Key result
Eptifibatide administration in an 80-year-old man with acute coronary syndrome induced profound acute thrombocytopenia, with platelet count dropping to 1 thou/μL and subcutaneous hematomas.
Why the study?
Glycoprotein IIb/IIIa inhibitors may be considered during percutaneous coronary interventions for acute coronary syndrome, but severe drug-induced thrombocytopenia is a rare adverse event warranting detailed reporting.
Does eptifibatide cause profound thrombocytopenia in an elderly patient with acute coronary syndrome?
Case Report (n=1)
Does eptifibatide cause profound thrombocytopenia in an elderly patient with acute coronary syndrome?
Eptifibatide can induce profound, acute thrombocytopenia in elderly patients with acute coronary syndrome, requiring prompt discontinuation and monitoring.
Alerts clinicians to monitor platelets with eptifibatide in elderly ACS; case report leaves incidence and risk factors open.
Introduction: Glycoprotein (Gp) IIb/IIIa is a platelet receptor participating in platelet aggregation. According to ESC guidelines, glycoprotein IIb/IIIa inhibitors might be considered during percutaneous coronary interventions in patients with the acute coronary syndrome. Purpose: A case study of profound thrombocytopenia in 80-year-old man with the acute coronary syndrome. Case presentation: An 80-year-old, medicationnaive man with acute coronary syndrome was admitted to the Department of Invasive Cardiology. Due to the unsuccessful invasive strategy, an intracoronary bolus of Gp IIb/IIIa inhibitor – eptifibatide - was administered. During the following intravenous infusion, large subcutaneous hematomas were observed. Eptifibatide infusion was discontinued. Drop in platelet count to 1 thou/μL without significant anemia was registered. A control sample in sodium citrate showed similarly low platelet count - 2 thou/uL. Acetylsalicylic acid and clopidogrel were discontinued, steroids were introduced. Neither PLT nor FFP transfusion were necessary. Consecutive lab tests showed the gradual increase of PLT up to 35 thou/μL at discharge. A week later, the patient did not complain of any cardiovascular or bleeding symptoms; hematomas resented significant involution. Laboratory findings were normal. During follow-up visit 30 days after the discharge, the patient presented no cardiovascular symptoms. Conclusions: There are patients at risk of druginduced thrombocytopenia, especially those with impaired kidney function and the elderly. In such cases, decisions concerning anti-platelet and antithrombotic therapy should be taken cautiously. Because of its rare occurrence, every case of severe thrombocytopenia in ACS patients should be reported. Moreover, such patients should be followed-up to minimalize risk of similar adverse events in the future.
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Kuźma et al. (2018) conducted a case report in Acute coronary syndrome (n=1). Eptifibatide was evaluated on Profound thrombocytopenia. Eptifibatide administration in an 80-year-old man with acute coronary syndrome induced profound acute thrombocytopenia, with platelet count dropping to 1 thou/μL and subcutaneous hematomas.
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