Severe thrombocytopenia after an infusion of abciximab
Rubio Antonio, González
Consuelo, Majado Maria Juliana, Salido Eduardo, García-
Candel Faustino, *González-Carrillo Josefa.
Servicios de Hematología y *Cardiología. Hospital V.
Arrixaca. Murcia.
Correspondence: Majado Maria Juliana. E-mail: mjmajado@huva.es
A case of severe acute thrombocytopenia related to Abciximab
therapy in a patient after coronary stent placement is presented,
emphasizing the importance of thinking about this rare
complication. The incidence of this adverse event in our hospital
seems lower (0.3%) than reported. The abciximab treatment (AT) in
acute coronary syndromes has proved to be of significant clinical
value, preventing ischemic complications and improving patient
outcome during acute coronary syndromes and after percutaneous
transluminal coronary angioplasty (PTCA) interventions, The AT is
associate with rare cases of severe acute thrombocytopenia (SAT),
less than 1%.1 SAT can produce excessive
bleeding,2 increasing the risk of hemorrhagic
complications in PTCA. A 82 year old male, with previous several
episodes of unstable angina and a coronariographic study showing
an obstruction in right coronary artery and severe lesion of left
coronary trunk, was submitted to our hospital for PTCA and
stenting, after a new episode of angina. The intervention on his
right anterior descending coronary artery lasted 26 min and was
without incidences. He was treated during the procedure with
ticlopidine 250 mg bolus, heparin 5000 units bolus, and
nitroglicerin 0.4 mg intracardiac. Prevention of acute thrombosis
was performed with abciximab (Reopro, Lilly-Dista) 0,25 mg/k bolus
and 10 microg/min/12h. Baseline platelet count (PC) was normal.
Two hours after the start of AT, PC dropped to 11x109/L in EDTA-,
citrate- and heparin- anticoagulated blood samples. AT was
discontinued. Two hours later PC was 3x109/L and 8
units of platelets were transfused. On the seventh hour post-PTCA
the PC was 25x109/L and other 8 units of random donor
platelets were given. After that the PC improved, reaching
110x109/L in the next 12 hours. The patient remained
all time stable, without bleeding signs, so 24 h after PTCA he was
discharged. Abciximab is the fragment Fab of the chimeric
monoclonal antibody c7E3, directed against the glycoprotein
IIb/IIIa platelet surface receptor, inhibiting platelet activation
and aggregation. SAT during AT is due to a rare idiosyncratic
reaction, but incidence, mechanisms and clinical relevance are not
still clear and data are limited. AT potentially results in
significant alterations of platelet surface that might alter the
adhesive properties of platelets with subsequent sequestration and
development of SAT.3 In a review of the
literature,4, the PC nadir ranged
1-16x109/L, appeared within 2-31 hours after AT,
platelet transfusions were useful in increasing the platelet level
in less than 24 hours, but Immunoglobulins IV were useless.
Pseudothombocytopenia is present in 1/3 of these
patients.5 Other causes of thrombocytopenia, as heparin
related thrombocytopenia, need to be excluded. Although severe
bleeding complications are usually no observed,6 fatal
cases have been reported.7.
In our institution, from last April to December, more than 1100 PTCA were made and, in a total of 334 patients who had received AT, this is the only case of SAT we have had. Although the incidence of SAT related to AT is very low; we have to bear its abrupt onset in mind, because it is unpredictable and the use of this drug is likely to be growing. So we have to emphasize the importance of monitoring PC after initiating AT to avoid hemorrhagic episodes.
