Febrile nonhemolytic transfusion reactions to platelets
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abstract
Although febrile nonhemolytic transfusion reactions to erythrocytes and platelets are not life threatening, the clinical symptoms associated with them cause discomfort for the patient, result in the use of premedicative drugs, and utilize nursing and laboratory resources. For many years it was assumed that febrile nonhemolytic transfusion reactions were caused by an interaction between leukocyte antibody in the patient's plasma and leukocytes present in the transfused product. Thus prevention has focused on the removal of leukocytes from the blood product by centrifugation or filtration just prior to transfusion. Recent data suggest that most febrile nonhemolytic transfusion reactions to platelets do not involve an immune-mediated event but are caused by the accumulation of biologic response modifiers in the platelet product during storage. Potential biologic response modifiers that have been investigated include histamine, lipids, complement fragments, and cytokines. The concentrations of these substances have been shown to increase in erythrocytes or platelet products or both during storage, and there is some clinical evidence that supports an association between elevated cytokine levels and the risk of reaction. If biologic response modifiers play a major role in febrile nonhemolytic transfusion reactions to platelets, then interventions to prevent these reactions should focus on ways to stop production of these substances or on mechanisms to remove these substances from the platelet product before transfusion. Possible interventions include prestorage leukoreduction, plasma removal from the platelet product before transfusion, and reduction of the platelet storage period to 3 days. Clinical studies to identify the most effective approach for preventing febrile nonhemolytic transfusion reactions have not yet been reported.
