Abciximab-induced Thrombocytopenia Research Articles

Abciximab-induced thrombocytopenia: Correct management

Thrombocytopenia is a possible side effect of routinely administered medical agents. Abciximab is one of the three potent intravenous glycoprotein IIb/IIIa receptor inhibitors (along with eptifibatide and tirofiban) that have shown significant positive outcomes when used in patients with intracoronary thrombus. The use of abciximab was associated with the risk of thrombocytopenia. This case reported the development of thrombocytopenia and treatment management after using abciximab.

Delayed severe abciximab-induced thrombocytopenia: A case report

BackgroundThrombocytopenia is a possible side effect of routinely administered medical agents widely used in the management of patients with acute coronary syndromes (ACS). It is usually observed within 24 h after abciximab infusion. Differential diagnosis is challenging and the management controversial. MethodsWe present a case of abciximab-induced thrombocytopenia which occurred after a standard treatment. ResultsA 57-year-old male was admitted with ST-segment elevation ACS. Coronary angiography revealed an acute occlusion of the diagonal branch by massive thrombus. The patient was administered clopidogrel and acetylsalicylic acid followed by unfractionated heparin and abciximab according to the current guidelines. A rapid progression of thrombocytopenia up to 1 × 109/L was observed. A total of 5 pooled platelet units were transfused and intravenous dexamethasone. Dual antiplatelet therapy was continued. ConclusionAlthough specific mechanisms of abciximab-related thrombocytopenia are still unclear and the management is not well established, the patient responded well to the therapy and his recovery was uneventful.

ABCIXIMAB INDUCED THROMBOCYTOPENIA – “TWO CASES OF A KIND”

ABCIXIMAB INDUCED THROMBOCYTOPENIA – “TWO CASES OF A KIND”

Abciximab‐Induced Thrombocytopenia: Management of Bleeding in the Setting of Recent Coronary Stents

This case report and subsequent literature review describes the management difficulties in a patient who developed abciximab-induced thrombocytopenia and gastrointestinal bleeding. Abciximab was used to treat the no-reflow phenomenon, which occurred during insertion of three sequential Taxus coronary artery stents. Resuscitation of this bleeding patient with fluids, blood, and platelet transfusion, and the cessation of antiplatelet agents, was complicated by acute stent thrombosis. We discuss the risk factors for stent thrombosis and discuss abciximab-induced thrombocytopenia, looking at its incidence, pathophysiology, differential diagnosis, investigation, course, management, preventative strategies, and prognostic implications.

A Case of Abciximab Induced Acute Profound Thrombocytopenia Resulting in Compartment Syndrome of the Forearm from Massive Bleeding at the Brachial Artery Access Site

Abciximab is one of the glycoprotein IIb/IIIa receptor inhibitors, and it is known to be effective for preventing and treating the thrombotic complications of percutaneous coronary intervention (PCI). On the other hand, there is an increasing risk of hemorrhagic complications when using abciximab, especially in the case of abciximab-induced thrombocytopenia. Acute profound thrombocytopenia is a rare, but life threatening adverse reaction to abciximab, and it can even occur within a few hours of the first exposure. We report here on a case of 56 yearold woman who experienced massive bleeding of her brachial artery access site. This was caused by abciximab-induced acute profound thrombocytopenia after performing PCI concomitant with using abciximab. (Korean Circ J 2007;37:594-598)

Detection and Mechanisms of GPIIb-IIIa Antagonist Induced Thrombocytopenia: Role for Antibody Induced Platelet Activation.

After the administration of GPIIb-IIIa antagonists, 1 – 3% of patients become thrombocytopenic, and 0.5 – 1% of patients develop profound thrombocytopenia. This GPIIb-IIIa antagonist-induced thrombocytopenia may be antibody mediated. In this study we demonstrated that GPIIb-specific monoclonal antibody 5B12 augmented platelet activation, as determined by platelet surface P-selectin and leukocyte-platelet aggregation) in the presence of therapeutic concentrations of abciximab, but not epitifibatide or tirofiban. Furthermore, the GPIIIa-specific monoclonal antibody Y2/51 augmented platelet activation in the presence of therapeutic concentrations of eptifibatide or tirofiban, but not abciximab. This activation was abolished by an FcγRII receptor (CD32)-specific antibody and was absent when Fab fragments 5B12 or Y2/51 were used. These results suggest that (i) GPIIb-IIIa antagonists cause conformational changes in GPIIb-IIIa; resulting in (ii) antibody binding to GPIIb-IIIa; and, consequently (iii) platelet activation via the FcγRII receptor. To determine whether this mechanism is operative in vivo, plasma from patients who developed abciximab-induced thrombocytopenia (n=2), eptifibatide-induced thrombocytopenia (n=5) and normal donors (n=7) was incubated with ABO Rh matched donor whole blood with and without therapeutic concentrations of GPIIb-IIIa antagonists. Platelet activation was assessed by flow cytometric measurement of platelet surface P-selectin. Abciximab, but not eptifibatide or tirofiban, increased platelet surface P-selectin in patients who developed abciximab-induced thrombocytopenia. Eptifibatide, but not abciximab or tirofiban, increased platelet surface P-selectin in patients who developed eptifibatide-induced thrombocytopenia. Platelet surface P-selectin in normal donors was not changed by abciximab, tirofiban or eptifibatide. These data (i) provide novel insight into the mechanisms of GPIIb-IIIa antagonist induced thrombocytopenia; and (ii) suggest a possible assay for the clinical diagnosis and prediction of this phenomenon.Platelet surface P-selectin after addition of a GPIIb-IIIa antagonist (% baseline fluorescence). *p<0.05AbciximabEptifibatideTirofibanNormal donors10310599Eptifibatide-induced thrombocytopenia103170 *104Abciximab-induced thrombocytopenia1571 *108105

Delayed thrombocytopenia after treatment with abciximab: a distinct clinical entity associated with the immune response to the drug

Acute thrombocytopenia is a recognized side-effect of treatment with the fibrinogen receptor antagonist, abciximab, a chimeric (human/mouse) Fab fragment. The etiology of this complication is not fully understood. Generally, abciximab-induced thrombocytopenia occurs within a few hours of starting treatment with the drug. We have characterized a group of 13 patients who first developed thrombocytopenia 3-6 days after abciximab was discontinued. To characterize clinical and serological aspects of this newly recognized clinical entity. Clinical information was obtained from attending physicians and review of hospital records. Antibodies reactive with abciximab-coated platelets were characterized by flow cytometry. In each patient, IgG and/or IgM antibodies reactive with abciximab-coated platelets were identified. These antibodies could be distinguished from similar antibodies present in many normal persons by two criteria-they were relatively resistant to inhibition by normal Fab fragments, and they reacted preferentially with platelets coated with 7E3, the murine monoclonal antibody from which peptide sequences in abciximab are derived. Antibodies with these characteristics were not found in pretreatment serum from three of the thrombocytopenic patients or in patients given abciximab who did not develop thrombocytopenia. 'Delayed thrombocytopenia' after treatment with abciximab is caused by antibodies produced in response to the drug. These antibodies may be specific for murine peptide sequences in abciximab but could recognize other target epitopes on abciximab-coated platelets. Physicians administering abciximab should be aware of this potential complication of treatment, which usually occurs after discharge from hospital.

Delayed thrombocytopenia following abciximab therapy.

Inhibitors of glycoprotein (GP) IIb/IIIa are currently approved for the treatment of acute coronary syndromes and during performance of percutaneous coronary interventions (PCIs). More than 500 000 patients annually undergo PCIs in the USA alone. Of these, 35% are receiving GPIIb/IIIa inhibitors. Currently, three different intravenous GPIIb/IIIa inhibitors are commercially available. Profound thrombocytopenia occurs almost exclusively with abciximab. Usually thrombocytopenia develops within 24 hours following abciximab administration. This paper describes three patients who developed delayed profound thrombocytopenia, occurring five days following abciximab therapy. These cases of thrombocytopenia were self-limited and reversible. Absence of serious bleeding complications was noted. The pathophysiology, differential diagnosis, natural history and management of the coronary patients with abciximab-induced thrombocytopenia are discussed.

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 x 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.

Mechanism proposed for abciximab-induced thrombocytopenia

Mechanism proposed for abciximab-induced thrombocytopenia