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PubMed1986

The value of a 51Cr platelet lysis assay as crossmatch test in patients with leukaemia on platelet transfusion therapy.

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.

Acute Disease↗
PubMed1995

Clinical perspectives of platelet transfusions: defining the optimal dose.

To halt bleeding in patients with severe thrombocytopenia due to bone marrow failure, it is desirable to achieve a post-transfusion blood platelet count of 40 x 10(9)/L by platelet transfusions. Based on calculations of corrected count increments, each 1 x 10(11) platelets transfused will increase the blood platelet count approximately 10 x 10(9)/L per each square meter of patient body surface area. Thus, the post-transfusion blood platelet count will be approximately 20 x 10(9)/L following transfusion of 3 x 10(11) platelets to a 5 foot, 8 inch patient weighing 170 pounds (2.0 m2), who is bleeding because of a pre-transfusion platelet count of 5 x 10(9)/L. The post-transfusion platelet count likely will be even lower in sick patients (sepsis, amphotericin B plus antibiotic therapy, splenomegaly, graft-vs.-host disease, etc.) or if platelets are lost from the unit by leukofiltration before transfusion. Although a dose of 3 x 10(11) platelets is acceptable, in a regulatory sense for product quality, it is inadequate to control bleeding in most thrombocytopenic adult patients. Adjusting dose for body size, bleeding patients with pre-transfusion blood platelet of < 10 x 10(9)/L and weighing > 120 pounds should receive approximately 6 x 10(11) platelets, those weighing 30 to 120 pounds should receive 3 x 10(11) platelets, and infants weighing < 30 pounds (15 kg) should receive 5-10 ml/kg of platelet concentrate.

Bone Marrow Diseases↗
PubMed2002

Serial aggressive platelet transfusion for fetal alloimmune thrombocytopenia: platelet dynamics and perinatal outcome.

OBJECTIVES: Our purpose was to describe the fetal loss rate and platelet dynamics in fetal alloimmune thrombocytopenia managed by serial platelet transfusions. METHODS: Retrospective analysis over 10 years of consecutive pregnancies affected by fetal alloimmune thrombocytopenia requiring in utero platelet transfusions. RESULTS: There were 2 perinatal losses in 12 pregnancies managed by 84 platelet transfusions. One was obviously procedure related from exsanguination despite platelet transfusion. The attributable procedure related fetal loss rate was 1.2% per procedure but 8.3% per pregnancy. The median rate of fall in fetal platelet count per day after transfusion was lower at the placental cord insertion (n = 54) 40.5 x 10(9)/L (range, 5.4-96.1 x 10(9)/L) compared with that at the intrahepatic vein (n = 30) 50.9 x 10(9)/L,(range, 29.5-91 x 10(9)/L) (P = .0009). CONCLUSION: Pooling our results with those previously published yields a cumulative risk of serial weekly transfusions of approximately 6% per pregnancy, indicating the need for development of less invasive approaches.

Blood Specimen Collection↗
PubMed1990

[Comparison of 4 crossmatching methods for predicting the success of platelet transfusion].

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%.

Adolescent↗
PubMed2000

Clinical and laboratory factors that affect the post-transfusion platelet increment.

Transfusion of platelet concentrates (PC) reduced the incidence of fatal hemorrhages in several thrombocytopenic conditions. Unfortunately, long-term platelet supportive care may be complicated by the development of a state of refractoriness, resulting in inadequate recovery of functional platelets. PC handling, clinical conditions of the patients and alloimmunization are the main factors affecting refractoriness. We evaluated the post-transfusion platelet increase in 25 patients (M=6, F=19) with hypomegakaryocytic thrombocytopenia receiving random ABO-compatible PC within 24 h after collection. Quality of PC was assessed by platelet count, pH measuring, LDH release, glycocalicin levels, CD-62 and CD-42b expression. Besides history, clinical status and therapy, we searched for the presence of anti-HLA class 1 and anti-HPA 1-4-5 antibodies. Only six patients (24%) were refractory to PC transfusion, as assessed by a corrected count increment (CCI)<5000. Four of such six patients (67%) had anti-HLA antibodies, as compared to zero of 19 responders (P<0.02). No other investigated clinical or laboratory feature was significantly different in refractory and responsive patients. Although post-transfusion bleeding time was shorter in responders than in refractory patients (297.33+/-249.95 versus 673.33+/-409.96; P<0.02), it did not significantly change even in patients with adequate correct count increment. Our data confirm the importance of anti-HLA antibodies in determining adequate post-transfusion recovery or refractoriness.

Adult↗
PubMed1997

[Platelet transfusion refractoriness and effective management of platelet alloimmunization].

Platelet transfusion recipients become alloimmunized to foreign HLA and HPA antigens, impairing their responses to further platelet transfusions (platelet transfusion refractoriness; PTR). Anti-HLA and HPA antibodies account for the majority of clinically significant alloimmunizations. Poor transfusion responses due to alloimmunization may be overcome by selection of HLA or HPA-compatible donors. Several approaches including use of white cell-depleted products have been shown to prevent or delay alloimmunization in transfusion recipients. This paper focused on: 1) factors involved in the development of platelet alloimmunization, 2) diagnosis of PTR and platelet alloimmunization, 3) effective management of the alloimmunization.

Blood Platelets↗
PubMed1998

The rational use of platelet transfusions in children.

Platelet transfusions are undoubtedly effective in securing hemostasis in bleeding children with absent or nonfunctioning platelets. They are, however, abused in some circumstances and are not without risk. The use of platelet transfusions to prevent rather than to treat bleeding in children with malignant disease has increased several times over the last two decades. When joining in this widespread practice, physicians should be aware that there is a relatively unimpressive evidence base supporting it and also that for patients with uncomplicated myelo-suppression the most persuasive studies suggest that a threshold platelet count of 10 x 10(9)/L is no less effective than the more customary 20 x 10(9)/L is. Still lower thresholds await evaluation. For children with nonmalignant conditions the use of platelet transfusions should be carefully evaluated on a case-by-case basis, but they should normally be avoided in the absence of clinically important bleeding. Neonates with thrombocytopenia, particularly those with immune disease due to a maternal alloantibody, are considered an exception to this generalization. The serious hazards of platelet transfusions include alloimmunization and the induction of refractoriness, graft-versus-host (GVH) disease, and the transmission of infection, all of which can be life threatening. Less risky alternative therapeutic approaches may become more widely available in the future, including recombinant thrombopoietin and lyophilized heat-treated platelet membrane preparations.

Child↗
PubMed1986

[Component transfusion in cancer chemotherapy--platelet transfusion and granulocyte transfusion].

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.

Adult↗
PubMed2003

Strategies for managing refractoriness to platelet transfusions.

The availability of platelet transfusions made possible intensive, myelosuppressive therapy. Chronic transfusion support is often complicated by refractoriness to platelet transfusions characterized by inadequate post-transfusion platelet count increments. Refractoriness is most commonly associated with a variety of clinical factors. Aggressive treatment of these clinical conditions often corrects the response to platelet transfusions. Fewer patients develop immune-mediated platelet destruction associated with alloantibodies to class I human leukocyte antigens (HLAs) and occasionally to platelet-specific antigens. The majority of these patients are successfully supported with HLA-matched or cross-match compatible single-donor platelet concentrates.

Antigens, Human Platelet↗
PubMed1995

Platelet transfusion and alternatives to transfusion in patients with malignancy.

Platelet transfusions have long had an important role in the treatment of patients with thrombocytopenia due to disease or myelotoxic treatment or in patients with reduced platelet function. However, platelet transfusions are associated with numerous risks, both immunologic (e.g., transfusion reactions, alloimmunization, immunosuppression) and infectious (e.g., viral, bacterial). In addition, several laboratory and clinical factors can influence post-transfusion platelet recovery. Recent technological advances have introduced the potential for using alternatives to platelet transfusions, such as cytokines or platelet substitutes, which may avoid the risks of transfusion. Platelet development from megakaryocytes is a process that is highly regulated by cytokines and animal research suggests that selected cytokines involved in this process may be useful in the treatment of thrombocytopenia. Newer developments, including the utilization of recombinant cytokines with relatively selective stimulation of platelet production (e.g., interleukin 6 [IL-6]) and the recent discovery of a megakaryocyte colony stimulating factor (thrombopoietin), represent major therapeutic opportunities in the treatment of thrombocytopenia. Platelet substitutes, e.g., thromboerythrocytes, also show promise in the management of platelet deficiencies.

Blood Transfusion↗
PubMed1996

Platelet transfusion therapy.

Although platelet transfusion is a vital part of modern hemotherapy, many related issues are unresolved. The most appropriate trigger point of transfusion and the clinical utility of prophylactic transfusion are still debated, but the importance of patient-specific transfusion decisions is clear. Leukocyte reduction and single donor platelets may have important roles in avoiding complications, but more data are needed. Establishment of a standardized protocol for managing patients receiving ongoing platelet transfusions may facilitate application of special techniques and the use of specially chosen units that provide better platelet support for thrombocytopenic patients.

Blood Component Removal↗
PubMedDate not supplied

Glanzmann's thrombasthenia; assessment of the response to platelet transfusions.

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.

Adenosine Diphosphate↗
PubMed1981

Alloimmunization against the MHC antigens after platelet transfusions is due to contaminating leukocytes in the platelet suspension.

Repeated platelet transfusion to thrombocytopenic patients frequently induce anti HLA antibodies, which are responsible for transfusion refractoriness. As the transfused platelet suspensions usually contain 15-30% of the leukocytes originally present in the blood, it is not known whether these antibodies are raised by the platelets or by the contaminating leukocytes in the platelet suspensions. In the mouse, pure platelet suspensions are not able to induce a primary antibody response, as measured by the NIH test and the indirect immunofluorescence test on platelets and leukocytes, despite repeated injections. However, when the platelet suspensions are contaminated with leukocytes (10(3) or more/injection) an antibody response is induced. This response is higher than the response indiced by an equal amount of leukocytes alone. As in man the use of leukocyte poor platelets postpones the development of refractoriness to random platelets it is concluded that transfusions with leukocyte free platelets will probably prevent immunization against the HLA antigens.

Animals↗