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Stabilization of von Willebrand factor in banked blood by leucocyte depletion
A Farrugia1, A Street, S Douglas
1Development Section, Red Cross Blood Bank, South Melbourne, Victoria, Australia.
The von Willebrand factor (vWf) activity, as measured by the ristocetin co-factor (vWf:RCo) and collagen binding (vWf:CBA) assays, declined progressively in standard blood units stored at 4 degrees C after a 2-day storage period. This loss of activity was accompanied by a loss and degradation of high molecular weight (HMW) vWf multimers. In studies using a paired design, filtration of blood with a high efficiency leucocyte-removal filter, prior to storage at 4 degrees C, led to significantly improved maintenance of vWf:RCo and vWf:CBA compared with unfiltered units (P < 0.01 after 8 days). Loss and degradation of HMW vWf decreased when blood was filtered prior to 4 degrees C storage. Filtration had no effect on vWf-associated activities when blood was stored at 22 degrees C for 10 days. These results indicate that part of the storage lesion of vWf in banked blood is due to leucocyte-mediated removal and degradation of HMW vWf. This has implications when specifying plasma for the production of vWF concentrates and may also play a role in the haemostatic lesion associated with massive transfusion of stored blood.
The von Willebrand factor (vWf) activity, as measured by the ristocetin co-factor (vWf:RCo) and collagen binding (vWf:CBA) assays, declined progressively in standard blood units stored at 4 degrees C after a 2-day storage period. This loss of activity was accompanied by a loss and degradation of high molecular weight (HMW) vWf multimers. In studies using a paired design, filtration of blood with a high efficiency leucocyte-removal filter, prior to storage at 4 degrees C, led to significantly improved maintenance of vWf:RCo and vWf:CBA compared with unfiltered units (P < 0.01 after 8 days). Loss and degradation of HMW vWf decreased when blood was filtered prior to 4 degrees C storage. Filtration had no effect on vWf-associated activities when blood was stored at 22 degrees C for 10 days. These results indicate that part of the storage lesion of vWf in banked blood is due to leucocyte-mediated removal and degradation of HMW vWf. This has implications when specifying plasma for the production of vWF concentrates and may also play a role in the haemostatic lesion associated with massive transfusion of stored blood.