Acute profound thrombocytopenia associated with glycoprotein IIb/IIIa receptor inhibitor after percutaneous coronary intervention: therapy insights from a single center 6-year experience

Background Acute profound thrombocytopenia is an infrequent, but potentially serious, even fatal complication associated with intravenous glycoprotein IIb/IIIa receptor inhibitors (GPI), which are widely used in acute coronary syndrome and percutaneous coronary intervention (PCI). Treatment with steroids and intravenous immunoglobulin (IVIg) is recommended for GPI-induced thrombocytopenia (GIT), but its efficacy is rarely reported. Methods In this retrospective study, we enrolled 21 patients who developed acute profound thrombocytopenia (defined as a platelet count < 20 ×10⁹/L) following PCI with GPI treatment. We analyzed their clinical characteristics, the timing of detected thrombocytopenia, the use of steroid and IVIg treatment, and the subsequent platelet count trends and outcomes. Results Among the 21 patients, 7 were female, and the median age was 63 years. Tirofiban and eptifibatide were administered to 12 and 9 patients, respectively. Thrombocytopenia was detected on the day of PCI in 9 patients. Among the remaining 12, one case was identified following the onset of intracerebral hemorrhage with coma, while the other 11 were discovered during routine blood tests on postoperative day 1. The median platelet count dropped sharply from 143 × 10⁹/L preoperatively to 4 × 10⁹/L after GPI treatment. Following the onset of profound thrombocytopenia, 11 patients underwent treatment with both steroids and IVIg, 6 received steroids alone, and 4 received neither intervention. Patients were categorized into three treatment groups (steroid plus IVIg, steroid alone, or no-intervention) with the aim of analyzing whether steroid/IVIg therapy promoted platelet recovery. No such beneficial effect was found. A separate analysis, grouping patients by whether thrombocytopenia was detected on the day of PCI (early-detection group and later-detection group), showed that those with an early diagnosis and consequent prompt withdrawal of the GPI exhibited a statistically significant faster platelet recovery. The median time to platelet recovery > 20×10⁹/L was significantly shorter in the early-detection group (24 hours) than in the later-detection group (72 hours) with p = 0.017. Conclusions GIT is characterized by rapid onset. Early detection of thrombocytopenia is essential for immediate GPI discontinuation, which is the cornerstone of platelet recovery. Steroids and IVIg did not improve platelet recovery in our cohort.