Abstract
Febrile, nonhemolytic reactions have been a clinical problem since the beginning of transfusion therapy. In the 1960s, antileukocyte antibodies were identified as a cause of these reactions, an observation that led to the discovery of the HLA antigens. The importance of antileukocyte antibodies has been shown by the Italian transfusion program for children with thalassemia, in which the use of leukocyte-depleted red cells virtually abolished febrile, nonhemolytic reactions1. However, febrile transfusion reactions to red cells are not always due to antileukocyte antibodies. Therefore, it is still reasonable to allow two or three reactions to occur before a costly regimen . . .