05).
566 citations
Cites background from "Pulmonary infiltrates associated wi..."
...The phenomenon of transfusion-related acute lung injury (TRALI) produced by sera from highly immunized pregnant women was first described in 1970 (9), and reviewed in 1985 (10) and 2001 (11)....
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261 citations
TL;DR: Techniques for removing the buffy coat when blood is prepared for transfusion offer a means of preventing the dangerous reactions that occur when patients, after multiple transfusions, become isoimmunized to donor leukocytes.
Abstract: The hypothesis that some otherwise unexplained febrile reactions to blood transfusions may be caused by isoimmunization of patients against the donors' leukocytes was tested in 10 patients who needed transfusions. Five patients (group A) had previously had from 20 to 85 transfusions, had histories of repeated transfusion reactions, and had demonstrable antibodies against the specific normal leukocytes administered during this study. The other five patients (group B) had had only seven or less previous transfusions, with no histories of transfusion reactions. Group A did not experience adverse effects when the blood used for transfusion was so prepared, by centrifuging, as to remove as much as possible of the buffy layer, but all reacted with fever, typical symptoms, and characteristic laboratory findings to subsequent transfusion of the buffy coat which had been so removed. Group B did not react adversely to either fraction of the donors' blood. Immunologic evidence suggested that it was the leukocytes rather than the platelets in the buffy layer that caused the reactions. Techniques for removing the buffy coat when blood is prepared for transfusion offer a means of preventing the dangerous reactions that occur when patients, after multiple transfusions, become isoimmunized to donor leukocytes.
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TL;DR: It is concluded thatwhite cell antibodies were the primary cause of nonhemolytic febrile transfusion reactions in this series, and that the detection of white cell antibodies and preparation of leukocyte‐poor blood continue to be procedures of practical importance in modern transfusion therapy.
Abstract: Summary
The conditions under which nonhemolytic febrile transfusion reactions developed in eight afebrile patients were investigated. Recipients invariably developed a reaction on transfusion of incompatible white cells if a sufficient quantity of leukocytes was infused. The sensitivity of each patient differed with respect to the number of incompatible white cells which could be tolerated without a reaction. In general, the in vivo reaction to blood from an individual donor could be predicted by the routine leukocyte agglutination test. Mild febrile reactions were inconstantly observed in three patients transfused with presumably compatible leukocytes. Further investigation suggested that the cells inducing reaction were probably incompatible, and that in vivo reactions were a more sensitive index than the in vitro test. Granulocytes, lymphocytes or platelets, separately administered, all induced febrile reactions, provided that the routine leukocyte agglutinin test demonstrated an incompatibility. There was no direct evidence that febrile reactions had occurred in response to plasma infusion. It is concluded that white cell antibodies were the primary cause of nonhemolytic febrile transfusion reactions in this series, and that the detection of white cell antibodies and preparation of leukocyte-poor blood continue to be procedures of practical importance in modern transfusion therapy.
Resume
Les conditions sous lesquelles des reactions febriles transfusionnelles non-hemolytiques se sont developpees chez huit patients afebriles ont ete recherchees. Les receveurs ont developpe invariablement une reaction transfusionnelle a l'egard de leucocytes incompatibles si la quantite de leucocytes infuses etait suffisante. La sensibilite de chaque patient differait selon le nombre de leucocytes incompatibles qui pouvait etre tolere sans provoquer de reaction. En general, les reactions in vivo a l'egard du sang de tel ou tel donneur pouvait etre predite en pratiquant le test d'agglutination leucocytaire de routine. Des reactions febriles moyennes ont ete observees d'une maniere inconstante chez trois patients transfuses vraisemblablement avec des leucocytes compatibles. D'autres investigations laissent suggerer que les cellules ayant provoque la reaction etaient probablement incompatibles et que les reactions observees in vivo etaient un index plus sensible que les reactions obtenues in vitro. Les granulocytes, les lymphocytes ou les plaquettes, administres separement, peuvent tous provoquer des reactions febriles lorsque le test d'agglutination leucocytaire de routine demontrait une incompatibilite. Il n'y a pas eu de demonstration evidente directe que les reactions febriles soient provoquees a la suite d'une infusion de plasma. On conclut que les anticorps anti-leucocytaires sont la cause primaire des reactions transfusionnelles febriles nonhemolytiques dans cette recherche et que la mise en evidence des anticorps anti-leucocytaires et la preparation de sang pauvre en leucocytes constituent un mode de faire d'une importance pratique non negligeable dans la therapeutique transfusionnelle moderne.
Zusammenfassung
Die Bedingungen, unter welchen bei acht afebrilen Patienten nicht-hamolytische febrile Transfusionsreaktionen zustande kamen, wurden genau untersucht. Die Empfanger zeigten ausnahmslos eine Reaktion im Anschlus an die Transfusion von inkompatiblen weisen Blutkorperchen, sofern ihnen solche Zellen in genugender Menge infundiert wurden. Die Sensibilitat hinsichtlich der Menge weiser Zellen, die eben noch reaktionslos ertragen wurden, wechselte von Patient zu Patient. Im allgemeinen gelang es, die in vivo-Reaktion auf Blut eines Einzelspenders an Hand des Leukozytenagglutinationstestes voraus zu sagen. Bei drei Patienten wurden bei Transfusion von augenscheinlich kompatiblen Leukozyten mitunter leichte febrile Reaktionen beobachtet. Bei der weiteren Abklarung zeigte sich, das es sich hochstwahrscheinlich auch in diesen Fallen um inkompatible Leukozyten gehandelt hat. Die in vivo-Reaktionen erwiesen sich als empfindlicher als die in vitro-Tests. Falls der Leukoagglutinintest positiv war, traten nach separater Transfusion von Granulozyten, Lymphozyten und Plattchen Fieberreaktionen auf. Direkte Hinweise, das auch durch Plasma solche Fieberreaktionen erzeugt wurden, konnten nicht beigebracht werden. Nachdem auf Grund dieser Untersuchungsreihe anzunehmen ist, das Leukozytenantikorper die Hauptursache fur nicht-hamolytische Fieberreaktionen darstellen, erweist sich der Nachweis von Leukozytenantikorpern und die Herstellung von leukozytenarmem Blut als bedeutsame Masnahme im modernen Transfusionswesen.
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