Tirofiban-Associated Profound Thrombocytopenia in a Patient With Glucose-6-Phosphate Dehydrogenase Deficiency Undergoing Primary Percutaneous Coronary Intervention: A Case Report
Research article published in Case reports in cardiology (2026)
Abstract
BACKGROUND: Profound thrombocytopenia after tirofiban exposure during primary percutaneous coronary intervention (PCI) is rare but clinically important. Causal attribution may be challenging when unfractionated heparin is coadministered, and the relevance of glucose-6-phosphate dehydrogenase (G6PD) deficiency remains uncertain. CASE PRESENTATION: A 34-year-old man with known G6PD deficiency presented with an inferior ST-segment elevation myocardial infarction and underwent primary PCI. He received aspirin, ticagrelor, and unfractionated heparin. Coronary angiography showed multivessel coronary disease with complete occlusion of the mid-to-distal right coronary artery and a large thrombus burden. After aspiration thrombectomy and drug-eluting stent implantation, intracoronary tirofiban (2500 μg bolus), followed by intravenous tirofiban infusion (0.15 μg/kg/min), was administered as bailout antithrombotic therapy. Within 6 h, the platelet count fell from 207 × 109 to 1 × 109/L. Peripheral blood smear showed no platelet clumping or abnormal cells. Sepsis and disseminated intravascular coagulation were not supported by laboratory findings. Heparin-induced thrombocytopenia was considered highly unlikely because the 4Ts score was 1, reflecting the extremely early onset, absence of new thrombosis, and the presence of a more plausible alternative explanation. The clinical course was therefore most consistent with acute tirofiban-associated profound thrombocytopenia. INTERVENTIONS AND OUTCOMES: Tirofiban and heparin were discontinued immediately, and intravenous immunoglobulin (20 g/day) was administered. The platelet count recovered to 25 × 109/L at 48 h, 48 × 109/L at 72 h, and 124 × 109/L on Day 4. Clopidogrel was restarted at 48 h, followed by indobufen at 72 h. No major bleeding or thrombotic complications occurred. CONCLUSIONS: This case supports tirofiban-associated acute profound thrombocytopenia as the most likely diagnosis and underscores the importance of prompt drug withdrawal, structured differential diagnosis against heparin-induced thrombocytopenia, and individualized antithrombotic reinitiation. The contribution of G6PD deficiency remains hypothetical and requires further study.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Summary
Peer-reviewed clinical and outcomes research relevant to anticoagulation, leech therapy, and microsurgical flap management. Indexed in PubMed and verified against the NCBI record.
Why This Matters for Hirudotherapy
This single case report describes a 34-year-old man with G6PD deficiency who developed profound thrombocytopenia (platelet count falling from 207 to 1 x 10^9/L within 6 hours) after receiving the GP IIb/IIIa inhibitor tirofiban during primary PCI for STEMI; the authors judged heparin-induced thrombocytopenia unlikely (4Ts score of 1) and attributed the event to tirofiban, with recovery after drug withdrawal and intravenous immunoglobulin. For the ASH evidence picture, it is a reminder of how challenging it is to pin a sudden platelet drop on the right agent when heparin and antiplatelet drugs are co-administered, and it reinforces why interest persists in anticoagulants — including leech-derived direct thrombin inhibitors — that avoid the immune-mediated platelet complications tied to heparin. As a single case report it carries the lowest evidentiary weight: it cannot establish causation or incidence, the role of G6PD deficiency is explicitly called hypothetical by the authors, and it has no bearing on leech therapy efficacy.
Citation
Tirofiban-Associated Profound Thrombocytopenia in a Patient With Glucose-6-Phosphate Dehydrogenase Deficiency Undergoing Primary Percutaneous Coronary Intervention: A Case Report.
Zhao et al. · Case reports in cardiology, 2026
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