Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The leading cause of transfusion-related morbidity and mortality in the United States is transfusion-related acute lung injury (TRALI). Diagnostic criteria for TRALI have recently been developed and primarily consist of hypoxia and bilateral pulmonary edema occurring during or within 6 h of a transfusion in the absence of cardiac failure or intravascular volume overload. The primary differential diagnosis is transfusion-associated circulatory overload and differentiation can be difficult. Treatment is supportive with oxygen and mechanical ventilation. Diuresis is not indicated and the role of steroids is unproven. Patients typically recover within a few days. All types of blood products have been associated with TRALI, however, the plasma-rich components, such as fresh frozen plasma and apheresis platelets, have been most frequently implicated. The pathogenesis of TRALI is not completely understood. Leukocyte antibodies in donor plasma have been implicated in most cases with antibodies directed at human leukocyte antigen (HLA) class I, HLA class II or neutrophil-specific antigens, particularly HNA-3a. Activation of pulmonary endothelium is important in the development of TRALI and may account for most cases being observed in surgical or intensive care unit patients. Transfused leukoagglutinating antibodies bind to recipients' neutrophils localized to pulmonary endothelium resulting in activation and release of oxidases and other damaging biologic response modifiers that cause capillary leak. In a minority of TRALI cases, no antibodies are identified and it is postulated that neutrophil priming factors in the transfused component can mediate TRALI in a patient with pulmonary endothelial activation, the so called "two hit" mechanism. Recognition of the role of anti-leukocyte antibodies has led to new strategies to reduce the risk of TRALI. Female blood donors with a previous pregnancy frequently have HLA antibodies with an overall prevalence of 24% and increasing prevalence related to the number of previous pregnancies. Since HLA antibodies have been implicated in TRALI, blood centers have adopted policies to produce plasma components primarily from male donors. Strategies to reduce the risk from apheresis platelets are problematic and are likely to involve testing female apheresis platelet donors for HLA antibodies. Much more research is needed to understand the blood component and patient risk factors for TRALI so that novel strategies for treatment and additional measures to reduce the risk of TRALI can be developed.
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PMID:Transfusion-related acute lung injury: current concepts for the clinician. 1922 81

Transfusion-related acute lung injury (TRALI) is a serious adverse transfusion reaction that is presented as acute hypoxemia and non-cardiogenic pulmonary edema, which develops during or within 6 hr of transfusion. Major pathogenesis of TRALI is known to be related with anti-HLA class I, anti-HLA class II, or anti-HNA in donor's plasma. However, anti-HLA or anti-HNA in recipient against transfused donor's leukocyte antigens also cause TRALI in minor pathogenesis and which comprises about 10% of TRALI. Published reports of TRALI are relatively rare in Korea. In our cases, both patients presented with dyspnea and hypoxemia during transfusion of packed red blood cells and showed findings of bilateral pulmonary infiltrations at chest radiography. Findings of patients' anti-HLA antibodies and recipients' HLA concordance indicate that minor pathogenesis may be not as infrequent as we'd expected before. In addition, second case showed that anti-HLA class II antibodies could be responsible for immunopathogenic mechanisms, alone.
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PMID:Two cases of transfusion-related acute lung injury triggered by HLA and anti-HLA antibody reaction. 2080 91

Transfusion-related acute lung injury (TRALI) is primarily caused by transfusion of fresh frozen plasma or platelet concentrates and occurs by definition within 6 hours after transfusion with acute shortness of breath, hypoxemia and radiographically detectable bilateral infiltrates of the lung. Mostly leucocyte antibodies in the plasma of the blood donor (immunogenic TRALI) are responsible. Apart from antibodies, other substances such as biologically active lipids, mainly arising from the storage of platelet and red blood cell concentrates, can activate neutrophilic granulocytes and trigger a non-immunogenic TRALI. Pathophysiologically, granulocytes in the capillaries of the lung vessels release oxygen radicals and enzymes which damage the endothelial cells and cause pulmonary edema. Therapeutically, nasal oxygen administration may be sufficient. In severe cases, mechanical ventilation, invasive hemodynamic monitoring and fluid intake are required. Diuretics should be avoided. The administration of glucocorticoids is controversial. Antibody-related TRALI reactions occurred mainly after transfusion of fresh frozen plasma, which had been obtained from womenimmunized during pregnancy against leukocyte antigens. Therefore, in Germany, since 2009 only plasma from female donors without a history of prior or current pregnancy or negative testing for antibodies against HLA I, II or HNA has been used with the result that since then no TRALI-related death has been registered.
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PMID:[Transfusion-related acute lung injury (TRALI)]. 2504 84