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  • Title: Paradoxical platelet activation was not observed on dissociation of abciximab from GpIIb-IIIa complexes.
    Author: Ndoko S, Poujol C, Combrié R, Nurden A, Nurden P.
    Journal: Thromb Haemost; 2002 Feb; 87(2):317-22. PubMed ID: 11858493.
    Abstract:
    The ability of abciximab to bind and dissociate from platelets raises the question of the conformational state of GPIIb-IIIa complexes losing abciximab and the risk of paradoxical drug-induced platelet activation. Platelets incubated with abciximab and mixed in vitro with c7E3 Fab-free platelets lost the drug to the new platelets giving a single platelet population with a unimodal abciximab distribution within 17 h. Prelabeling the receiving platelets with phycoerythrin-labeled anti-GPIb monoclonal antibody (MoAb), permitted their identification by flow cytometry. Binding of PAC-1 and AP6, two MoAbs specific for activated GPIIb-IIIa, was then assessed to both losing and receiving platelet populations during transfer of abciximab. The subpopulation losing c7E3 Fab failed to show increased binding of these MoAbs. However, PAC-1 binding increased in both subpopulations after addition of ADP. Thus GPIIb-IIIa complexes are not in an activated state after dissociation of abciximab unless there is an additional source of activation.
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