THE ASSOCIATION OF BIOLOGICALLY-ACTIVE LIPIDS WITH THE DEVELOPMENT OFTRANSFUSION-RELATED ACUTE LUNG INJURY - A RETROSPECTIVE STUDY

Citation
Cc. Silliman et al., THE ASSOCIATION OF BIOLOGICALLY-ACTIVE LIPIDS WITH THE DEVELOPMENT OFTRANSFUSION-RELATED ACUTE LUNG INJURY - A RETROSPECTIVE STUDY, Transfusion, 37(7), 1997, pp. 719-726
Citations number
25
Categorie Soggetti
Hematology
Journal title
ISSN journal
00411132
Volume
37
Issue
7
Year of publication
1997
Pages
719 - 726
Database
ISI
SICI code
0041-1132(1997)37:7<719:TAOBLW>2.0.ZU;2-6
Abstract
BACKGROUND: Transfusion-related acute lung injury (TRALI) is clinicall y similar to the adult respiratory distress syndrome (ARDS) and has be en linked to the transfusion of leukocyte antibodies in blood componen ts. Animal models have implicated neutrophil (PMN)-priming agents in A RDS; however, two agents were required. Previous studies showed the ge neration of PMN-priming agents during blood storage. Thus, the associa tion of PMN-priming agents with TRALI was examined. STUDY DESIGN AND M ETHODS: Ten patients with TRALI and IO with febrile or urticarial reac tions (control group) were evaluated. The presence of PMN-priming acti vity was tested in the patients' pretransfusion and posttransfusion bl ood samples by incubating PMNs with these samples followed by activati on of the respiratory burst. Plasma lipids were separated by normal-ph ase high-performance liquid chromatography (HPLC), and the priming act ivity was evaluated. The presence of leukocyte antibodies was determin ed in the blood donors and patients with TRALI. RESULTS: Significantly more PMN-priming activity was present in the posttransfusion sera (11 .4 +/- 1.8 nmol superoxide anion/min, mean rt SEM; n = 10) and plasma of patients with TRALI than in their pretransfusion sera (6.5 +/- 1.5; n = 10) or in the pretransfusion and posttransfusion sera (5.1 +/- 1. 3, n = 10; and 4.5 +/- 1.4, n = 10, respectively) and from the control s (p<0.05). HPLC separation of lipids demonstrated that three active s pecies were present in the posttransfusion plasma samples of TRALI pat ients. All the patients with TRALI had underlying clinical factors, su ch as infection, cytokine administration, recent surgery, or massive t ransfusion, while only 2 of 10 control patients had these clinical con ditions. None of the donors had significant titers of HLA or HLA-DR an tibodies; however, 50 percent had weak positivity for granulocyte anti bodies. CONCLUSION: TRALI is the result of two clinical events, the fi rst being a predisposing clinical condition and the second being the t ransfusion of biologically active lipids in stored blood.