Eptifibatide-Associated Acute, Profound Thrombocytopenia

Coons, James C.; Barcelona, Robert; Freedy, Tucker; Hagerty, Michael F

doi:10.1345/aph.1e244

Cited by 30 publications

(26 citation statements)

References 19 publications

(22 reference statements)

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“…Thrombocytopenia in patients treated with RGD ligandmimetic platelet inhibitors can be life-threatening, 5,7,46,47 and drugs that are equally effective but do not cause thrombocytopenia would be desirable. Zhu and coworkers recently described an inhibitor designated RUC-1, which like eptifibatide and tirofiban, blocks binding of fibrinogen to the activated integrin.…”

Section: Discussionmentioning

confidence: 99%

Antibodies causing thrombocytopenia in patients treated with RGD-mimetic platelet inhibitors recognize ligand-specific conformers of αIIb/β3 integrin

Bougie

Rasmussen

Zhu

et al. 2012

Blood

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Section: Discussionmentioning

confidence: 99%

Antibodies causing thrombocytopenia in patients treated with RGD-mimetic platelet inhibitors recognize ligand-specific conformers of αIIb/β3 integrin

Bougie

Rasmussen

Zhu

et al. 2012

Blood

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“…Thrombocytopaenia is a well known complication of these drugs with an incidence of between 0.2% and 4.6% in clinical trials, depending on whether thrombocytopaenia was defined as a platelet count of lower than 20×10 9 /L, 50×10 9 /L or 100×10 9 /L [25]. Haematemesis, life-threatening bleeding, intracranial haemorrhage or fatal shock have been described as complications [26][27][28][29]. In contrast to other types of DITP, GP IIb/ IIIa-antagonist-associated thrombocytopaenia usually develops rapidly within a few hours after drug exposure, although delayed onset thrombocytopaenia has been described in several patients exposed to abciximab [30,31].…”

Section: Discussionmentioning

confidence: 99%

Drug-induced immune thrombocytopaenia: results from the Berlin Case–Control Surveillance Study

Garbe

Andersohn

Bronder

et al. 2011

Eur J Clin Pharmacol

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“…Historically, dyspnea did not appear to represent a safety concern for any of the antiplatelet agents [3], until the introduction of ticagrelor in 2011. Few anecdotal observations suggested that aspirin [4], hirudin [5], or eptifibatide [6] may be associated with dyspnea. In contrast, recent randomized evidence consistently suggests that reversible platelet P2Y12 receptor inhibitors are associated with dyspnea.…”

Section: Tablementioning

confidence: 99%

Dyspnea and Reversibility of Antiplatelet Agents: Ticagrelor, Elinogrel, Cangrelor, and Beyond

2013

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Context: Oral reversible platelet P2Y12 receptor inhibitors (ticagrelor and elinogrel) cause double-digit rates of dyspnea, while irreversible oral antiplatelet drugs (aspirin, ticlopidoine, clopidogrel, and prasugrel) or intravenous glycoprotein IIb/IIIa inhibitors (abciximab, eptifibatide, or tirofiban) do not increase the incidence of dyspnea in randomized trials. Dyspnea after oral reversible antiplatelet agents remains unexplained. A transfusion-related acute lung injury (TRALI) hypothesis has been proposed. The dyspnea risks after cangrelor, an intravenous reversible antiplatelet agent, are not well defined but may offer a universal mechanism linking TRALI, dyspnea, and reversible platelet inhibition. Objective: We analyzed safety data from recent head-to-head randomized trials with reversible antiplatelet agents (ticagrelor, elinogrel, and cangrelor) compared to irreversible (clopidogrel/placebo) comparators. Results: All three reversible antiplatelet agents cause excess dyspnea. In contrast to the high double-digit rates after oral ticagrelor or elinogrel, the dyspnea risks after intravenous cangrelor were smaller (<2%) but still consistently and significantly higher than in the corresponding control arms. Conclusions: The clinical utility of reversible antiplatelet strategies has been challenged. Despite a potential advantage of fewer bleeding events during heart surgery, reversible antiplatelet agents carry the risk of potential autoimmune reactions manifesting as dyspnea. Repeated binding and unbinding cycles, impaired platelet turnover, and lung sequestration or apoptosis of overloaded destructive platelets are among the potential mechanism(s) responsible for dyspnea after reversible antiplatelet agents.

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Eptifibatide-Associated Acute, Profound Thrombocytopenia

Abstract: Increasing use of the glycoprotein IIb/IIIa inhibitors and enhanced recognition of the potential for acute, profound thrombocytopenia reinforce the need for more vigilant monitoring and alternative management strategies.

Cited by 30 publications

References 19 publications

Antibodies causing thrombocytopenia in patients treated with RGD-mimetic platelet inhibitors recognize ligand-specific conformers of αIIb/β3 integrin

Antibodies causing thrombocytopenia in patients treated with RGD-mimetic platelet inhibitors recognize ligand-specific conformers of αIIb/β3 integrin

Drug-induced immune thrombocytopaenia: results from the Berlin Case–Control Surveillance Study

Dyspnea and Reversibility of Antiplatelet Agents: Ticagrelor, Elinogrel, Cangrelor, and Beyond

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