Platelet dysfunction and inhibition of multiple electrode platelet aggregometry caused by penicillin
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CASE REPORT
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Platelet dysfunction and inhibition of multiple electrode platelet aggregometry caused by penicillin Christian Schulz*, Olga von Beckerath, Rainer Okrojek, Nicolas von Beckerath, Steffen Massberg Abstract Beta-lactam antibiotics, e.g. penicillin, may inhibit platelet function and lead to reduced response in light transmission aggregometry and adhesion. However, influence on platelet function tests more commonly used in clinical practice, such as multiple electrode platelet aggregometry (MEA), have not been described so far. We report a case of a patient with local streptococcus infection. Treatment with penicillin resulted in mild bleeding tendency after 3 days. While coagulation parameters were normal, assessment of platelet function by MEA revealed strong platelet inhibition of both ADP and arachidonic acid induced platelet aggregation comparable to normal responders to antiplatelet therapy. Change of antibiotic regime resulted in recovery of platelet function. Thus, penicillin therapy may impact on platelet function and consecutively commonly used platelet function assays, e.g. MEA. Case report Inhibition of platelet function in the presence of beta-lactam antibiotics was first described decades ago. In the first documented report in 1973, Cazenave et al. found that beta-lactam antibiotics (BLA), e.g. penicillin, inhibit all major types of platelet functions in vitro, such as secretion, adhesion and also aggregation [1]. Postulated mechanisms are inhibition of agonist-stimulated platelet calcium influx [2], and impairment of agonist binding to their specific receptors on the platelet surface [3]. Importantly, penicillin binds irreversibly to platelets [4]. This results in a dose- and time-dependent effect of BLA on platelet function in animals and humans, which occurs within 24 to 72 hours after therapy induction [4-6]. A 46-year old female patient presented to our clinic with a perimandibular abscess following surgical removal of a third molar. The patient had no medical therapy upon admission. Despite elevated inflammation parameters other blood tests were normal. The patient was treated with surgical drainage and intravenous penicillin (12 million IU/day) because of local infection with penicillin-sensitive streptococcus species. Due to swelling of the neck and jaw the patient required mechanical * Correspondence: [email protected] Deutsches Herzzentrum and 1. Medizinische Klinik, Klinikum rechts der Isar, Technische Universität München, Munich, Germany
ventilation for three days. In addition to antibiotic therapy, the patient received fentanyl and midazolam intravenously for analgo-sedation, and enteral feeding by tube. On postoperative day 3 bleeding tendency during invasive procedure (routine placement of arterial catheter) was noticed. Platelet counts (174000 [150000450000]/μl), partial thromboplastin time (PTT 31 [25-39] sec) and international normalized ratio (INR 1.0) were normal. However, multiple electrode platelet aggregometry (MEA)[7] revealed significant inhibition in
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