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Prepublished online as a Blood First Edition Paper on September 5, 2002; DOI 10.1182/blood-2002-03-0958.

Submitted March 27, 2002
Accepted August 23, 2002
Transfusion-related acute lung injury: epidemiology and a prospective analysis of etiologic factors
Christopher C Silliman, Lynn K Boshkov*, Zahra Mehdizadehkashi, David J Elzi, William O Dickey, Linda Podlosky, Gwen Clarke, and Daniel R Ambruso
Department of Research, Bonfils Blood Center, Denver, CO, USA; Department of Pediatrics, University of Colorado School of Medicine, Denver, CO, USA; Department of Surgery, University of Colorado School of Medicine, Denver, CO, USA
Department of Pathology, Oregon Health Sciences University, Portland, OR, USA
The American Red Cross, Portland, OR, USA
Department of Research, Bonfils Blood Center, Denver, CO, USA
Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB, Canada
Department of Research, Bonfils Blood Center, Denver, CO, USA; Department of Pediatrics, University of Colorado School of Medicine, Denver, CO, USA
* Corresponding author; email: boshkovl{at}ohsu.edu.
Transfusion-related acute lung injury (TRALI) is a life threatening complication of hemotherapy. We report a series of 90 TRALI reactions in 81 patients secondary to transfusion with whole blood platelets (72), apheresis platelets (2), packed red cells (15) and plasma (1). The overall prevalence was 1/1,120 cellular components. To examine the epidemiology of TRALI we completed a nested case control study of the first 46 patients with TRALI compared to 225 transfused controls. We then completed a prospective analysis possible biologic response modifiers responsible for 51 of the TRALI cases, including HLA Class I, Class II, and granulocyte antibodies in donors, and neutrophil (PMN) priming activity in the plasma of the implicated units and recipients. Two groups were at risk: patients with hematologic malignancies (p<0.0004) and patients with cardiac disease (p<0.0006), and TRALI was associated with older platelets (p=0.014). In the prospective study, anti-leukocyte antibodies were found in only 3.6% of cases. The implicated blood components had greater PMN priming activity than controls (p<0.05), and as compared to pre-transfusion, TRALI patients' plasma demonstrated increases in both IL-6 and lipid priming activity, consisting of neutral lipids and lysophosphatidylcholines (p<0.05). We conclude that TRALI may be more frequent than previously recognized, and patient susceptibility, product age, and increased levels of bioactive lipids in components may predispose patients to TRALI. TRALI, like the acute respiratory distress syndrome may be a two-event phenomenon with both recipient predisposition and factors in the stored units playing major roles.

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