Sudden onset of EDTA-dependent pseudothrombocytopenia after therapy with the glycoprotein IIb/IIIa antagonist c7E3 Fab

 The development of thrombocytopenia following exposure to the platelet glycoprotein (GP) IIb/IIIa receptor antagonist abciximab (c7E3 Fab, ReoPro) is associated with adverse clinical outcome and excessive bleeding. Pseudothrombocytopenia is an important differential diagnosis in sudden onset of thrombocytopenia in a patient treated with c7E3 Fab. We report on a case of documented sudden onset of EDTA-dependent pseudothrombocytopenia in a 63-year-old woman who was admitted for emergency coronary intervention. Four hours after bolus administration of c7E3 Fab, the platelet concentration in EDTA-anticoagulated blood decreased from 385×10⁹/l to 119×10⁹/l, and it showed a further decrease to 57×10⁹/l at the end of a 12-h infusion. Despite no warnings or abnormalities of the automated cell counter, platelet aggregates were observed by microscopic evaluation of the blood smear. Repeated platelet counts in citrate-anticoagulated samples revealed platelet concentrations within the reference range. EDTA-dependent pseudothrombocytopenia due to therapy with c7E3 Fab is an important differential diagnosis that needs to be excluded rapidly from other causes of thrombocytopenia to avoid unnecessary further examinations, discontinuation of therapy, or even initiation of inappropriate therapy. Received: April 10, 1999 / Accepted: July 2, 1999     

Occurrence and clinical significance of pseudothrombocytopenia during abciximab therapy

OBJECTIVES: This study determined the incidence of pseudothrombocytopenia during abciximab therapy administered for percutaneous coronary interventions and compared the clinical course of patients with pseudothrombocytopenia with the clinical courses of patients with thrombocytopenia and patients with normal platelet counts. BACKGROUND: Although pseudothrombocytopenia has been previously reported during therapy with abciximab, the incidence and significance of this occurrence are unknown. The failure to differentiate pseudothrombocytopenia from thrombocytopenia could lead to unnecessary interruption of abciximab infusions or to platelet transfusions. METHODS: The incidences of pseudothrombocytopenia and thrombocytopenia were determined in four large placebo-controlled abciximab trials: c7E3 Fab Antiplatelet Therapy in Unstable Refractory Angina (CAPTURE), Evaluation of 7E3 for the Prevention of Ischemic Complications (EPIC), Evaluation of Percutaneous Transluminal Coronary Angioplasty to Improve Long-term Outcome of c7E3 GpIIb/IIIa Receptor Blockade (EPILOG) and Evaluation of Platelet IIb/IIIa Inhibitor for Stenting (EPISTENT). The clinical features, bleeding complications and major clinical outcomes of patients with pseudothrombocytopenia and those with thrombocytopenia were compared with each other and with those of patients with normal platelet count. RESULTS: Pseudothrombocytopenia occurred in 2.1% (95% confidence intervals [CI]: 1.7%, 2.5%) of abciximab-treated patients and in 0.6% of placebo-treated patients (p < 0.001). Thrombocytopenia occurred in 3.7% (95% CI: 3.2%, 4.2%) of abciximab-treated patients and in 1.8% (95% CI: 1.3%, 2.3%) of placebo-treated patients (p < 0.001). Patients with thrombocytopenia had significantly higher rates of major bleeding, major decreases in hemoglobin and increased transfusion requirements of both blood and platelets compared with those without thrombocytopenia. By contrast, pseudothrombocytopenic patients did not differ from patients with normal platelet counts in any of the measures of blood loss or transfusion requirements. Thrombocytopenic patients, but not those with pseudothrombocytopenia, had increased rates of revascularization at 30 days and six months. As previously reported, there was also a higher rate of death and myocardial infarction in the thrombocytopenic patients. CONCLUSIONS: Pseudothrombocytopenia is the cause of more than one third (36.3%) of low platelet counts in patients undergoing coronary interventions who are treated with abciximab. This study demonstrates that pseudothrombocytopenia is a benign laboratory condition that does not increase bleeding, stroke, transfusion requirements or the need for repeat revascularization. It is important to recognize pseudothrombocytopenia so that the beneficial effects of abciximab are not lost by premature termination of therapy.     

Acute profound thrombocytopenia following C7E3 Fab (Abciximab) therapy: case reports, review of the literature and implications for therapy.

Platelets play a crucial role in the ischemic complications of percutaneous coronary procedures. The recent availability of C7E3 Fab (Abxiximab or ReoProtrade mark), a chimeric monoclonal antibody Fab fragment directed against the platelet glycoprotein IIb/IIIa receptor, has reduced abrupt closure and other adverse events and lessened the need for revascularization procedures. As the use for this drug has increased, rare cases of severe thrombocytopenia have been revealed. From August 1995 to June 1997, 452 patients at Charleston Area Medical Center who underwent percutaneous coronary revascularization procedures and were treated with abciximab were evaluated for the development of severe thrombocytopenia (i.e., platelet count less than 20,000 within 48 hr of treatment). A review of published reports of severe thrombocytopenia was also reviewed. A review of published reports of abciximab-induced severe thrombocytopenia, as well as our three cases, reveals that: 1) the incidence is less than 0.7%; 2) the nadir platelet count (range 1, 000-16,000) was noted within 2-31 hr after abciximab infusion; 3) the platelet count increases to greater than 100,000 within 12 days in all patients; 4) bleeding episodes were treated with platelet transfusion with an improvement in platelet count within 24 hr in all patients in whom they were given; and 5) in the one patient treated with gamma globulin alone, no significant rise in platelet count was noted. Acute severe thrombocytopenia can occur after ReoProtrade mark administration. Its development is not predictable and may occur within 2 hr of administration. Thrombocytopenia, therefore, requires consideration in every patient treated with this drug. It appears prudent to obtain a platelet count 2 hr after initiating ReoProtrade mark. If thrombocytopenia develops, then the drug can be stopped in a timely manner and platelet transfusion can be given.     

Occurrence and clinical significance of thrombocytopenia in a population undergoing high-risk percutaneous coronary revascularization

Objectives. This study sought to determine the frequency of thrombocytopenia and its relation with clinical outcomes in high risk patients undergoing percutaneous coronary revascularization who received either the platelet glycoprotein (GP) IIb/IIIa receptor antagonist abciximab (ReoPro, c7E3 Fab) or conventional therapy.Background. The development of thrombocytopenia on exposure to GPIIb/IIIa antagonists threatens the utility and economic viability of this drug class for patients with vascular disease.Methods. We analyzed data from the Evaluation of c7E3 for the Prevention of Ischemic Complications trial (EPIC), a 2,099-patient, randomized trial of placebo, abciximab bolus or abciximab bolus plus a 12-h infusion during high-risk coronary revascularization.Results. Thrombocytopenia (nadir platelet count <100 × 10⁹/liter) developed in 81 patients (3.9%) during their hospital stay, with 19 (0.9%) developing severe (<50 × 10⁹/liter) thrombocytopenia. Both thrombocytopenia and severe thrombocytopenia were more frequent in the bolus-plus-infusion arm (5.2% and 1.6%, respectively) than in the bolus-only and placebo arms combined (p = 0.020 and p = 0.025, respectively). Acute profound thrombocytopenia developed in two patients in the bolus-plus-infusion arm. Patients with thrombocytopenia experienced more unfavorable clinical outcomes than those who did not develop thrombocytopenia, regardless of treatment assignment, but those with thrombocytopenia who received abciximab had fewer worse outcomes at 30 days. Multivariable logistic modeling revealed a lower baseline platelet count, older age and lighter weight to be important predictors of thrombocytopenia. In a logistic regression model, bolus-plus-infusion treatment was a significant predictor of thrombocytopenia (p = 0.016) and remained so after adjustment for procedures and baseline risk factors (p = 0.0077).Conclusions. Thrombocytopenia was associated with adverse clinical outcomes and excessive bleeding, but patients receiving abciximab fared better than those receiving placebo.     

Severe thrombocytopenia refractory to platelet transfusions, secondary to abciximab readministration, in a patient previously diagnosed with idiopathic thrombocytopenic purpura. A possible etiopathogenic link

Acute severe thrombocytopenia is a serious although infrequent complication following abciximab infusion that is usually managed with platelet transfusions. We present a patient who underwent multivessel percutaneous coronary intervention with concomitant abciximab administration. Soon after the procedure the patient developed severe thrombocytopenia that persisted despite multiple platelet transfusions. This patient had been previously diagnosed as having idiopathic thrombocytopenic purpura, although this diagnosis was not recorded in our medical records, and at the time of the intervention the patient had a normal platelet count. He was successfully managed with IgG administration. The clinical and therapeutic implications of this case are discussed.     

Acute profound thrombocytopenia after abciximab therapy during coronary angioplasty

Since the extensive use of abciximab, a potent antiplatelet agent directed against GP IIb/IIIa platelet receptors, to prevent ischemic complications of percutaneous transluminal coronary angioplasty, few cases of thrombocytopenia have been observed. This paper reports a case of acute profound thrombocytopenia (platelet count: 800/mm3) occurring 16 h after abciximab therapy during coronary angioplasty. As thrombocytopenia occurrence is not predictable, platelet count should be evaluated periodically after drug administration. Mechanisms of this adverse effect remain unknown. Platelet transfusion results in a rapid and sustained improvement of platelet count, avoiding the occurrence of major hemorrhagic complications.     

Acute thrombocytopenia associated with eptifibatide therapy

BACKGROUND: Platelet glycoprotein (GP) IIb/IIIa receptor blockade improves clinical outcomes in percutaneous coronary interventions and in acute coronary syndromes. Thrombocytopenia is a serious complication well described with the use of the prototype GPIIb/IIIa inhibitor abciximab. Its association with other agents of this class has been underemphasized. OBJECTIVES: To determine the incidence of thrombocytopenia in a cohort of patients treated with eptifibatide at a tertiary cardiac centre. PATIENTS AND METHODS: Chart review of consecutive patients treated with eptifibatide at the study institution. RESULTS: There were four (1.3%) cases of acute thrombocytopenia (platelet count less than 100 x 10(9)/L) among 305 patients reviewed. One patient had been previously exposed to eptifibatide. The other three patients are described. In each case, platelet counts declined within 6 h of receiving eptifibatide. Recovery of platelet counts was noted within 6 to 30 h after withdrawal of eptifibatide. No patient suffered an adverse clinical event related to thrombocytopenia. CONCLUSIONS: It is important to monitor platelet counts closely after initiation of GPIIb/IIIa inhibitor therapy, not only for abciximab, but also for small molecule inhibitors such as eptifibatide. Monitoring of platelet counts at 2 to 6 h and 24 h will detect most cases of acute thrombocytopenia. Adverse events may be prevented by prompt discontinuation of GPIIb/IIIa inhibitor therapy.     

Acute severe thrombocytopenia after c7E3 Fab (abciximab) therapy in a patient with unstable angina and stenting of the right coronary artery. Occurrence of subacute stent thrombosis and safe readministration of the GPIIb/IIIa inhibitor tirofiban

This paper reports a case of acute severe thrombocytopenia (platelet count: 1 &#50 10 9 /liter) occurring within minutes of an initial abciximab bolus during coronary angioplasty and stenting in a patient with unstable angina. After six days with platelets again in the normal range the patient developed stent thrombosis. The stent was reopened and the glycoprotein receptor inhibitor tirofiban (Aggrastat) was administered without any adverse effects on platelet count. Antibodies against heparin-platelet factor 4 complexes could be excluded. Allo- and autoantibodies (IgG, IgA, IgM) directed against platelets with and without binding of abciximab could not be detected by indirect and direct platelet fluorescence antiglobulintest. A possible activation or lysis of the platelets by abciximab could also be excluded by an in vitro bleeding test investigating the effect of abciximab on heparin and citrate blood of the patient and two healthy donors. The mechanisms of abciximab-induced thrombocytopenia in this case remain unclear. The possible mechanisms are discussed. (Int J Cardiovasc Intervent 2000; 3: 185-188)     

Acute profound thrombocytopenia without bleeding complications after re-administration of abciximab

Abciximab (c7E3) is the Fab fragment of the chimeric (murine/human) monoclonal antibody directed against the platelet glycoprotein IIb/IIIa receptor, which is the final common pathway for platelet aggregation. Abciximab has been widely used for patients undergoing angioplasty who are at high risk for ischemic complications. Severe thrombocytopenia (defined as platelet count < 50,000 platelet/mm3) has been observed in both first-time administration and re-administration of abciximab. Platelet transfusion as treatment for the reversal of thrombocytopenia is ubiquitously accepted. Intravenous corticosteroid as an adjunctive therapy is being explored. We previously reported our experience with platelet transfusion combined with corticosteroid treatment for acute thrombocytopenia following first-time abciximab administration. We now report a case of acute profound thrombocytopenia following re-administration of abciximab successfully treated with a combination of platelet transfusion and intravenous corticosteroid.     

Transient appearance of EDTA dependent pseudothrombocytopenia in a patient with 2019 novel coronavirus pneumonia

Abstract

EDTA dependent pseudothrombocytopenia (EDTA-PCTP) is a phenomenon that characterized by a spurious decrease of platelets in vitro due to the aggregation of platelets in EDTA anticoagulant blood samples. We report the first case of a transient appearance of EDTA-PCTP in a patient with 2019 novel coronavirus pneumonia (COVID-19). A 59-year-old woman was admitted to the isolated ward for severe type of 2019 novel coronavirus pneumonia. At the time of admission, her platelet count was in a normal range. Two days later, her platelet count decreased gradually without any signs or symptoms of bleeding. Since the peripheral blood smear showed a platelet aggregation, a blood sample anticoagulanted with citrate was tested and the number of platelet was normal. The phenomenon disappeared after 17 days when the patient was cured. This case emphasized the importance of peripheral blood smear and clinical manifestation, especially in the differential diagnosis of thrombocytopenia.     

Uneventful use of tirofiban as an adjunct to coronary stenting in a patient with a history of abciximab-associated thrombocytopenia 10 months earlier

A 52-year-old male undergoing a percutaneous coronary intervention after an inferior infarction treated with thrombolytic therapy was given abciximab with development of early severe reversible thrombocytopenia (platelet count nadir of 50,000 per mm3). The same patient underwent another percutaneous coronary intervention 10 months later and was given tirofiban without development of thrombocytopenia. This observation suggests that the development of thrombocytopenia with abciximab is not necessarily generalizable to other unique IIb/IIIa receptor antagonists. Tirofiban may be an appropriate consideration for patients who would benefit from a IIb/IIIa receptor antagonist and who are not candidates for abciximab therapy due to an episode of abciximab-associated thrombocytopenia. Further investigation of thrombocytopenia associated with IIb/IIIa receptor antagonists is warranted to determine appropriate approaches to the management of patients with a history of abciximab-associated thrombocytopenia.     

Alveolar hemorrhage as a complication of treatment with abciximab.

STUDY OBJECTIVE: The use of abciximab, a chimeric monoclonal antibody Fab fragment specific for platelet glycoprotein IIb/IIIa receptors, is associated with improved outcome after angioplasty and stent placement. Major complications include bleeding, but pulmonary hemorrhage has been reported rarely. This study was done to identify patients with pulmonary hemorrhage following abciximab infusion and to define, if possible, any specific risk factors. DESIGN: Retrospective review of institutional coronary angiography and bronchoscopy databases to identify patients who received abciximab and developed pulmonary hemorrhage. SETTING: Tertiary-care teaching hospital. PATIENTS: All patients who underwent coronary angiography and received abciximab between June 1995 and March 2000. INTERVENTION: None. Measurements and results: Seven of 2,553 patients (0.27%) had documented severe pulmonary hemorrhage associated with chest radiographic abnormalities, impaired oxygenation, and the need for blood product transfusions. The initial symptom was hemoptysis in four of the seven patients. There were two early deaths and one late death. No cases of pulmonary hemorrhage were identified in 5,412 patients who underwent coronary procedures without abciximab infusion. No other risk factors predicting hemorrhage were identified. CONCLUSIONS: Severe pulmonary hemorrhage is a complication of abciximab use. Although hemoptysis is an important alerting symptom, it may not be present initially and the diagnosis may be missed or considered late, with the potential for inappropriate treatment until the diagnosis is established. Lesser degrees of bleeding are potentially easily missed, and this report should alert physicians to this complication so that it can be considered early in the evaluation of patients presenting with pulmonary events after abciximab use.     

Extreme thrombocytopenia following abciximab therapy

Antagonists of the glycoprotein IIb/IIIa receptor block the binding of fibrinogen and Von Willebrand factor to the platelet receptor. This effect can lead to bleeding and thrombocytopenia. We analyzed the incidence and clinical repercussions of severe thrombocytopenia (< 20 000 /microl) secondary to abciximab treatment in a prospective study of 375 patients (74% men) who underwent percutaneous coronary revascularization and received abciximab at our hospital. We recorded clinical and demographic characteristics, angiographic findings, laboratory results and platelet counts (before, 4 hours after and 12 hours after the procedure) and hematocrit. The incidence of severe acute thrombocytopenia was 1.1%. All patients were men, and none had relevant bleeding complications. Management consisted of monitoring the bleeding, discontinuing the drug and transfusing platelets. Clinicians should be alert to this complication during the initial hours after the administration of abciximab.     

Incidence and time course of thrombocytopenia with abciximab and eptifibatide in patients undergoing percutaneous coronary intervention

Thrombocytopenia is recognized as a potential adverse effect in patients treated with glycoprotein IIb/IIIa inhibitors. We monitored platelet counts at baseline and at 10 minutes and at 1, 8, and 24 hours after initiation of therapy with either abciximab (n = 74) or eptifibatide (n = 26) in a series of 100 consecutive patients who underwent percutaneous coronary intervention. Thrombocytopenia (platelet count <100,000 m(3) occurred in 11 patients treated with abciximab (15%) and in none of those treated with eptifibatide. The inhibition of platelet adhesion to fibrinogen-coated material by abciximab and eptifibatide was similar, indicating that the reduction in platelet count with abciximab is unrelated to inhibition of platelet function.     

Administration of abciximab to patients receiving tirofiban or eptifibatide: effect on platelet function.

OBJECTIVES: The goal of this study was to evaluate platelet function and to preliminarily assess the clinical safety of sequential treatment with tirofiban or eptifibatide followed by abciximab in patients undergoing percutaneous coronary intervention (PCI). BACKGROUND: An increasing number of acute coronary syndrome (ACS) patients are treated early with tirofiban or eptifibatide. Some later require PCI and may benefit from switching to abciximab, for which long-term benefits have been reported. METHODS: Fifty ACS patients planned for PCI were enrolled. Twenty-five patients received tirofiban followed by abciximab. Ten patients received eptifibatide followed by abciximab. Fifteen patients received only abciximab. All patients had blood samples drawn six times during the therapeutic course. Platelet function was evaluated by ADP- and TRAP-induced aggregation, flow cytometry analysis of fibrinogen binding and the cone and plate(let) analyzer, which tests shear rate-dependent platelet activation. RESULTS: Administered after tirofiban, abciximab caused a significant further decline in platelet function, as evidenced by all methods. Administered after eptifibatide, abciximab caused a significant further reduction in platelet function, as assessed by the cone and plate(let) analyzer and fibrinogen binding methods. The platelet inhibition achieved by the combination therapy was always greater than or equal to that achieved by abciximab alone. There were no major bleeding or severe thrombocytopenia episodes. Three of the 35 combination therapy patients and one of the 15 who received abciximab alone had minor bleeding. CONCLUSIONS: This is the first in vivo study of combination intravenous platelet glycoprotein IIb/IIIa inhibitor therapy. Administration of abciximab immediately after tirofiban or eptifibatide therapy effectively inhibits platelet function and appears to be safe.     

Successful use of eptifibatide as an adjunct to coronary stenting in a patient with abciximab-associated acute profound thrombocytopenia

A 72-year-old male who was given abciximab for unstable angina developed acute profound thrombocytopenia with a platelet count nadir of 6,000/mm3. He was treated with steroids and platelet transfusion. Four days later, he underwent coronary angioplasty after pretreatment with eptifibatide without development of thrombocytopenia. This suggests that the development of thrombocytopenia with abciximab is not necessarily a contraindication to subsequent use of glycoprotein (GP) IIb/IIIa receptor antagonists. Eptifibatide may be an appropriate consideration in high-risk patients who would benefit from a GP IIb/IIIa receptor antagonist, in spite of acute profound thrombocytopenia due to abciximab therapy.     

Clinical correlates and course of thrombocytopenia during percutaneous coronary intervention in the era of abciximab platelet glycoprotein IIb/IIIa blockade

BACKGROUND: Thrombocytopenia is infrequently associated with abciximab therapy but may contribute to hemorrhagic risk. Factors associated with development of thrombocytopenia, the role of weight-adjustment in concomitant heparin administration, and clinical outcomes in patients with thrombocytopenia are not well defined. METHODS AND RESULTS: Pooled data from 3 placebo-controlled, randomized trials (EPIC, EPILOG, and EPISTENT) of abciximab therapy during percutaneous coronary intervention identified 178 patients (2. 4% of 7290 patients) in whom thrombocytopenia (platelet count <100 x 10(9)/L) developed after enrollment. Multivariate regression analysis identified age (>65 years; P <.001), weight (<90 kg; P =. 023), baseline platelet count (<200 x 10(9)/L; P <.001), abciximab therapy (P =.002), and enrollment into the EPIC trial (P <.001) to be associated with development of thrombocytopenia. Major and minor nonsurgical hemorrhage and transfusion were more frequent (all P <. 001) in thrombocytopenic patients. Although the primary composite clinical end point of these trials (death, myocardial infarction, or urgent revascularization to 30 days) was observed with similar frequency in patients with (11.2%) and those without (7.9%; P =.114) thrombocytopenia, 30-day mortality rate was higher in thrombocytopenic patients (8.4% vs 0.6%, respectively; P <.001). This excess mortality rate persisted after excluding patients in whom thrombocytopenia was first noted after the performance of coronary bypass surgery (4.8% vs 0.6%; P <.001). Among patients in whom thrombocytopenia developed during these trials, those who received prophylactic abciximab had fewer primary end point events (7.1% vs 23.1%; P =.056) and had a lower 30-day mortality rate (3.5% vs 15.4%; P =.048) than patients with thrombocytopenia who had received prophylactic placebo. CONCLUSIONS: Thrombocytopenia associated with abciximab therapy for percutaneous coronary intervention was more frequent in older, lighter-weight patients, those with lower baseline platelet counts, and in those patients who were enrolled into the EPIC trial. Both bleeding and transfusion events occur more frequently in patients with thrombocytopenia. Patients in whom thrombocytopenia developed during these trials had increased mortality rates to 30 days not attributable to the performance of coronary bypass surgery. Among patients with thrombocytopenia, those who received prophylactic abciximab had better clinical outcomes including survival than those who did not.     

Impact of in-hospital acquired thrombocytopenia in patients undergoing primary angioplasty for acute myocardial infarction

Thrombocytopenia that develops after percutaneous coronary intervention (PCI) may result in hemorrhagic complications, requirement for blood product transfusions, and potentially thrombotic or ischemic complications. The incidence and prognostic significance of thrombocytopenia, in patients with acute myocardial infarction (AMI) who undergo primary PCI have not been evaluated. In the CADILLAC trial 2,082 patients who had AMI within 12 hours of onset without shock were prospectively randomized to receive balloon angioplasty with or without abciximab versus stenting with or without abciximab. Acquired thrombocytopenia, defined as a nadir platelet count <100 x 10(9)/L in patients who did not have baseline thrombocytopenia, developed in 50 of 1,975 qualifying patients (2.5%) after primary PCI. By multivariate analysis, acquired thrombocytopenia developed more frequently in patients who had non-insulin-requiring diabetes mellitus (odds ratio 3.88 [OR], p = 0.0002), previous statin administration (OR 3.28, p = 0.002), and use of abciximab (OR 2.06, p = 0.02) and less frequently in patients who had previous aspirin use (OR 0.26, p = 0.002), a higher baseline platelet count (OR 1.20, p < 0.0001), and greater body mass index (OR 0.90, p = 0.006). Patients who developed thrombocytopenia versus those who did not had higher in-hospital rates of major hemorrhagic complications (10.0% vs 2.7%, p = 0.01), greater requirement for blood transfusions (10.0% vs 3.9%, p = 0.05), longer hospital stay (median 4.8 vs 3.6 days, p = 0.008), and increased costs (median dollar 14,466 vs dollar 11,629, p = 0.001). All-cause mortality was markedly increased at 30 days (8.0% vs 1.6%, p = 0.0008) and at 1 year (10.0% vs 3.9%, p = 0.03) in patients who developed thrombocytopenia. In conclusion, thrombocytopenia that develops after primary PCI for AMI, although uncommon, is associated with increased hemorrhagic complications and decreased survival.     

Efficacy of abciximab readministration in coronary intervention

Abciximab, an Fab monoclonal antibody fragment that blocks the platelet glycoprotein IIb/IIIa receptor, is increasingly used as an adjunct to coronary intervention. Little is known, however, about the efficacy and safety of readministration of abciximab. This study examined and characterized outcomes of patients receiving abciximab for a second time. From April 1995 to June 1997, 164 consecutive patients were readministered abciximab at our 3 institutions. We retrospectively examined and analyzed in-hospital outcomes in this cohort. The median time to readministration was 95 days. The angiographic success rate of percutaneous intervention was 99.5%. Rates and 95% confidence intervals of in-hospital events were death 2% (0.7% to 6.1%), myocardial infarction 3% (1% to 7%), coronary bypass surgery 0% (0% to 2.2%), and intracranial hemorrhage 2% (0.4% to 5.3%). Severe thrombocytopenia was observed in 4% of patients (1.4% to 7.8%) after readministration. Allergic or anaphylactic reactions were not observed. Major bleeding was associated with excessive concomitant antithrombotic therapy. Patients undergoing readministration of abciximab within 2 weeks of first administration experienced a higher incidence of severe thrombocytopenia (12% vs. 2%, p = 0.046). Thus, abciximab remains clinically efficacious when readministered as an adjunct to percutaneous coronary intervention. However, concomitant heparin administration must be carefully monitored and warfarin therapy should be avoided. Vigilant surveillance for thrombocytopenia should be employed. Reduced dosing may be necessary when abciximab is readministered within days of the initial administration.     

Abciximab readministration: A single-operator community-hospital experience

Abciximab, a monoclonal antibody to the platelet glycoprotein IIb/IIIa receptor, reduces ischemic complications of coronary interventions after first administration. In this study, We sought to determine whether readministration of abciximab is associated with equal efficacy and safety. We retrospectively reviewed the charts of 35 patients who received two doses of abciximab at separate intervals. We monitored patients clinically for recurrent ischemia, bleeding complications, and thrombocytopenia. We measured hemoglobin and platelet counts before and after readministration of abciximab. There was no cardiac-related death, myocardial infarction, or recurrent ischemia. No obvious bleeding occurred in any of the 35 patients, although 1 patient had a drop of hemoglobin >3 gm/dl. We observed one episode of severe thrombocytopenia without any complication, and this patient improved without requiring platelet transfusion. There was no profound thrombocytopenia. We conclude that readministration of abciximab was well tolerated without any evidence of altered efficacy or safety. Cathet. Cardiovasc. Intervent. 47:294–296, 1999. © 1999 Wiley-Liss, Inc.