Key result
High-dose GP IIb/IIIa inhibitors reduce sCD40L release by up to ~85%, whereas suboptimal doses increase it.
Why the study?
The effects of glycoprotein IIb/IIIa antagonists on the release of soluble CD40 ligand during platelet stimulation were not well understood.
Do GP IIb/IIIa antagonists and aspirin inhibit the release of soluble CD40 ligand during platelet stimulation?
Population
Platelets in vitro and platelets from aspirin-treated individuals
Comparison
Glycoprotein IIb/IIIa antagonists and aspirin versus suboptimal doses or no antagonist
Design
Preclinical in vitro study
Authors
Loading...
Suboptimal GP IIb/IIIa dosing may potentiate sCD40L release; leaves open clinical relevance for thrombotic inflammation.
Do GP IIb/IIIa antagonists and aspirin inhibit the release of soluble CD40 ligand during platelet stimulation?
Optimal doses of GP IIb/IIIa antagonists and aspirin inhibit the release of the prothrombotic and proinflammatory protein sCD40L, whereas suboptimal doses may paradoxically increase its release.
Nannizzi‐Alaimo et al. (2003) studied this question. Glycoprotein IIb/IIIa antagonists (eptifibatide, abciximab, tirofiban) and aspirin was evaluated on Release of soluble CD40 ligand (sCD40L). Glycoprotein IIb/IIIa antagonists at doses inhibiting platelet aggregation by ≥80% inhibited sCD40L release by 57% to 85%, whereas suboptimal doses potentiated its release by 19% to 26%.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: