Q J Med 2002; 95: 635-636
© 2002 Association of Physicians
Correspondence |
Abciximab-induced thrombocytopenia
Division of Cardiology, University Hospital of Wales, Cardiff
Sir,
Abciximab is a potent platelet glycoprotein IIb/IIIa receptor antagonist, currently indicated as adjunctive therapy during percutaneous coronary intervention and acute coronary syndromes. Potential future indications include acute myocardial infarction, peripheral arterial disease and ischaemic stroke, thus more widespread use is likely in the future. We present a case which highlights one of its major complications.
A 55-year-old man with a 7-day history of chest pain was admitted to hospital; investigations suggested an established anteroseptal myocardial infarction. He was commenced on low molecular weight heparin, aspirin, oral nitrates, atenolol and simvastatin. He continued to complain of anginal pain and a Bruce Protocol exercise test was positive after 3 min. He was then referred to our institution for further investigation. Examination on arrival was unremarkable, and routine bloods were normal, including a platelet count of 199x109/l. Clopidogrel was commenced in addition to the existing therapy.
At angiography, a severe lesion in the left anterior descending artery was successfully stented, and abciximab was commenced with intravenous heparin at a rate of 7 IU/kg/h until abciximab infusion was completed, and then continued at 14 IU/kg/h. Approximately 4 h later, a medical review was sought, as the patient had started to ooze from his gums. Samples were sent for a coagulation profile; coagulation was normal but the platelet count was 4x109/l. The platelet count was repeated from samples taken with EDTA and citrate as the anticoagulant, to exclude EDTA-dependent pseudothrombocytopenia, and again the platelet count was 3x109/l. Abciximab and heparin were therefore discontinued, as were the aspirin and clopidogrel. One unit of platelets was given immediately, and the platelet count improved to 21x109/l. During the remainder of the patient's admission, three further units of platelets were required to correct the thrombocytopenia. On discharge the platelet count was 196x109/l.
The incidence of acute profound thrombocytopenia (platelet count <20x109/l) following abciximab, is cited as 0.3–0.69% after a first exposure,1 2% if administered for a second time, and greater still if readministered within 2 weeks.2 Typically, the thrombocytopenia occurs within 2–4 h after commencing treatment1 and resolution is usually seen after 5–10 days.
Predictors of thrombocytopenia include older age (>65 years), lower body weight (<80 kg) and lower baseline platelet count (<200x109/l).2 The proposed mechanism is an antibody-mediated reaction directed against a currently unknown target; platelet damage occurring as a consequence of complement activation. In this case, the use of heparin therapy raises the possibility of heparin-induced thrombocytopenia (HIT), which is well recognized as being the most frequent drug-induced thrombocytopenia, with an approximate frequency of 1–2%.3 However, HIT typically develops after 6–10 days of heparin use, whereas our patient had received LMWH for 9 days, and had a platelet count of 199x109/l at that time. HIT is also an immune-mediated response, with formation of antibodies which are usually directed against platelet factor 4 (PF4)/heparin complexes.4 On the advice of the haematologist, samples were sent for these antibodies and were negative.
A final differential diagnosis would be thrombotic thrombocytopenic purpura/haemolytic uraemic syndrome induced by clopidogrel;5 this is unlikely, as the coagulation profile remained within the normal range, excluding a consumptive coagulopathy. We therefore conclude that the severe thrombocytopenia reported here was abciximab-induced.
References
1. Coller B. Anti-GPIIb/IIIa drugs: current strategies and future directions. Thromb Haemost2001; 86:427–43.[Web of Science][Medline]
2. Madan M, Kereiakes D, Hermiller J, Rund M, Tudor G, Anderson L, Mcdonald M, Berkowitz S, Sketch M, Phillips H, Tcheng J. Efficacy of abciximab readministration in coronary intervention. Am J Cardiol2000; 85:435–40.[Web of Science][Medline]
3. Weimann G, Lubenow N, Selleng K, Eichler P, Albrecht D, Greinacher A. Glucosamine sulfate does not cross-react with the antibodies of patients with heparin-induced thrombocytopenia. Br J Haematol2001; 66:195–9.
4. Baumgärtel M, Eichler P, Glöckner M, Ranze O, Greinacher A. Heparin-induced thrombocytopenia (HIT): in vitro and in vivo cross-reactivity to danaparoid sodium and successful treatment with recombinant hirudin (lepirudin). Eur J Haematol2000; 65:148–9.[Medline]
5. Bennett CL, Connors JM, Carwile JM, et al. Thrombotic thrombocytopenic purpura associated with clopidogrel. N Engl J Med2000; 342:1773–7.
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