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Prepublished online as a Blood First Edition Paper on September 5, 2002; DOI 10.1182/blood-2002-03-0958.
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Blood, 15 January 2003, Vol. 101, No. 2, pp. 454-462
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
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
From the Bonfils Blood Center and the Departments of
Pediatrics and Surgery, University of Colorado School of Medicine,
Denver; the Department of Pathology, Oregon Health Sciences University,
Portland; the American Red Cross, Portland, OR; and the Department of
Laboratory Medicine and Pathology, University of Alberta, Edmonton, AB,
Canada.
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 reactions), apheresis platelets (2), packed red cells (15), and plasma
(1). The overall prevalence was 1 in 1120 cellular components. To
examine the epidemiology of TRALI, we completed a nested case-control
study of the first 46 patients with TRALI compared with 225 controls
who had received transfusions. We then completed a prospective analysis
of possible biologic response modifiers responsible for 51 of the TRALI
cases, including human leukocyte antigen (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 < .0004) and patients with cardiac disease
(P < .0006). TRALI was associated with older platelets
(P = .014). In the prospective study, antileukocyte antibodies were found in only 3.6% of cases. The implicated blood components had greater PMN priming activity than controls
(P < .05), and compared with pretransfusion samples,
TRALI patients' plasma demonstrated increases in both interleukin 6 (IL-6) and lipid (neutral lipids and lysophosphatidylcholines) priming
activity (P < .05). We conclude
that 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. TRALI, like the
acute respiratory distress syndrome, may be a 2-event phenomenon with
both recipient predisposition and factors in the stored units playing
major roles.

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