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1/15. Transfusion-related acute lung injury associated with interdonor incompatibility for the neutrophil-specific antigen HNA-1a.

    BACKGROUND AND OBJECTIVES: A patient transfused with two pooled platelet concentrates became breathless. Bilateral infiltrates were seen on chest X-ray. A diagnosis of transfusion-related acute lung injury (TRALI) was made. The patient received 100% oxygen and recovered after 5 days. MATERIALS AND methods: Antibody screening, cross-matching for granulocyte and lymphocyte antibodies and typing for granulocyte antigens was undertaken. RESULTS: The patient typed as HNA-1b/HNA-1b. Granulocyte and lymphocyte antibodies were not detected in the patient's serum or in any of the donor sera by cross-match. In antibody screening against typed panel granulocytes, complement-fixing anti-HNA-1a IgM antibodies were detected in the serum of one female donor. Two of the other donors who contributed to the pooled platelet concentrate containing the HNA-1a IgM antibodies typed as HNA-1a/HNA-1b. CONCLUSION: Anti-HNA-1a IgM antibodies may have formed immune complexes with white cell fragments or soluble FcgammaRIII from HNA-1a donors in the pooled platelet concentrate and initiated TRALI.
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2/15. Transfusion-related acute lung injury caused by human leucocyte antigen class II antibody.

    Fcgamma receptor (FcgammaR)-mediated destruction of immunoglobulin-coated red blood cells (RBCs) is the underlying mechanism of haemolytic disease of the newborn. Human leucocyte antigen (HLA) antibodies in vitro are able to block monocyte FcgammaRs and prevent phagocytosis. The intention was to demonstrate this effect in vivo upon a volunteer. plasma containing a non-cytotoxic HLA-DR alloantibody was infused into the subject. The FcgammaR blockade was achieved and persisted for about 2.5 d, but, unexpectedly, a mild transfusion-related acute lung injury (TRALI) was also caused. monocytes disappeared completely from the peripheral blood within the first hour after infusion and a mild pulmonary oedema was observed within 3-4 h. The subject recovered within 2 d.
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3/15. Common features in the onset of ARDS after administration of granulocyte colony-stimulating factor.

    STUDY OBJECTIVE: Respiratory disturbance caused by ARDS has been reported during administration of granulocyte-colony stimulating factor. The clinical features of such respiratory distress were investigated in this study. DESIGN: Retrospective case review. SETTING: A 1,100-bed university teaching hospital. patients: Five patients who had dyspnea caused by ARDS develop after chemotherapy or bone marrow transplantation (BMT) at our hospital. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Levels of cytokines, human leukocyte antigen (HLA) typing, and the clinical course were analyzed to clarify common features. All five patients possessed HLA-B51 or HLA-B52, and all had fever and an enhanced inflammatory response at the time of the WBC nadir. The tumor necrosis factor (TNF)-alpha and interleukin (IL)-8 levels increased when respiratory distress syndrome occurred. CONCLUSIONS: If patients with HLA-B51 or HLA-B52 have infection develop at the time of WBC nadir after chemotherapy or BMT, ARDS may occur in association with elevation of TNF-alpha and IL-8 during WBC recovery.
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4/15. Investigations into the role of anti-HLA class II antibodies in TRALI.

    BACKGROUND: TRALI is thought to be triggered by recipient-specific anti-HLA class I or antibodies against neutrophils in donor plasma. Recently, anti-HLA class II have also been implicated. The prevalence of anti-HLA class II was investigated in normal volunteer platelet donors and in two nonfatal TRALI cases utilizing a flow-based assay. Potential target antigens also were investigated. STUDY DESIGN AND methods: Commercial flow cytometry-based assays (FlowPRA, One Lambda, Inc.) for anti-HLA class I and II were compared with standard lymphocytotoxicity tests. Subsequently, 151 volunteer platelet donors and two clinical cases of TRALI were screened with FlowPRA. Immunohistochemical studies were performed on lung tissue from a surgical case, an autopsy case, and a fatal TRALI case. RESULTS: The FlowPRA assays showed moderate concordance for anti-HLA class I (kappa = 0.448) and good concordance for class II antibodies (kappa = 0.801), when compared to standard lymphocytotoxicity assays. Ten and 9 percent of female platelet donors were positive for anti-HLA class I and class II, respectively. Two nonfatal cases of TRALI showed both anti-HLA class I and anti-HLA class II. Immunohistochemical analysis of a TRALI case revealed granulocyte aggregation in alveolar capillaries with activated vascular endothelial cells. HLA class II antigen expression was not present on vascular endothelium or intravascular WBCs; however, strong expression was seen on alveolar macrophages. CONCLUSION: FlowPRA assays often detect anti-HLA class I not detected by conventional lymphocytotoxicity assays. These assays reveal anti-HLA class II in normal female donor plasma and in sera implicated in TRALI. Immunohistochemical studies failed to reveal endothelial or intravascular-WBC HLA class II antigen expression in lung tissue derived from TRALI cases or controls, but demonstrated HLA class II expression on pulmonary macrophages.
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5/15. Postoperative pulmonary edema, transfusion-related?--a case report.

    Transfusion-related acute lung injury (TRALI) is a severe reaction between leukocyte antigen and antibody during transfusion of plasma-containing components. Recently, biologically active lipids have been also suggested to cause the disorder. It is a rare, but rather benign pulmonary edema. We report a postoperative pulmonary edema, which was temporally and clinically compatible with TRALI. Because the patient received blood products from 3 or 4 donors and the disorder was not recognized right away, the laboratory task for the definite diagnosis was difficult. Nevertheless, the patient had fully recovered in 36 hours after supportive therapies. Without identifying the blood donor implicated in the disorder, transfusion reactions or TRALI will be inevitable.
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6/15. pulmonary edema after transfusion in a patient with end-stage renal disease.

    AIMS: To describe a patient with end-stage renal disease who developed non-cardiogenic pulmonary edema after transfusion of packed red blood cells. DESIGN: Case report and literature review. RESULTS: The patient under consideration is a 60-year-old woman who developed acute pulmonary edema after transfusion of packed red blood cells without concomitant dialysis. The initial diagnosis of fluid overload was managed by isolated ultrafiltration. Minimal fluid removal led to significant hypotension that was resistant to vasopressors. Subsequent pulmonary artery catheter readings were consistent with non-cardiogenic pulmonary edema. The patient improved spontaneously over the next few days with supportive care only. plasma from the donors was checked for granulocyte antibodies and antibodies to HLA class I antigens. No granulocyte antibodies were detected in donor plasma but of one the HLA antibodies detected in donor plasma had specificity for a recipient HLA-A antigen. These characteristics supported a final diagnosis of transfusion-related acute lung injury (TRALI). CONCLUSIONS: Acute pulmonary edema following blood transfusion in a dialysis-dependent patient does not always signify fluid overload and nephrologists should be aware of the alternative diagnosis of TRALI. Proper awareness of TRALI will lead to prompt diagnosis and appropriate management.
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7/15. Transfusion-related acute lung injury or acute chest syndrome of sickle cell disease? - A case report.

    PURPOSE: To describe how to differentiate transfusion-related acute lung injury from acute chest syndrome of sickle cell disease. Clinical features: A neurosurgical patient with sickle cell disease received two units of packed red blood cells postoperatively. Four hours later she developed progressive respiratory distress, diffuse geographical airspace disease and bilateral pulmonary edema. The patient recovered sufficiently to be transferred from the intensive care unit within four days. The temporal relationship to transfusion, features on computerized tomographic scan, and the rapid resolution of severe edema point to a diagnosis of transfusion related acute lung injury. Granulocyte or human leukocyte antigen antibodies in donor plasma may confirm a diagnosis of transfusion injury. CONCLUSION: The clinician should appreciate that erythrocyte transfusion to prevent or treat acute chest syndrome may cause transfusion related acute lung injury, a condition that mimics, exacerbates or possibly triggers the syndrome it was intended to treat.
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8/15. Transfusion-related acute lung injury caused by two donors with anti-human leucocyte antigen class II antibodies: a look-back investigation.

    Transfusion-related acute lung injury (TRALI) is considered as one of the most important complications of blood transfusion. Previous look-back investigations have revealed unrecognized cases. We report two cases of TRALI in brief and the outcomes of transfusion in the recipients of previous components from the implicated donors. This look-back investigation was a retrospective case-note study assessing whether there were any untoward events associated with the previous transfusions. 18 patients were identified as having received a blood component transfusion from one of the two donors with anti-human leucocyte antigen (HLA) antibodies to antigens occurring frequently in the local population. One of the five patients receiving a unit of fresh frozen plasma had an evidence of TRALI, which was not diagnosed at the time. A second patient, who had been HLA typed and who carried a full match of antigens for the antibody specificities of the plasma received, had no evidence of a reaction. There were no documented reactions in 13 recipients of red cells in optimal additive (OA) solution. Cases of TRALI may go unrecognized. Not all patients with antibody/antigen concordance will develop clinical signs. Red cells in OA solution from donors with anti-HLA antibodies appear to have a low risk of causing clinically evident lung damage.
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9/15. Transfusion-related acute lung injury following allogeneic bone marrow transplantation in a patient with acute lymphoblastic leukemia.

    Transfusion-related acute lung injury (TRALI) is a clinical syndrome characterized by bilateral pulmonary edema in association with transfusions. We encountered a 23-year-old woman with acute lymphoblastic leukemia, in whom TRALI without anti-human leukocyte antigen class I and anti-granulocyte antibodies developed following allogeneic bone marrow transplantation. TRALI improved mainly in association with treatment of saline and ventilation support after several days, but graft-versus-host disease and thrombotic microangiopathy developed, resulting in death due to multiple organ failure. This case indicates that TRALI can also occur following allogeneic bone marrow transplantation.
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10/15. Legionella pneumonia associated with adult respiratory distress syndrome caused by legionella pneumophila serogroup 3.

    A 68-year-old man developed pneumonia 2 days after nearly drowning in a bathtub of a hot spring spa. Chest radiography revealed bilateral consolidation shadows associated with adult respiratory distress syndrome. Initial treatment with antibiotics and pulse therapy with methylprednisolone was not effective. The patient died on the 4th hospital day. A urinary antigen test for Legionella was positive. legionella pneumophila serogroup 3 was recovered from an intratracheal specimen. The same serotype of Legionella was isolated from the hot spring water. Restriction enzyme analysis by pulse-field gel electrophoresis revealed identical restriction fragments. We conclude that the water at the hot spring spa could have been the source of infection.
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