title: Transfusion-related acute lung injury: epidemiology and a prospective analysis of etiologic factors.
abstract: 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.
authors.affiliation: Bonfils Blood Center and the Department of Pediatrics, University of Colorado School of Medicine, Denver, USA.
authors.forename: Christopher C
authors.initials: CC
authors.lastname: Silliman
authors.forename: Lynn K
authors.initials: LK
authors.lastname: Boshkov
authors.forename: Zahra
authors.initials: Z
authors.lastname: Mehdizadehkashi
authors.forename: David J
authors.initials: DJ
authors.lastname: Elzi
authors.forename: William O
authors.initials: WO
authors.lastname: Dickey
authors.forename: Linda
authors.initials: L
authors.lastname: Podlosky
authors.forename: Gwen
authors.initials: G
authors.lastname: Clarke
authors.forename: Daniel R
authors.initials: DR
authors.lastname: Ambruso
mesh_terms: D017677:Age Distribution; D016022:Case-Control Studies; D006098:Granulocytes; D006680:HLA Antigens / Q000276:immunology; D006801:Humans; D007155:Immunologic Factors / Q000097:blood; D007518:Isoantibodies / Q000097:blood; D007519:Isoantigens / Q000276:immunology; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects; D011446:Prospective Studies; D012128:Respiratory Distress Syndrome / Q000453:epidemiology / Q000209:etiology*; D018570:Risk Assessment; D065227:Transfusion Reaction
chemical_list: D006680:HLA Antigens; D007155:Immunologic Factors; D007518:Isoantibodies; D007519:Isoantigens; D009240:N-Formylmethionine Leucyl-Phenylalanine