Platelet Febrile Reactions
Read this first. For many years, the mechanism described in the Red Cell FNH section was all we knew about Febrile Reactions.
Soon, however, people started noticing that FNHs occurred much more often in platelet transfusions than they did during red cell transfusions (somewhere between 20 to 30% of the time in platelet transfusion, vs. only about 1% with red cells). From a physiologic perspective, this didn't really make sense, since red cells, in general, contain more white blood cells than platelets! People began to realize that something else must be at work in platelet transfusions, and research began to focus on substances which were present in platelets prior to transfusion which would directly induce fever on transfusion. These substances have come to be known as "Biological Response Modifiers" or BRMs.
Most of the exhaustive research that has been done on BRMs point toward a group of cytokines that accumulate in platelets during storage. Interleukin 1-beta (IL-1b), Interleukin 6 (IL-6), and Tumor Necrosis Factor (TNF) should sound familiar to you, since we discussed them as the "pyrogenic cytokines" in the section on Red Cell FNH reactions. These cytokines, along with some other substances such as complement components and so-called "neutrophil priming factors", increase day-by-day in bags of platelets as they are stored, in direct proportion to the number of white blood cells present in each bag. So, to beat a dead point, the more white cells present in a bag of platelets, the more pyrogenic cytokines will accumulate.
Transfusion of components that contain high levels of these cytokines has been shown to result in a higher number of febrile reactions. A very elegant study published in 1994 in the New England Journal of Medicine (NEJM 1994;331,10:625-8) showed clearly that the culprit in most febrile reactions from platelets is contained in the plasma and not in the cellular parts of the platelet component.
So, the most important thing to remember about platelet-type febrile reactions is this: Everything a unit of platelets needs to cause a fever is already present in the bag at the time of transfusion! No immune interaction between antigens on donor white cells and recipient antibodies is necessary. This has obvious consequences in terms of how we will try to prevent platelet-type febrile reactions, which we will discuss in a moment. Next, though, let's briefly hit on the treatment of a febrile reaction.
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