Objective: To determine the prevalence of heparin-dependent platelet antibodies (HDPA) in children requiring heparin for >5 days after cardiopulmonary bypass surgery.
Design: Prospective, observational study.
Setting: Tertiary care pediatric intensive care unit.
Patients: Thirty children were enrolled: 15 patients <30 days old and 15 patients between 30 days and 12 yrs of age.
Interventions: Detection of HDPA by heparin-platelet factor 4 enzyme-linked immunosorbent assay after 5-10 days of postoperative heparin exposure. Positive or equivocal results were confirmed with serotonin release assay.
Measurements And Main Results: There were no confirmed cases of HDPA in this study (95% confidence interval 0-11.6%). Despite the lack of HDPA, the study population was at high risk of thrombosis with symptomatic clot developing in six patients (20%). Clinical models developed in adults to determine the pretest risk of heparin-induced thrombocytopenia were not valid in this study population.
Conclusions: The prevalence of HDPA in children after cardiopulmonary bypass surgery is low. After bypass surgery, critically ill children are at risk of developing thrombosis from multiple etiologies, and suspicion of heparin-induced thrombocytopenia needs to be confirmed with laboratory testing including a functional assay.
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http://dx.doi.org/10.1097/01.PCC.0000269398.10804.7F | DOI Listing |
Lab Med
March 2018
Department of Laboratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Spurious thrombocytopenia is a well-known phenomenon observed with the widespread use of hematology analyzers (HAs). In this study, 355 specimens with pseudo-thrombocytopenia (PTCP) were evaluated via epidemiology, identification, remedies, and platelet (PLT) count. Data showed that anticoagulants such as citrate and/or heparin-dependent PTCP (16.
View Article and Find Full Text PDFBlood
October 2016
Division of Hematology, and.
Heparin-induced thrombocytopenia is a prothrombotic disorder caused by antibodies to platelet factor 4 (PF4)/heparin complexes. The mechanism that incites such prevalent anti-PF4/heparin antibody production in more than 50% of patients exposed to heparin in some clinical settings is poorly understood. To investigate early events associated with antigen exposure, we first examined the interaction of PF4/heparin complexes with cells circulating in whole blood.
View Article and Find Full Text PDFThromb Res
July 2014
Department of Internal Medicine, Division of Vascular Medicine/Haemostaseology, Goethe University Hospital, Frankfurt/M., Germany.
Blood
April 2013
Division of Hematology, Duke University Medical Center, Durham, NC 27710, USA.
Protamine is routinely used to reverse heparin anticoagulation during cardiopulmonary bypass (CPB). Heparin interacts with protamine to form ultralarge complexes that are immunogenic in mice. We hypothesized that patients exposed to protamine and heparin during CPB will develop antibodies (Abs) to protamine/heparin (PRT/H) complexes that are capable of platelet activation.
View Article and Find Full Text PDFRheumatology (Oxford)
September 2012
Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, Japan.
Objective: Antibodies that recognize complexes formed by platelet factor 4 (PF4) and heparin are involved in the pathogenesis of heparin-induced thrombocytopenia (HIT). This study was undertaken to investigate the prevalence and clinical correlations of anti-PF4 autoantibodies in patients with SLE.
Methods: We studied 118 patients with SLE, 78 with primary immune thrombocytopenia (ITP), 27 with primary APS, 2 with HIT (as positive controls) and 47 healthy controls.
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