Key result
Intravenous penicillin therapy caused significant inhibition of platelet function, reducing MEA AUC to 250 for ADP and 109 for arachidonic acid, comparable to the effects of antiplatelet therapy.
Why the study?
Does intravenous penicillin inhibit platelet function as measured by multiple electrode platelet aggregometry?
Case Report (n=1)
No
Does intravenous penicillin inhibit platelet function as measured by multiple electrode platelet aggregometry?
High-dose intravenous penicillin therapy can cause significant platelet inhibition that mimics the effects of antiplatelet therapy on multiple electrode platelet aggregometry (MEA).
Answers are grounded in this paper and cite their sources.
Clinicians should consider recent penicillin when interpreting MEA; single case leaves open bleeding risk implications.
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.
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Schulz et al. (2010) conducted a case report in Perimandibular abscess with local streptococcus infection (n=1). Penicillin was evaluated on Platelet function assessed by multiple electrode platelet aggregometry (MEA) area under the curve (AUC) in response to ADP and arachidonic acid (AA). Intravenous penicillin therapy caused significant inhibition of platelet function, reducing MEA AUC to 250 for ADP and 109 for arachidonic acid, comparable to the effects of antiplatelet therapy.
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