Abstract

Abstract : Live platelets have many complex functions other than clot formation. These include the modulation of fibrinolysis, inflammation, vascular tone, and cellular growth through substances released from cytoplasmic granules or direct interaction with endothelial cells, leukocytes, and macrophages. Many of these functions are poorly understood and serve as a reminder of the complexity of the cell that researchers seek to mimic.1 Despite improvements in the production of 22 C liquidstored platelets, conventional PCs have several drawbacks. Recipients continue to be at risk for febrile nonhemolytic transfusion reactions; the transmission of bacterial, viral, and protozoan infections; alloimmunization resulting in refractoriness to future platelet transfusions; and graft-versus-host disease. The potential for transfusion-associated immunosuppression has also been a concern. Shortages in platelet supply occur frequently, and the stockpiling of platelets is not feasible because of the short shelf life of conventional platelet concentrates. The result is often wastage owing to the expiration of platelet products, which is inevitable under current transfusion medicine practices. The decline in the donor pool and increase in platelet use over the past decade compounds the problem. These drawbacks have led to efforts to minimize the exposure of recipients to allogeneic blood products and to develop safe and effective platelet products and substitutes with longer shelf lives.2 Ideally, modified platelet products and substitutes should function hemostatically as live platelets do without causing pathologic thrombosis or a consumptive coagulopathy. A platelet substitute should not transmit infection, nor should it be immunogenic or cause reticuloendothelial blockade. Novel platelet products and platelet substitutes should have a long duration of action to allow long dosing intervals.

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