Transfusion of PCs in PAS-2 significantly reduces the incidence of reactions. The 1-hour and 20-hour CCIs after transfusion of PCs in PAS-2 were significantly lower than the CCIs after transfusion of PCs in plasma. Because storage conditions of both PCs were found to be optimal, the decrease in CCIs after transfusion of PCs prepared in PAS-2 may be caused by rapid elimination of a subpopulation of P-selectin-positive platelets from the circulation.
We studied the value of leukocyte depletion of platelet transfusions for the prevention of secondary human leukocyte antigen (HLA)- alloimmunization in patients with a high-risk of prior immunization induced by pregnancies. Seventy-five female patients with hematologic malignancies (mostly acute leukemia) and a history of pregnancy were randomized to receive either standard random single-donor platelet transfusions (mean leukocytes, 430 x 10(6) per transfusion) or leukocyte-depleted random single-donor platelet transfusions. Leukocyte depletion to less than 5 x 10(6) leukocytes per platelet transfusion (mean leukocytes, 2 x 10(6) per transfusion) was achieved by filtration. Of the 62 evaluable patients, refractoriness to random donor platelets occurred in 41% (14 of 34) of the patients in the standard group and in 29% (8 of 28) of the patients in the filtered group (P = .52); anti-HLA antibodies developed in 43% (9 of 21) of individuals in the standard group and 44% (11 of 25) of cases in the filtered group. The time toward refractoriness and development of anti- HLA antibodies was similar for both groups. We conclude that leukocyte depletion of random single-donor platelet products to less than 5 x 10(6) per transfusion does not reduce the incidence of refractoriness to random donor platelet transfusion because of boostering of anti-HLA antibodies.
A prospective study was carried out to determine whether use of cytomegalovirus (CMV) unscreened red blood cells and platelet concentrates, white blood cell (WBC) depleted with high-efficiency filters, would prevent transfusion-associated (TA) CMV infection in CMV seronegative bone marrow transplant recipients. Blood components were filtered in the bloodcentre under quality control and after filtration residual WBC counts were always below 5 x 10(6) cells/U. Since 1990, 23 consecutive allogeneic and 37 autologous CMV seronegative marrow transplant recipients, have been transfused with filtered blood components and followed for 6 months for evidence of CMV infection by monitoring culture and CMV serology. None of the patients showed clinical symptoms of CMV infection, and CMV cultures during episodes of fever were always negative. IgM anti-CMV antibodies were negative during the study in all patients. Low titres of IgG anti-CMV antibodies (5-12 relative ELISA units) were found in 24/60 patients during the first month after bone marrow transplantation (BMT), probably due to passive transfer of IgG administered with the platelet transfusions. 3 and 6 months after BMT, 56 and 48 patients respectively were still alive; and CMV serology was negative in all patients. The results show that TA-CMV infection is preventable by filtration of blood through high-efficiency filters in patients undergoing autologous and allogeneic BMT.
Previous studies have shown that ultraviolet B (UVB) radiation causes platelet aggregation by exposing fibrinogen binding sites via activation of an intracellular mechanism. In the present study we have further investigated the routes of platelet activation following UVB exposure. Evidence is provided that UVB radiation does not activate the platelets via the classical Phospholipase A2 and Phospholipase C routes. Despite this observation, UVB-induced fibrinogen binding was found to be correlated with a 40% increase in phosphorylated 47 kD protein. Both findings could be completely inhibited in the presence of staurosporine, a potent inhibitor of protein kinase C (PK-C). In efforts to explain the mechanism of PK-C activation by UV radiation we found that both UV-induced PK-C activation and platelet aggregation were significantly reduced in the presence of specific scavengers for reactive oxygen species including superoxide dismutase and catalase. We conclude that exposure of platelets to UVB radiation can activate PK-C via oxygen radicals, resulting in exposure of fibrinogen binding sites and subsequent platelet aggregation.
Five days storage of pooled platelet concentrates (PCs) with high yields often results in a pH fall and poor platelet morphology despite the use of specific containers. In this study we evaluated two techniques for prolonged storage of PCs with high platelet counts, by measuring pH and platelet swirl. In routine procedures, 90 PCs, prepared from five buffy coats, were stored in a single 1-litre PL 732 container. After 5 days storage, 51 PCs with platelet counts below 3.1 x 10(11)/U showed a pH above 6.8 and optimal swirling scores. 29 of 39 PCs (74%) with yields above 3.1 x 10(11)/U showed pH values below 6.8 and poor swirling scores. These poor results can be prevented by shortening the duration of storage. PCs with high yields can be stored for 5 days either by dividing the concentrate into two containers or by adjusting the platelet count to 3.1 x 10(11)/U. In the latter procedure, we reduced the volume of the concentrate and found that of 102 PCs, only 9 showed poor values for pH and platelet swirl. The data clearly indicate the importance of measuring the prestorage platelet count to select the optimal procedure for concentrate storage.
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