Acute lung injury (ALI) is an infrequently recognized complication of transfusion therapy. Although the role of passive transfer of leukoagglutinating antibodies has been acknowledged, there is little documentation of the relationship of these antibodies in transfused blood to the human leukocyte antigen (HLA) phenotype of the recipient. Recently, we observed 5 cases of transfusion-related ALI, and in all cases leukoagglutinating and lymphocytotoxic antibodies were found in serums of the transfused blood products. In 3 cases, the antibodies corresponded to the HLA antigens of the recipient. Multiparous blood donors whose plasma contains these antibodies represent a potential transfusion hazard. It is recommended that blood component usage from donors implicated in these reactions be restricted to frozen or washed red blood cells. The incidence of leukoagglutinin-associated ALI may be more frequent than previously appreciated. Current concepts of the mechanism of microvascular pulmonary injury are discussed in relation to these cases.

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The recent publication of Seeger et all regarding an ex vivo lung model for transfusion-related acute lung injury (TRALI) provides important information for understanding the mechanism of this life-threatening, but often under-diagnosed complication of transfusion. First, the time course of the physiologic changes (ie, microvascular alterations) strongly parallels the onset of hypoxemia, cyanosis, and acute pulmonary edema seen in published reports.* Second, the physiologic changes seen in the investigators" model did not occur when anti-5b was administered but the granulocytes were negative for the 5b epitope. In most cases of TRALI noted to date, it is HLA, rather than neutrophil-specific antibodies, that are identified in donor plasma of implicated blood components. We have recently demonstrated the relationship of the specificity of the donor's HLA antibody and the corresponding epitope in patients in about 60% of cases of TRALI. Seeger et al's' data suggest that both the donor antibody and the corresponding epitope must be present for the microvascular physiologic alterations to occur. Clearly, more data are needed to explain these cases in which this relationship does not exist. However, it should be noted that in most of the published reports, neutrophil-specific antibodies were not assayed. MARK A. POPOVSKY American Red Cross Services-Northeast Region Harvard Medical School Dedham, M A