Changes in Platelet Function and Platelet Counts During Substitution Therapy in Haemophiliacs and Produced by Plasmapheresis in Patients Suffering from Inhibitors

1979 ◽  
Author(s):  
E. Dumitrescu ◽  
I. Ambrus ◽  
Kh. Nienhaus ◽  
B. Podolsak ◽  
E. Wenzel
Keyword(s):  
Factor Viii ◽  
Platelet Function ◽  
Clinical Signs ◽  
Bleeding Complications ◽  
Substitution Therapy ◽  
Drug Induced ◽  
Platelet Counts ◽  
Before And After ◽  
Factor Viii Concentrates ◽  
Laboratory Investigations

We noticed a systematic increase in small platelets (evaluated by electronical analysis of platelet volune distribution, using the Coulter Counter equipment, Wenzel 1977) during substitution therapy in patients suffering from haemophilia (N = 60). Laboratory investigations on these patients were performed before substitution and then 30 min., 60 min., 120 min. and 24 hours after infusion of factor-VIII-concentrationa (Inmuno, Schwab, Behring, factor-VIII-concentrates 20 U/kg b.w.). The same investigations were performed before and after plasmapheresis using a Hemonetric cell separator (N = 7}. in 48 of the patients, the clinical signs were insignificant (bleeding time, according to Duke, was found to be normall, although the platelet changes ware considerable (decrease in platelet count and increase of the percentage of platelets smaller than 4.5 μ3). However, significant test results were noticed in a haemophiliac patient suffering from inhibitory- and drug-induced platelet disorders during and after plasmapheresis. We observed bleeding complications only in 2 cases (Duke; 7 min. and 9 min.). Yet, a coneiderable decrease in platelet counts was observed as well as a significant increase in the percentages of small platelets (4.5 μ3, N = 48) in all cases. Controlling platelet function in haemophiliacs following substitution therapy could be essential as well as controlling the usual hemolysis parameters after plasmapheresis.

Determination and Treatment of Disorders of Primary Haemostasis

1999 ◽  
Vol 19 (04) ◽  
pp. 168-175 ◽  
Author(s):  
M. Weippert-Kretschmer ◽  
V. Kretschmer
Keyword(s):  
Platelet Function ◽  
Bleeding Risk ◽  
Bleeding Complications ◽  
Bleeding Tendency ◽  
Platelet Counts ◽  
Platelet Function Disorders ◽  
Perioperative Bleeding ◽  
Before And After ◽  
Low Sensitivity

SummaryPerioperative bleeding complications due to disorders of primary haemostasis are often underestimated. Routine determination of primary haemostasis is still problematic. The in vivo bleeding time (BT) shows low sensitivity and high variability. In this contribution the results and experiences with the IVBT having been obtained in various studies and during 10 years of routine use are reported. Patients and Methods: Blood donors before and after ASA ingestion, patients with thrombocytopenia as well as congenital and acquired platelet function disorders. Monitoring of desmopressin efficacy. IVBT with Thrombostat 4000 (tests with CaCl2 = TST-CaCl2 and ADP = TST-ADP) and PFA-100 (test cartridges with epinephrine = PFA-EPI and ADP = PFA-ADP). Results and Conclusions: IVBT becomes abnormal with platelet counts <100,000/μl. With platelet counts <50,000/μl the results are mostly outside the methodical range. IVBT proved clearly superior to BT in von Willebrand syndrome (vWS). All 16 patients with vWS were detected by PFA-EPI, whereas with BT 7 of 10 patients with moderate and 1 of 6 patients with mild forms of vWS were spotted. The majority of acquired and congenital platelet function disorders with relevant bleeding tendency were detectable by IVBT. Sometimes diagnostic problems arose in case of storage pool defect. Four to 12 h after ingestion of a single dose of 100 mg ASA the TST-CaCl2 became abnormal in all cases, the PFA-EPI only in 80%. However, the ASA sensitivity of TST-CaCl2 proved even too high when looking for perioperative bleeding complications in an urological study. Therefore, the lower ASS sensitivity of the PFA-100 seems to be rather advantageous for the estimation of a real bleeding risk. The good efficacy of desmopressin in the majority of cases with mild thrombocytopenia, congenital and acquired platelet function disorders and even ASS-induced platelet dysfunction could be proven by means of the IVBT. Thus IVBT may help to increase the reliability of the therapy. However, the IVBT with the PFA-100 is not yet fully developed. Nevertheless, routine use can be recommended when special methodical guidelines are followed.

TT virus contaminates first-generation recombinant factor VIII concentrates

Blood ◽  
2001 ◽  
Vol 98 (8) ◽  
pp. 2571-2573 ◽  
Author(s):  
Alberta Azzi ◽  
Riccardo De Santis ◽  
Massimo Morfini ◽  
Krystyna Zakrzewska ◽  
Roberto Musso ◽  
...  
Keyword(s):  
Factor Viii ◽  
First Generation ◽  
Second Generation ◽  
Human Albumin ◽  
Factor Ix ◽  
Recombinant Factor Viii ◽  
Tt Virus ◽  
Recombinant Product ◽  
Before And After ◽  
Factor Viii Concentrates

Abstract Recombinant factor VIII and factor IX concentrates, human-plasma–derived albumin, and samples from previously untreated patients with hemophilia were examined for the presence of TT virus (TTV) by using polymerase chain reaction testing. Blood samples from the patients were obtained prospectively before and every 3 to 6 months after therapy was begun. TTV was detected in 23.5% of the recombinant-product lots and 55.5% of the albumin lots tested. Only first-generation factor VIII recombinant concentrates stabilized with human albumin were positive for TTV, whereas all second-generation (human protein–free) concentrates were negative for the virus. In 59% of patients treated with either first- or second-generation recombinant factor concentrates, TTV infection developed at some point after the initial infusion. Infection with TTV in these patients before and after treatment did not appear to be clinically important. Thus, first-generation recombinant factor VIII concentrates may contain TTV and the source of the viral contamination may be human albumin.

The Role of Platelets in the Pathogenesis of Thrombosis and Hemorrhage in Patients with Thrombocytosis

1977 ◽  
Vol 38 (04) ◽  
pp. 1085-1096 ◽  
Author(s):  
Peter N. Walsh ◽  
Scott Murphy ◽  
William E. Barry
Keyword(s):  
Platelet Function ◽  
Bleeding Complications ◽  
Platelet Counts ◽  
Normal Platelet ◽  
Coagulant Activity ◽  
Hemorrhagic Complications ◽  
Myeloproliferative Diseases ◽  
Thrombotic Complications ◽  
Preliminary Study

SummarySome patients with thrombocytosis due to myeloproliferative diseases or other etiologies experience thromboembolic complications and others may bleed excessively. It seems unlikely that elevations in platelet count per se are a direct cause either of thrombosis or of hemorrhage. In an effort to ascertain whether variations in platelet function might determine whether an individual patient experiences thrombotic or hemorrhagic complications we have evaluated platelet function in 22patients with thrombocytosis due to a variety of etiologies. The results of platelet counts, bleeding time determinations, and studies of platelet aggregation were similar in patients with thrombosis, in patients with bleeding and in patients with neither complication. Therefore, detailed studies of platelet coagulant activities were carried out in 8patients. The results of platelet coagulant activity assays were normal in all 3patients with thrombocytosis and neither thrombotic nor bleeding complications and an additional 3patients with myeloproliferative diseases, normal platelet counts and no thrombohemorrhagic complications. In 2patients with thrombotic complications significant elevation of platelet coagulant activities concerned with the early phases of intrinsic coagulation were observed whereas in 2patients with severe hemorrhagic complications deficiences of either contact forming activity or collagen-induced coagulant activities were evident. This preliminary study suggests the possibility that variations in platelet coagulant activities concerned with the early stages of intrinsic coagulation may determine whether patients with thrombocytosis will experience bleeding or thrombotic complications.

Factor VIII concentrates and the immune system—laboratory investigations

1995 ◽  
Vol 6 (Sup 2) ◽  
pp. S65-S79 ◽  
Author(s):  
M. Wadhwa ◽  
T. W. Barrowcliffe ◽  
A. R. Mire-Sluis ◽  
R. Thorpe
Keyword(s):  
Immune System ◽  
Factor Viii ◽  
Factor Viii Concentrates ◽  
Laboratory Investigations

scholarly journals The "Platelet Boilermaker" Is an Option for Quickly Raising Platelet Counts in IVIG Refractory ITP

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 5023-5023 ◽  
Author(s):  
Thomas G. Deloughery
Keyword(s):  
Therapeutic Option ◽  
Combined Therapy ◽  
Bleeding Complications ◽  
Drug Induced ◽  
Platelet Counts ◽  
The Past ◽  
First Line Therapy ◽  
Transient Rise ◽  
Warfarin Reversal ◽  
Refractory Itp

Abstract Most patients with immune thrombocytopenia (ITP) respond to first line therapy. Rarely there are patients who remain with very low platelet counts despite administration of intravenous immune globulin (IVIG). A protocol at our institution (colloquially known as the "platelet boilermaker") for these refractory patients is to give 1 gram/kg of IVIG continuously over 24 hours concurrent with one unit of plateletpheresis product given over 6 hours repeated times 4. We examined the charts of 10 patients in the past 6 years who have received combined therapy. 70% were male; all were refractory to steroids and IVIG. Results are in table: Abstract 5023. TableAgeGenderDiseaseBleedingPlts PreDay +1Day+2Day+3Results65MEvansGIB1110510Stopped bleeding59MITP, CLLBruising3656No response34FITPPregnancy2583175150Delivered81FITPEpistaxis15384167Splenectomy day +123FITPEpistaxis552165Splenectomy day +164MDITPEpistaxis, ruising252427Stopped bleeding89MITPEpistaxis4655046Splenectomy day +157MITPBruising9586946Splenectomy day +128MITPICH14133325326No extension78MITPGIB27354498Splenectomy day +1 Plt = platelet count x 109/L DITP = drug induced ITP, ICH - intracranial hemorrhage. GIB - gastrointestinal bleeding 9/10 patients had at least a transient rise in platelets greater than 30x109/L - 5 patients underwent emergent splenectomy with no bleeding complications. The patient with ICH had no extension and while the other patients who responded had cessation of bleeding. In summary for patients with IVIG refractory ITP who either have bleeding or need urgent splenectomy combined continuous platelets/IVIG is a therapeutic option. Disclosures Off Label Use: profilnine - warfarin reversal rVIIa - warfarin reversal.

Hemostatic Challenges In Patients Treated with Eltrombopag

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2511-2511 ◽  
Author(s):  
Michael D. Tarantino ◽  
Patrick F. Fogarty ◽  
Bhabita Mayer ◽  
Sandra Y. Vasey ◽  
Andres Brainsky
Keyword(s):  
Clinical Trials ◽  
Platelet Count ◽  
Research Funding ◽  
Bleeding Complications ◽  
Blood Products ◽  
Invasive Procedures ◽  
Platelet Counts ◽  
Chronic Itp ◽  
Number Of Patients ◽  
Before And After

Abstract Abstract 2511 Introduction: Chronic immune thrombocytopenia (ITP) is an autoimmune disease in which antiplatelet-antibodies induce platelet destruction and impair platelet production, resulting in chronically low platelet counts. Patients with chronic ITP may require invasive procedures associated with bleeding (hemostatic challenges) that cannot be undertaken if the platelet count is unacceptably low. Eltrombopag is an oral, nonpeptide, thrombopoietin receptor (TPO-R) agonist developed to increase platelet counts in various conditions associated with thrombocytopenia; its use may facilitate undertaking invasive procedures in patients with chronic ITP, reducing the need for additional supportive requirements including cellular blood products. Methods: Across the eltrombopag ITP clinical trials, information about hemostatic challenges was collected retrospectively (TRA100773A and B) and prospectively (REPEAT, RAISE, EXTEND). Basic demographic information, platelet counts before and after the procedures, type of procedure, need for additional treatment to increase platelet counts (one week before and after the intervention), use of blood products, and where possible, assessment of bleeding and bleeding complications were recorded. For the purpose of this analysis, minor invasive procedures (eg, dental cleaning, endoscopy, bone marrow biopsy) were distinguished from major invasive procedures (splenectomy, laparotomy, hip replacement, aortic aneurysm repair, arthroplasty). Results: Seventy-seven patients underwent 120 invasive procedures while enrolled in clinical trials with eltrombopag. The median age of patients undergoing invasive procedures was 54 years; the median duration of treatment at the time of all procedures was 131 days. 112 invasive procedures were performed in patients while receiving eltrombopag, compared to 8 procedures among patients while receiving placebo. 65 (54%) were considered to be major and 55 (46%) were considered to be minor. The median platelet count closest to minor or major invasive procedures in patients receiving eltrombopag was higher than in those receiving placebo (Table). For minor procedures, rescue ITP medication was required in 9/52 (17%) procedures in patients treated with eltrombopag and in 1/3 (33%) procedures in patients receiving placebo. For major procedures, rescue ITP medication was required in 14/60 (23%) procedures in patients treated with eltrombopag and 3/5 (60%) procedures in patients receiving placebo. One bleeding complication was reported in an eltrombopag-treated patient with colon cancer who, on the first post-operative day after a colectomy, experienced a pulmonary embolism requiring anticoagulation and had an intra-abdominal hemorrhage on post-operative day 2. Conclusions: No difference in use of periprocedural blood products between groups was discernable, possibly due to the low frequency of bleeding events reported. Although the number of patients who did not undergo procedures due to thrombocytopenia was not captured, data from 77 patients undergoing 120 invasive procedures suggest that by achieving a sustained platelet increase in patients with chronic ITP, eltrombopag facilitates the undertaking of medical and surgical procedures associated with bleeding. Disclosures: Tarantino: GlaxoSmithKline, Novo Nordisk, Talecris, Baxter, Cangene: Honoraria, Research Funding, Speakers Bureau. Fogarty: GlaxoSmithKline: Honoraria, Research Funding. Mayer: GlaxoSmithKline: Employment, Equity Ownership. Vasey: GlaxoSmithKline: Employment. Brainsky: GlaxoSmithKline: Employment.

IVIG Ameliorates Thrombin Activation of Platelets and Endogenous Thrombin Potential In Pediatric Patients with ITP.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3706-3706
Author(s):  
Sabine Kroiss ◽  
Oliver Speer ◽  
Jeannine Winkler ◽  
Alexandra Förderer ◽  
Markus Schmugge
Keyword(s):  
Platelet Count ◽  
Platelet Function ◽  
Surface Expression ◽  
Ivig Treatment ◽  
Healthy Children ◽  
Platelet Surface ◽  
Platelet Counts ◽  
Before And After ◽  
Healthy Control ◽  
Thrombin Activation

Abstract Abstract 3706 Immune thrombocytopenia (ITP) is a common hematological disorder in children that can lead to severe bleeding symptoms. Previous studies in ITP patients have found autoantibodies that bind to glycoprotein (GP) complex GPIIb/IIIa or GPIb/IX (Kiefel V et al. Br J Hematol 1991) and thus can alter platelet function (Olsson A et al. Thromb Res 2002; Nissner H et al. Blood 1986). Although platelet function has been studied in chronic ITP and in pediatric ITP (Panzer S et al. Europ J Haemat 2007; Semple et al. Blood 1996), so far platelet function was not studied in response to IVIg treatment, which leads to an increase of platelet counts and reduced bleeding symptoms. Next to platelet count no other biological markers have been correlated to bleeding symptoms. Therefore we studied the effect of IVIg treatment on platelet function and endogenous thrombin potential (ETP) in children with newly diagnosed primary ITP. Bleeding symptoms were assessed according to a pediatric bleeding score for ITP at the time of diagnosis and venous blood samples were obtained at the time of diagnosis and after IVIg therapy for measurement of platelet count and for flow cytometric analyses of platelets. In citrated platelet-rich plasma platelets were identified as CD42 positive events; CD62p, CD63 and PAC-1 binding were measured as % platelets with bound fluorescence before and after thrombin stimulation. All patients (median age 6.5 yrs, n=18) presented with typical symptoms of acute ITP with bleeding scores of 2 – 3 and had platelet counts < 20×109/L. (fig. 1). Results from ITP patients were compared to healthy children (median age 6.8 yrs, n = 18) with normal platelet counts and to children with thrombocytopenia as a result of chemotherapy for malignancies (cTP; median age 10.2 yrs, n = 9; platelet counts of 3 – 51×109/L). Results were expressed as the % of platelets expressing the antigen and were analyzed by ANOVA and Wilcoxon test. At initial presentation platelets of ITP patients showed an increased surface expression of CD62p (mean ± SEM: 14.4 ± 3.7 %, n = 17; p<0.05) and CD63 (27.21 ± 5.35 %, n = 17; p<0.05) compared to platelets from cTP patients (3.7 ± 1.1; 9.29 ± 1.7 %, n = 9) and healthy controls (4.9 ± 1.4; 9.5 ± 2.2 %, n = 9). PAC-1 binding was not increased in any of these groups. After thrombin stimulation, platelet surface expression of CD62p, CD63 and PAC1 increased significantly (p<0.0001). Among the groups, thrombin-stimulated expression of CD62p, CD63 and PAC1 was reduced in ITP (55.75 ± 7.77%; 57.07 ± 7.97%; 30.73 ± 7.71%; p<0.01) and in cTP (51.76 ± 7.59%; 55.22 ± 10.71%; 15.51 ± 5.05%; p<0.001) compared to healthy children (84.36 ± 4%; 91.94 ± 1.82%; 69.15 ± 6.91%). ETP was reduced in both, ITP (179.2 ± 52.3 nM thrombin; p<0.01) and cTP (185.0 ± 101.6 nM; p<0.05) compared to healthy children (353.4 ± 33.3 nM). After IVIg treatment all ITP patients showed a rise in platelet counts to >= 20 × 109/L (mean 46 × 109/L, range 20 – 123 × 109/L) and amelioration of bleeding symptoms. Concomitantly thrombin-stimulated platelet surface expression of CD62p, CD63 and PAC1 (84.51 ± 5.04%; 85.32 ± 5.79%; 56.8 ± 7.88%; p range 0.3 – 0.6) and ETP (316.6 ± 48.3 nM; p=0.3) improved and were not different from results in healthy children. In summary we demonstrated that platelets of children with primary ITP at baseline show an increased CD62p surface expression while thrombin-stimulated platelet activation of ITP and cTP patients is decreased compared to healthy children. After IVIg thrombin-stimulated platelet activation and ETP is similar to that seen in healthy children, even before normalization of the platelet counts. Figure 1. Pediatric ITP patients show increased proportions of platelets with p-selectin exposure and a decreased thrombin activation, which is normalized after IVIg treatment independent of the platelet count. (A) Platelet counts (Tc count), (B) proportion of platelets exposing p-selectin (% CD62p+ platelets) without and (C) with thrombin-stimulation (+ thrombin) were compared between children with ITP before and after IVIg treatment (ITP+IVIg), healthy control and cTP. The median and upper and lower quartiles are shown in boxes with whiskers for the range of data and open symbols for outliners. Figure 1. Pediatric ITP patients show increased proportions of platelets with p-selectin exposure and a decreased thrombin activation, which is normalized after IVIg treatment independent of the platelet count. (A) Platelet counts (Tc count), (B) proportion of platelets exposing p-selectin (% CD62p+ platelets) without and (C) with thrombin-stimulation (+ thrombin) were compared between children with ITP before and after IVIg treatment (ITP+IVIg), healthy control and cTP. The median and upper and lower quartiles are shown in boxes with whiskers for the range of data and open symbols for outliners. Disclosures: No relevant conflicts of interest to declare.

Effect of DDAVP on Platelet Activation and Platelet-Derived Microparticle Generation

2021 ◽  
Author(s):  
Matthieu Persyn ◽  
Nicolas Athanase ◽  
Marc Trossaërt ◽  
Marianne Sigaud ◽  
Catherine Ternisien ◽  
...  
Keyword(s):  
Factor Viii ◽  
Platelet Activation ◽  
Ex Vivo ◽  
Von Willebrand Disease ◽  
Factor Viii Deficiency ◽  
Platelet Counts ◽  
Definite Effect ◽  
Before And After ◽  
Combined Action ◽  
Von Willebrand

Abstract Background The way by which 1-deamino-8-D-arginine vasopressin (DDAVP) acts on platelets remains unclear. Data from the literature tend to show that there is no definite effect on platelet activation, but recent work has suggested that a subtype of platelets, activated by the combined action of collagen and thrombin, was triggered by DDAVP. Moreover, platelet microparticles (PMPs), which have been shown to be procoagulant, have rarely been studied in this context. The goal of this study was to analyze the effects of DDAVP on PMPs' release through platelet activation. Methods Fifteen out of 18 consecutive patients undergoing a therapeutic test with DDAVP were included. They were suffering from factor VIII deficiency or from von Willebrand disease. The expression of P-selectin and PAC-1 binding on platelets and the numbers of circulating PMPs were evaluated ex vivo before and after DDAVP infusion. Peripheral blood was collected on CTAD to limit artifactual platelet activation. Results DDAVP induced a significant decrease of platelet counts and volume. Only small changes of P-selectin expression and PAC-1 binding were observed. Considering PMPs, two populations of patients could be defined, respectively, with (120%, n = 6) or without (21%, n = 7) an increase of PMPs after DDAVP. The decrease in platelet counts and volume remained significant in the group of responders. Conclusion This study shows that DDAVP induces the generation/release of PMPs in some patients with factor VIII deficiency and von Willebrand disease 1 hour after DDAVP infusion.

Bleeding manifestations of congenital and drug-induced defects of the platelet P2Y12 receptor for adenosine diphosphate

2011 ◽  
Vol 105 (S 06) ◽  
pp. S67-S74 ◽  
Author(s):  
Marco Cattaneo
Keyword(s):  
Platelet Function ◽  
Thrombus Formation ◽  
Adenosine Diphosphate ◽  
New Drugs ◽  
Bleeding Complications ◽  
Bleeding Events ◽  
Drug Induced ◽  
High Concentrations ◽  
Therapeutic Doses ◽  
Induced Defects

SummaryP2Y12, one of the two platelet receptors for adenosine diphosphate (ADP), plays a central role in platelet function. Defects of P2Y12 should be suspected when ADP, even at high concentrations (≥10 μM), is unable to induce full, irreversible platelet aggregation. Patients with congenital P2Y12 defects display a mild-to-moderate bleeding diathesis of variable severity, characterised by mucocutaneous bleeding and excessive post-surgical and post-traumatic blood loss. Drugs that inhibit P2Y12 are potent antithrombotic drugs, attesting the central role played by P2Y12 in platelet thrombus formation. Clopidogrel, the most widely used drug that inhibits P2Y12, is effective both in monotherapy and in combination with acetylsalicylic acid (ASA). Its most important drawback is the inability to inhibit adequately P2Y12-dependent platelet function in about 1/3 of patients, at the recommended therapeutic doses. The incidence of bleeding events is similar in ASA-treated and clopidogrel-treated patients; however, the combination of ASA and clopidogrel causes more bleeding than each drug in monotherapy. Compared to clopidogrel, new drugs inhibiting P2Y12, such as prasugrel and ticagrelor, decrease the risk of cardiovascular events and increase the risk of bleeding complications, because they adequately inhibit P2Y12-dependent platelet function in the vast majority of treated patients.

scholarly journals Platelet Function Changes during Neonatal Cardiopulmonary Bypass Surgery: Mechanistic Basis and Lack of Correlation with Excessive Bleeding

2019 ◽  
Vol 120 (01) ◽  
pp. 094-106 ◽  
Author(s):  
Nicole M. J. Zwifelhofer ◽  
Rachel S. Bercovitz ◽  
Regina Cole ◽  
Ke Yan ◽  
Pippa M. Simpson ◽  
...  
Keyword(s):  
Platelet Count ◽  
Cardiopulmonary Bypass ◽  
Platelet Activation ◽  
Platelet Function ◽  
Platelet Transfusion ◽  
Adenosine Diphosphate ◽  
Bleeding Complications ◽  
Bleeding Events ◽  
Excessive Bleeding ◽  
Platelet Counts

AbstractThrombocytopenia and platelet dysfunction induced by extracorporeal blood circulation are thought to contribute to postsurgical bleeding complications in neonates undergoing cardiac surgery with cardiopulmonary bypass (CPB). In this study, we examined how changes in platelet function relate to changes in platelet count and to excessive bleeding in neonatal CPB surgery. Platelet counts and platelet P-selectin exposure in response to agonist stimulation were measured at four times before, during, and after CPB surgery in neonates with normal versus excessive levels of postsurgical bleeding. Relative to baseline, platelet counts were reduced in patients while on CPB, as was platelet activation by the thromboxane A2 analog U46619, thrombin receptor activating peptide (TRAP), and collagen-related peptide (CRP). Platelet activation by adenosine diphosphate (ADP) was instead reduced after platelet transfusion. We provide evidence that thrombocytopenia is a likely contributor to CPB-associated defects in platelet responsiveness to U46619 and TRAP, CPB-induced collagen receptor downregulation likely contributes to defective platelet responsiveness to CRP, and platelet transfusion may contribute to defective platelet responses to ADP. Platelet transfusion restored to baseline levels platelet counts and responsiveness to all agonists except ADP but did not prevent excessive bleeding in all patients. We conclude that platelet count and function defects are characteristic of neonatal CPB surgery and that platelet transfusion corrects these defects. However, since CPB-associated coagulopathy is multifactorial, platelet transfusion alone is insufficient to treat bleeding events in all patients. Therefore, platelet transfusion must be combined with treatment of other factors that contribute to the coagulopathy to prevent excessive bleeding.

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