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Acquired Bleeding Disorders Associated with Disease and Medications
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
William A. Rock, Sue D. Walker
The most common complication of Abciximab is bleeding, and treatment is associated with statistically significant increases in both major and minor bleeding events and in bleeding requiring transfusion. Bleeding sites include GI, GU, retroperitoneum, intracerebral, and arterial access sites.
Drug therapy in the cardiac catheterisation laboratory: A guide to commonly used drugs
Published in John Edward Boland, David W. M. Muller, Interventional Cardiology and Cardiac Catheterisation, 2019
John Edward Boland, Fuyue Jiang, Andrew Fenning
Abciximab is a monoclonal antiplatelet antibody that targets the platelet GP IIb/IIIa surface receptor. The other GP IIb/IIIa antagonists are the peptide eptifibatide (a derivative of rattlesnake venom) and a group of smaller peptides (tirofiban, lamifiban and xemilofiban). Abciximab was widely used in association with stent deployment, or as required to prevent or treat acute clotting scenarios. It is delivered intravenously according to a weight-adjusted chart. Initial administration is as an intravenous bolus in solution (0.25 mg/kg) followed by a 12-hours infusion at 0.125 mcg/kg/min (to a maximum of 10 ug/min). Again, side effects are bleeding complications and possible allergic reactions that drop the platelet count. The latter may be associated with formation of human anti chimeric antibodies. Abciximab is fast-acting, achieving receptor blockade greater than 80% after the first bolus. Its effects are irreversible and last for 24–36 hours. A platelet transfusion is necessary to effect reversibility. Abciximab also reduced the incidence of death and myocardial infarction in patients presenting with ACS,9,10 but demonstrated no added benefit to stable patients pre-treated with aspirin and clopidogrel prior to elective coronary intervention.11 Use of abciximab has declined considerably in recent years and is now used almost exclusively in association with thrombus formation during coronary intervention.
Vasopressors, Vasodilators, and Antithromboticsin The Catheterization Laboratory
Published in Debabrata Mukherjee, Eric R. Bates, Marco Roffi, Richard A. Lange, David J. Moliterno, Nadia M. Whitehead, Cardiovascular Catheterization and Intervention, 2017
Tracy E. Macaulay, David J. Moliterno
Several important pharmacologic factors define the useof abciximab. In contrast to other GP IIb/IIIa inhibitors,abciximab is a monoclonal antibody. Following IV bolus,antiplatelet effects occur within minutes and return to nor-mal within 48 hours in most cases.70 Because of its generalirreversibility and slower offset compared with small-mole-cule GP IIb/IIIa inhibitors, abciximab is not recommendedwhen there is a high likelihood of bleeding complicationsor surgical intervention. Since abciximab is an antibody,immune-mediated thrombocytopenia may occur, espe-cially with repeated use.71
Clinical pharmacology of antiplatelet drugs
Published in Expert Review of Clinical Pharmacology, 2022
Georg Gelbenegger, Bernd Jilma
Abciximab dose-dependently inhibits platelet function. A bolus infusion of 0.25 mg/kg inhibits >80% of GPIIb/IIIa receptors, reaching its peak effect 10 minutes after treatment initiation. Continuous abciximab infusion (0.125 µg/kg/min or 10 µg/min) maintains near maximal platelet inhibition [140]. Platelets were uniformly coated with abciximab within 30 minutes after start of intravenous infusion. Abciximab was still detected on platelets 14 days after infusion, suggesting continuous transfer of abciximab to platelets newly released into circulation [141]. Platelet function recovered gradually over 48 hours following end of infusion [141,142]. Human-antichimeric antibodies were detected in 5–6% of abciximab-treated patients but antibody titers were low in most patients [141,143] (Table 3).
Immunothrombosis and thromboinflammation in host defense and disease
Published in Platelets, 2021
Kimberly Martinod, Carsten Deppermann
Studies in the 1980s showed that following ischemia, platelets together with coagulation factors and VWF accumulate in the brain [106,107]. More recently, mouse studies have demonstrated the importance of the platelet VWF receptor GPIb in infarct development [108]. In contrast, blocking platelet integrin αIIbβ3 did not reduce infarct size and on the contrary increased the incidence of intracerebral hemorrhage and death. These results are in line with the outcome of a clinical trial that tested the safety and efficacy of abciximab in ischemic stroke and had to be stopped prematurely because of significantly increased hemorrhage and mortality [109]. A study using an elegant experimental design with crossed bone marrow transplantation in mice confirmed that platelet-derived VWF is an important contributor to immunothrombosis after stroke through a GPIb-dependent process [110]. In the past years another receptor has emerged as a major player in immunothrombosis after ischemia: Depleting platelet GPVI through a specific antibody led to significantly reduced infarct sizes after tMCAO [108]. Importantly, GPVI depletion did not lead to increased bleeding complications, making GPVI an attractive target for stroke therapy.
TEG®6s system measures the contributions of both platelet count and platelet function to clot formation at the site-of-care
Published in Platelets, 2020
Joao D. Dias, Carlos G Lopez-Espina, Kevin Bliden, Paul Gurbel, Jan Hartmann, Hardean E Achneck
Abciximab is a humanized, hybrid, monoclonal antibody that binds to the αIIbβ3 receptor, thereby blocking fibrinogen binding and subsequent platelet aggregation. Whole-blood samples were investigated with seven concentrations of abciximab (range 1.9–20.0 μg/mL), in addition to a baseline sample and a negative control with saline. These concentrations only required the addition of small volumes of abciximab, enabling coagulation factor levels and platelet counts to be preserved. The inhibitory effects of abciximab were confirmed by LTA with TRAP agonist. Previous studies have used threshold values of 70–81% [16,17], and so we used a threshold value of 75% for determining the presence or absence of platelet inhibition (i.e., platelet inhibition deemed to be present if the LTA TRAP value was ≤75%).