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Platelet transfusion without regard for AB0 compatibility is controversially discussed. Therefore, we studied the success of 136 AB0 compatible and 52 incompatible platelet applications in 37 patients. Our results suggest, that AB0 matching can improve the response of platelet transfusion.
Platelets play a pivotal role in hemostasis by forming the initial hemostatic plug and augmenting the formation of the more permanent fibrin thrombus. Thrombocytopenia may lead to bleeding, which can be treated with therapeutic platelet transfusions or prevented with prophylactic transfusions. While many advances have been made in platelet transfusion technology, problems remain. These include the short storage life of liquid-stored platelets and the frequent development of alloantibodies (the refractory state) in patients receiving a number of transfusions. Significant progress, however, is being made in both areas.
In thirty patients with acute leukemia and severe aplastic anemia receiving random single donor platelet transfusions, the development of refractoriness by consecutive platelet transfusions with cytapheresis and its relationship to the appearance of anti-platelet antibodies were investigated. The median number of platelet transfusions inducing refractoriness was 13 times, and 20% of the patients remained unrefractory despite of the repeated multiple platelet transfusions up to 20 to 25 times. The results of anti-platelet antibody tasts by the enzyme-linked immunosorbent assay(ELISA) and immunofluorescent techniques(IFT) showed no statistically significant relationship with the refractoriness (p greater than 0.1). Although there was significant correlation between the results of ELISA and IFT, both tests were insufficient to find out refractoriness even with the use of pooled platelets from multiple donors as target cells. This study shows that 13 single donor platelet transfusions result in refractoriness, that both ELISA and IFT are insufficient to detect refractoriness despite of their significant correlation, and that other methods than these are needed in order to detect alloimmunization.
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Thirty thrombocytopaenic patients of acute leukaemias and myelodysplastic syndrome were transfused platelets collected from ABO-matched donors using Haemonetics V30 and V50 blood processors. Twenty-seven patients had septicaemia and/or splenomegaly; 2 patients had disseminated intravascular coagulation (DIC). Pre-transfusion platelet count was 11.0 +/- 4.0 X 10(9)/L. The mean corrected count increments (CCI) 1 hour and 18 hours post-transfusion were 13.02 X 10(9)/L and 3.88 X 10(9)/L respectively, in the absence of DIC. Active bleeding stopped when platelet count was above 15.0 X 10(9)/L. There was no difference between the platelet yield from two blood processors.
The relationship between the 1 and 20 h post-transfusion platelet count and three parameters used to define refractory transfusions, namely the corrected increment (CI), platelet increment (PI), and percentage platelet recovery (%REC), was studied in 437 non-HLA matched platelet transfusions given to 102 patients with bone marrow failure. The percentage agreement between common definitions of refractoriness was calculated based on these parameters. As the maintenance of platelet counts above 20 x 10(9)/l is a relevant clinical goal for platelet support, the values of the CI, PI and %REC, which best corresponded to 1- and 20-h post-transfusion counts of 20 x 10(9)/l, were identified. A 1-h post-transfusion CI < 3 (PI < 7 x 10(9)/l or % REC < 8%) corresponded to clinically unsuccessful transfusions with a 1-h platelet count < 20 x 10(9)/l. A 1-h CI > or = 5.5 (PI > or = 12 x 10(9)/l or %REC > or = 14%) corresponded to clinically successful transfusions with a 20-h post-transfusion count of > or = 20 x 10/l. These data tie together the end points reported in the literature for defining refractory transfusions.
To better define the role of T-cells in alloimmunization, we induced purine nucleoside phosphorylase (PNP) deficiency in a dog platelet transfusion model. Short-term administration of eight different drug schedules using several combinations of the PNP inhibitor 8-aminoguanosine and/or deoxyguanosine did not induce significant toxicity in four treated animals as demonstrated by blood chemistries, cell counts, and autologous platelet recovery and survival measurements. However, continuous long-term daily administration of these agents produced significant renal and/or hepatic toxicity leading to death in five of six animals. Modification of the drug schedule to early short-term administration of both deoxyguanosine and 8-aminoguanosine, followed by long-term intermittent doses of only 8-aminoguanosine, was not only well tolerated by all the animals but also resulted in significant immunosuppression. Overall, six of nine evaluable dogs (67%) treated with some combination of PNP inhibitors did not become refractory to eight weekly transfusions of platelets from a single random donor dog, P less than 0.005, compared to untreated controls, only 3/21 (14%) not immunized. Furthermore, in four evaluable recipients, discontinuation of the 8-aminoguanosine while continuing platelet transfusions from their original donors did not result in refractoriness. In addition, these four recipients were also unable to recognize platelets from two other random donors. This suggests that both specific and non-specific tolerance to foreign platelet antigens had been induced by PNP-inhibitor therapy. Other evidence for the efficacy of this immunosuppressive treatment was the almost normal post-transfusion recovery and survival of donor platelets, both during and after treatment. This suggests failure to form even low levels of platelet alloantibodies in the immunosuppressed recipients. In contrast, B-cell immunity to soluble antigens was intact as demonstrated by a normal antibody response to keyhole limpet haemocyanin (KLH) antigen.
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Platelet transfusions are of unquestionably proven benefit for the correction of thrombocytopenia or functional platelet disorders, and they have allowed for more intensive antineoplastic therapy. With the advent of blood component therapy most modern blood banks now have the capabilities for supplying at least limited quantities of platelets. Refinements in procurement methods will inevitably lead to a greater supply of platelets and the establishment of larger transfusion programs. These programs will need to incorporate facilities for platelet storage, recruitment of suitable donors, selection of special donors for refractory patients, and methods for quality control. As antineoplastic therapy becomes more aggressive, such transfusion programs will become an integral part of the operation of cancer treatment centers.
Current platelet crossmatch testing still results in a significant percentage of false positive or false negative results in oncological patients during platelet support. A 51Cr platelet lysis assay was used for the detection of platelet alloantibodies. We determined the predictive value of this assay as crossmatch procedure on 28 occasions in 14 patients who received random single donor platelet transfusions. To deal with the problem of spontaneous lysis we included a panel of 10 control sera from normal individuals and applied several methods of statistical analysis to these data. It appeared that the use of only one control serum was sufficient when the percentage relative counts was used as the criterion variable, which is of advantage in the practical application of the test. The test values were retrospectively compared with the clinical transfusion response, determined as the 1 h post-transfusion platelet recovery. The 51Cr platelet lysis crossmatch showed false negative results in 1/21 cases and false positive results in 1/7 cases. These data indicate that the 51Cr platelet lysis assay adds a useful dimension to the solution of the problem of selecting compatible platelet donors. Spontaneous lysis of target platelets appeared not to be a problem in the interpretation of test results.
Long term platelet transfusion support often results in alloimmunization of the recipients and refractoriness to further platelet transfusions. Crossmatch tests between the recipients' serum and the donor platelets offer a potential solution to this problem. In the present study, 207 donor-recipient pairs were studied in 65 patients. We compared four assays (LCT, PAIFT, ELISA and MAIPA) in their ability to predict the response in patients receiving multiple platelet transfusions. All four techniques showed a similar predictability of transfusion outcome (79-80%). Of the four assays, the LCT had the highest specificity (100%) and the PAIFT had the highest sensitivity (70%). In comparison to the three other techniques, the MAIPA assay, a glycoproteinspecific immunoassay, offers the possibility to distinguish between HLA-specific (cytotoxic and noncytotoxic) and platelet-specific antibodies in the same serum specimens. Our results demonstrate that HLA antibodies are the major cause of platelet transfusion refractoriness. Platelet specific (i.e. anti-Zwb) and ABO antibodies are involved in approximately 10%.
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The role of component transfusion has become important in cancer chemotherapy. Recently, it has become possible to obtain large amounts of platelets and granulocytes by the mechanical development of continuous flow centrifugation or filtration leukopheresis. These methods have enhanced the clinical efficiency of platelet transfusion. Although, several reports of randomized controlled studies of granulocyte transfusion have been published, its effectiveness has not yet been clearly established.
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The response to platelet transfusions was studies in two patients with Glanzmann's thrombasthenia. Antibodies to platelets were detected in one patient who had failed to respond to platelet transfusions, and bled during and after surgery despite fresh whole blood transfusions. The other patient had no detectable antiplatelet antibodies, exhibited improved platelet function when normal platelets were added to her platelet-rich plasma and experienced a favorable response to platelet transfusions during major surgery. These cases demonstrate the importance of antiplatelet antibodies as a determinant of a patient's response to platelet transfusion, the value of this therapy in qualitative platelet disorders, and the potential usefulness of in vitro studies to predict the outcome of platelet transfusions in such patients.
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Platelet count, mean platelet volume (MPV), and plateletcrit (PCT) were studied in 51 patients after cardiopulmonary bypass (CPB). MPV was significantly lower in 10 patients who developed postoperative bleeding (bleeders) compared to 41 with no significant bleeding (nonbleeders) (7.7 +/- 0.86 vs 8.5 +/- 1.2 fl, p less than .05). Postoperative platelet count was significantly lower in the group of bleeders (93.3 +/- 22.4 vs 127.5 +/- 43 X 10(9)/liters, p less than .02). A cutoff point of MPV or platelet count that would include bleeders and exclude nonbleeders could not be found due to the large overlap between the two groups. However, such a cutoff point does exist for PCT (PCT = total platelet mass). PCT was significantly lower among the bleeders (0.072 +/- 0.02% vs 0.108 +/- 0.036%, p less than .05) and a cutoff point of PCT less than 0.1% included all the bleeders and excluded 65% of nonbleeders. The low PCT and bleeding tendency can be corrected by platelets transfusion. In 15 patients (eight bleeders and seven nonbleeders) with low postoperative PCT (0.078 +/- 0.014), transfusion of 10 platelet units increased platelet count from 101 +/- 32 to 169 +/- 22 X 10(9)/liter, increased PCT to 0.128 +/- 0.2%, and stopped bleeding in all bleeders. A finding of PCT less than 0.1% after CPB is a clear indication for platelet transfusion in patients who develop post-CPB bleeding. This supports the observation that large platelets are more active than smaller ones, and that PCT, rather than PLT counts, predicts the risk of bleeding in patients with thrombocytopenia.