The influence of bevacizumab on platelet function

Area of Science:

• Oncology
• Pharmacology
• Hematology

Background:

• Systemic bevacizumab is linked to increased arterial and venous thromboembolism and hemorrhage.
• The underlying pathophysiological mechanisms, particularly concerning platelet function, require investigation.

Purpose of the Study:

• To investigate the impact of bevacizumab on platelet adhesive and aggregatory functions.
• To determine if altered platelet function contributes to thromboembolic events associated with bevacizumab therapy.

Main Methods:

• In vitro study: Blood from 10 healthy volunteers incubated with bevacizumab and vascular endothelial growth factor.
• Clinical observation study: Assessed platelet function analyzer (PFA-100®) closure times and soluble P-selectin levels in 20 cancer patients treated with bevacizumab.
• Evaluated platelet activation and aggregation using PFA-100® and sP-selectin as a marker.

Main Results:

• No significant changes in PFA-100® closure times were observed in the in vitro study.
• Mean PFA-100® closure times remained unchanged in patients after bevacizumab treatment.
• Soluble P-selectin levels decreased by 18% (p = 0.045) post-bevacizumab infusion, suggesting potential platelet inhibition.

Conclusions:

• The study data do not support the hypothesis that increased platelet activation, adhesiveness, or aggregation by bevacizumab are key mechanisms for clinical thrombus formation.
• Bevacizumab may exert an inhibitory effect on platelets, as indicated by decreased sP-selectin levels.