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BACKGROUND: Coated platelets (PLTs), a subpopulation of PLTs observed upon dual agonist stimulation with collagen and thrombin, are known to retain several procoagulant a-granule proteins on their surface. By formation of a highly active membrane-bound prothrombinase complex, these PLTs represent an important step in the coagulation cascade as a consequence of their ability to generate thrombin at the site of vascular injury. Various clinical observations suggest that higher levels of coated PLTs are associated with thrombosis while a deficiency of coated PLTs results in a bleeding diathesis. Current quality control guidelines for in vitro PLT storage measure PLT viability but no routine evaluation of the hemostatic function of stored PLTs and particularly no estimation of coated PLT potential is performed. Our primary objective was to evaluate if the process of apheresis and storage of PLT units alters the levels of coated PLTs. In addition, we sought to determine how transfusion of stored PLTs into patients with thrombocytopenia affects the patient’s coated PLT levels. STUDY DESIGN AND METHODS: Coated PLT levels were analyzed in 13 voluntary PLT donors before donation, in the fresh apheresis product (Trima, CaridianBCT) and in the stored apheresis product just before transfusion. In addition, 10 patients with thrombocytopenia were analyzed for coated PLTs before and after transfusion of a stored PLT product. RESULTS: Coated PLT levels were significantly decreased after the process of apheresis (17% relative decline; p < 0.01) and with prolonged storage (1 to 5 days; 53% relative decline; p < 0.001). Transfusion of stored PLT units did not result in significant increment of coated PLT levels in patients with thrombocytopenia as expected considering the low level of coated PLTs in stored PLT units. Furthermore, there was no suggestion of regeneration of coated PLT potential upon reinfusion. CONCLUSIONS: Isolation and storage of apheresis PLTs by standard blood bank procedures results in a significant decline in coated PLT potential. Reinfusion of stored apheresis PLTs into patients with thrombocytopenia resulted in a predictable change in coated PLT potential with no suggestion of regeneration of lost coated PLT potential. P latelets (PLTs) have two critical roles in promoting hemostasis at the site of vascular injury. The firstisprimaryhemostasisinvolvingplugformation resulting from PLT adhesion to the subendothelial membrane and subsequent PLT aggregation. The other role is to provide a negatively charged membrane surface for formation of an active prothrombinase complex, resulting in thrombin generation for propagation of fluid-phase coagulation, often referred to as secondary hemostasis. Although all PLTs have an inherent capacity to satisfy the aggregation function, it is observed that a subpopulation of PLTs has an enhanced ability to form prothrombinase complexes and may, therefore, play an especially critical role in hemostasis. 1 |
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