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PubMed1989

Platelet transfusion therapy in thrombocytopaenia of haematologic malignancies.

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.

Acute Disease↗
PubMed2000

Plasma thrombopoietin concentrations in response to platelet transfusion therapy.

Studies performed in rabbit and mouse models and in a limited number of human subjects, show that transfused platelets bind thrombopoietin (TPO) and decrease its concentration in the circulation. The aim of the present study was to further examine this relationship. The material comprised 12 patients receiving a total of 21 transfusions, as part of the routine clinical treatment. Blood samples were collected from the patients immediately before and 30 min after completion of the platelet transfusion, and the corrected platelet count increment (CCI) was calculated. A commercially available ELISA kit was used to determine plasma TPO concentrations. Statistically significant reductions in median TPO concentration were observed in response to the platelet transfusions. Patients who were refractory to platelet transfusions showed the slightest decrease in TPO concentration. As for the linear regression between change in TPO level and CCI, only borderline significance was observed. Thus, our findings support the concept that platelets can remove TPO from the circulation.

Aged↗
PubMed2004

Streptococcus bovis septic shock due to contaminated transfused platelets.

Although most physicians and the public are primarily concerned about the risk of transmitting human immunodeficiency virus (HIV) or hepatitis virus during a platelet transfusion, bacterial contamination is actually the most common infectious complication. Unlike red blood cells, platelets are stored at room temperature (20-24 degrees C), which raises the risk of bacterial proliferation. The risk of bacterial sepsis is 2.5-fold higher for each unit of transfused platelets compared to each unit of red blood cells. We report an unusual case of Streptococcus bovis septic shock associated with a contaminated platelet transfusion.

Adult↗
PubMed2004

Optimizing platelet transfusion therapy.

Platelet transfusions are widely used. Prophylactic transfusions are employed in severely thrombocytopenic patients without evidence of bleeding, but no randomized trial data prove the safety or efficacy of this approach. Randomized trials have demonstrated the equivalence of transfusion triggers of 10,000 and 20,000/microl for prophylactic transfusions. The former threshold is potentially safer for the patient, conservative of donor resources and leads to lower costs, with perhaps a slightly greater risk of minor hemorrhage. Randomized trials have demonstrated the equivalence of pheresis or whole blood-derived platelet transfusions. The former present a lower risk for infectious agents, and the latter are less expensive and a more efficient use of limited donor resources. Randomized trials prove that leukoreduced and ABO identical platelet transfusions reduce the risks of HLA alloimmunization and platelet transfusion refractoriness (both leukoreduction and ABO matching), transfusion reactions (leukoreduction) and CMV transmission (leukoreduction). Leukoreduction and ABO matching of platelet transfusions also have been associated in preliminary observational studies with reduced morbidity and mortality in surgical patients and reduced infections in patients with leukemia. These results require further investigation. Future challenges include (1) determining the best approach to bacterial contamination of platelets, whether by detection methods or pathogen inactivation and (2) determining the threshold for prophylactic platelet transfusions in thrombocytopenic patients undergoing surgery or invasive procedures.

ABO Blood-Group System↗
PubMed2003

Immunoplatelet counting: potential for reducing the use of platelet transfusions through more accurate platelet counting.

Research is required to determine the optimal approach for prophylactic platelet transfusions in patients with haematological malignant disorders. It has been suggested that thresholds for prophylactic platelet transfusions of platelet counts below 10 x 109/l should be investigated, as these may be equivalent in clinical effectiveness and associated with lower costs and fewer complications. An important concern in such investigation is the accurate estimation of platelet counts below 10 x 109/l. This study aimed to further examine the potential reduction in platelet usage that could be made if a lowered platelet transfusion threshold of 5 x 109/l was used in conjunction with an immunoplatelet counting method. Clinical and laboratory data from 130 haematology patients were used. Standard platelet counting was performed using Bayer H3 and ABX Argos analysers. Immunoplatelet counting was performed by flow cytometry using anti-CD61. The potential for reducing platelet transfusions included consideration of clinical criteria that influence prophylactic platelet transfusion use. The results indicated that the use of an immunoplatelet count with a 5 x 109/l platelet transfusion threshold would potentially reduce the number of transfusions by 10.4% in comparison with a 10 x 109/l threshold and standard automated platelet counting with the ABX Argos analyser, and increase the number of transfusions by 5.4% in comparison with the same threshold using the Bayer H3 analyser. The immunoplatelet count may aid the clinical decision to transfuse platelets, but would not necessarily lead to a reduced use of platelet transfusions.

Flow Cytometry↗
PubMed1999

Prevention and management of platelet transfusion refractoriness.

Platelet transfusion refractoriness is a major complication of long-term platelet supportive care. Refractoriness may lead to fatal bleeding complications in thrombocytopenic patients. Major factors involved are factors related to the clinical condition of the patient as well as HLA alloimmunisation. Non-alloimmune factors may occur in up to 80% of the patients. However, platelet transfusion outcome is impaired in only 50% of the patients having these conditions. HLA alloimmunisation has been convincingly reduced by the use of leucocyte-depleted transfusions. UV-B irradiation of platelet transfusions may be alternatively used to reduce HLA alloimmunisation. Despite these measures, patients with a history of pregnancy or non-leucocyte-depleted transfusions form HLA antibodies in a high proportion (up to 50%). HPA antibodies play a minor but relatively important role in patients with HLA antibodies. ABO antibodies may play a role in refractoriness, which can be abolished by transfusion of ABO-identical platelets. Screening for the presence of HLA and/or HPA antibodies is indicated in case of transfusion failure after ABO-identical or HLA-matched platelets. If no alloantibodies are detected, further analysis to define a role of drug- related or autoantibodies is required. In case of HLA and/or HPA alloimmunisation associated with refractoriness, matched platelet transfusions are indicated. In case of non-alloimmune factors associated with increased platelet consumption, increasing the transfusion frequency can be considered. Additional investigations are still necessary to define risk factors for secondary HLA alloimmunisation and refractoriness due to non-immune factors to further decrease the incidence of refractoriness.

Humans↗
PubMed2000

Effect of premedication guidelines and leukoreduction on the rate of febrile nonhaemolytic platelet transfusion reactions.

Platelet transfusion reactions were prospectively studied in haematology/oncology patients at five university teaching hospitals over three consecutive summers. The initial summer study provided baseline information on the use of premedications and the rate of platelet transfusion reactions (fever, chills, rigors and hives). Most (73%) platelet recipients were premedicated and 30% (95% CI 28-33%) of transfusions were complicated by reactions. The second study followed implementation of guidelines for premedicating platelet transfusions. Despite a marked reduction in premedication (50%), there was little change in the platelet transfusion reaction rate, 26% (95% CI 24-29%), or the type of reactions. The third study followed implementation of prestorage platelet leukoreduction while maintaining the premedication guidelines. The reaction rate decreased to 19% (95% CI 17-22%). For nonleukoreduced platelets, there was a statistically significant association between the platelet age and reaction rate (P = 0.04). For leukoreduced platelets, there was no statistically significant association between platelet age and reaction rate (P = 0.5). Plasma reduction of nonleukoreduced platelet products also reduced the reaction rate. These prospective studies document a high rate of platelet transfusion reactions in haematology/oncology patients and indicate premedication use can be reduced without increasing the reaction rate. Prestorage leukoreduction and/or plasma reduction of platelet products reduces but does not eliminate febrile nonhemolytic platelet transfusion reactions.

Blood Preservation↗
PubMed1992

The definition of refractoriness to platelet transfusions.

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.

Blood Platelets↗
PubMed1990

Inhibition of the enzyme purine nucleoside phosphorylase (PNP) reduces refractoriness to transfused platelets in a dog model.

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.

Animals↗
PubMed1981

Delayed alloimmunisation by random single donor platelet transfusions. A randomised study to compare single donor and multiple donor platelet transfusions in cancer patients with severe thrombocytopenia.

The effects of single-donor (SD) and multiple-donor (MD) platelet transfusions in 34 cancer patients with severe thrombocytopenia and haemorrhages were compared in a randomised study. Platelet recovery values in both groups were similar after the first transfusion. After the second transfusion platelet recovery values were significantly better in those receiving SD transfusions. Platelet recovery values gradually declined with subsequent MD transfusions. These results suggest early alloimmunisation in the MD transfused patients only. MD transfusions were estimated to be no longer effective after about nine transfusions. Platelet recovery values were better indicators of early sensitisation than was the lymphocytotoxicity test. Restriction of the number of donors per transfusion may postpone the development of refractoriness to random-donor platelet transfusions in thrombocytopenic patients.

Blood Donors↗
PubMed1984

Supportive care for children with cancer. Guidelines of the Childrens Cancer Study Group. The use of platelet transfusions.

The indications for platelet transfusions in pediatric oncology remain largely undefined. Results of clinical studies suggest that transfusing platelets prophylactically can reduce the incidence of bleeding during remission induction of acute leukemia, but they have not been shown to decrease deaths due to hemorrhage or to increase the overall survival of patients so treated. The risk of alloimmunization due to frequent platelet transfusions is not great, but it represents a life-threatening complication for some patients. Following a critical analysis of the literature, the author offers guidelines for indications of platelet transfusions, platelet dose, and the means of reducing the risk of alloimmunization. Although only patients with leukemia were included in the studies reviewed in this article, the author believes that the guidelines developed apply to children with other oncologic diagnoses as well.

Acute Disease↗
PubMed2001

Prophylactic platelet transfusions from healthy apheresis platelet donors undergoing treatment with thrombopoietin.

Many patients receiving dose-intensive chemotherapy acquire thrombocytopenia and need platelet transfusions. A study was conducted to determine whether platelets harvested from healthy donors treated with thrombopoietin could provide larger increases in platelet counts and thereby delay time to next platelet transfusion compared to routinely available platelets given to thrombocytopenic patients. Community platelet donors received either 1 or 3 microg/kg pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF) or placebo and then donated platelets 10 to 15 days later. One hundred sixty-six of these platelet concentrates were then transfused to 120 patients with platelets counts 25 x 10(9)/L or lower. Pretransfusion platelet counts (11 x 10(9)/L) were similar for recipients of placebo-derived and PEG-rHuMGDF-derived platelets. Early after transfusion, the median platelet count increment was higher in patients receiving PEG-rHuMGDF-derived platelets: 19 (range, -12-66) x 10(9)/L, 41 (range, 5-133) x 10(9)/L, and 82 (range, -4-188) x 10(9)/L for placebo-, 1-microg/kg-, and 3-micro/kg-derived platelets, respectively. This difference was maintained 18 to 24 hours after transfusion. Transfusion-free intervals were 1.72, 2.64, and 3.80 days for the recipients of the placebo-, 1-microg/kg-, and 3-micro/kg-derived platelets, respectively. The rate of transfusion-related adverse events was not different in recipients of placebo-derived and PEG-rHuMGDF-derived platelets. Therefore, when transfused into patients with thrombocytopenia, platelets collected from healthy donors undergoing thrombopoietin therapy were safe and resulted in significantly greater platelet count increments and longer transfusion-free intervals than platelets obtained from donors treated with placebo.

Adolescent↗
PubMed1996

State of the art in platelet transfusion therapy.

Platelet transfusions are established as effective treatment for thrombocytopenic bleeding, and are commonly used prophylactically to prevent bleeding in thrombocytopenic patients. However, many issues in platelet supportive care remain to be resolved, including the optimal methods for the preparation of platelet concentrates, the best means for the prevention of complications such as platelet refractoriness, transfusion reactions and the transmission of infection, and the precise clinical indications for their use. The demand for platelet concentrates continues to rise, mainly due to the increasing number of patients undergoing myeloablative therapy. This is leading to considerable interest in the coming availability of recombinant thrombopoietin for clinical use.

Humans↗
PubMed2001

Design of clinical trials to evaluate the efficacy of platelet transfusion: the euroSPRITE trial for components treated with Helinx technology.

Methods of collection, preparation, and transfusion of platelet components have evolved markedly since the introduction of modern platelet transfusion therapy three decades ago. Despite these improvements, few randomized, prospective, controlled studies have been conducted to evaluate the effects of these innovations on the outcome of platelet transfusion--prevention and treatment of bleeding due to thrombocytopenia. The majority of studies have used posttransfusion platelet count increments (CIs) as the primary outcome variable rather than bleeding assessments. In general, these studies have only examined average values for platelet CIs or adjusted ratio measures such as corrected count increment (CCI). Because platelet transfusions are given repeatedly over variable periods of time, this type of analysis has not provided information about the effects of multiple platelet transfusions or about specific product or patient-related covariates that may impact the outcome. Longitudinal regression analysis of platelet CIs offers the potential to provide more information than simple average values of ratio measures. The euroSPRITE trial, a European, multicenter, phase III study undertaken to assess the clinical efficacy and safety of platelets prepared with Helinx technology (Cerus Corp, Concord, CA), used longitudinal regression analysis to characterize more fully the response to platelet transfusions with products prepared with this new pathogen inactivation technology. In contrast to previous studies, the euroSPRITE study examined peritransfusion hemostasis and global indices of hemostasis to correlate the effect of platelet CI with prevention and treatment of bleeding during a period of platelet transfusion support.

Blood Platelets↗
PubMed1977

Platelet transfusion therapy.

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.

Blood Cell Count↗
PubMed2001

Platelet transfusion refractoriness associated with HPA-1a (Pl(A1)) alloantibody without coexistent HLA antibodies successfully treated with antigen-negative platelet transfusions.

BACKGROUND: Alloimmune-mediated refractoriness to platelet transfusion is most commonly due to antibody to HLA antigens in multiply transfused or multiparous patients. Published reports of poor transfusion response due to antibodies to platelet-specific antigens are rare and often confounded by the presence of coexistent antibodies against HLA antigens. CASE REPORT: A case is presented of a multiparous woman with acute myelogenous leukemia whose sole cause of transfusion refractoriness was antibody to platelet antigen HPA-1a. She responded dramatically to HPA-1a-negative platelet transfusion. CONCLUSION: This case provides strong serologic and clinical evidence that platelet transfusion refractoriness may result from antibodies to platelet-specific antigens.

Antigens, Human Platelet↗
PubMed2006

Utilization of platelet transfusions in the intensive care unit: indications, transfusion triggers, and platelet count responses.

BACKGROUND: A description of current platelet (PLT) transfusion practice in the intensive care unit (ICU) is needed. STUDY DESIGN AND METHODS: All thrombocytopenic patients (PLT count, <150 x 10(9)/L) who received PLT transfusions were identified from a previous prospective study of consecutive medical-surgical ICU patients; trauma, orthopedic, and cardiac surgery were exclusions. Risk factors for ineffective transfusions were examined. RESULTS: Of 261 ICU patients, 118 (45.2%) had thrombocytopenia and a PLT count nadir of less than 50 x 10(9) per L (n = 22), 50 to 99 x 10(9) per L (n = 37), and 100 to 149 x 10(9) per L (n = 59). Twenty-seven (22.9%) patients received PLT transfusions (n = 76 transfusions) and 37 (31.4%) had major bleeding. PLT dose was approximately 3 to 4 x 10(11) per L transfusion. Therapeutic (n = 24) and prophylactic (n = 52) PLT transfusion triggers were 51 x 10(9) per L (interquartile range [IQR], 26 to 68) and 41 x 10(9) per L (IQR, 20 to 57), respectively, as measured at a median of 4.5 hours (IQR, <1.6 to 6.9) before transfusion. A single PLT transfusion resulted in a median PLT increase of 14 x 10(9) per L (IQR, -2 to 30) measured at 5.2 hours (IQR, 1.8 to 8.8) after the transfusion; however, no PLT count increase was observed after 17 transfusions given to 13 (48.1%) patients. No risk factors for ineffective transfusions were identified. CONCLUSIONS: Among critically ill patients, most PLT transfusions were administered to prevent, rather than to treat, bleeding, with a transfusion trigger of 40 to 50 x 10(9) per L. Nearly half of ICU patients who received transfusions failed to mount a PLT count increase after a single transfusion. Prospective studies are needed to determine the effects of PLT transfusions on bleeding and predictors of ineffective transfusions in the ICU.

Aged↗