Abstract Background: In systemic inflammatory diseases, thrombotic complications often cannot be fully explained by traditional risk factors, suggesting that the immune system directly affects hemostasis. The complement system, particularly C1q (the recognition molecule of the classical complement pathway), has been shown to enhance primary hemostasis in vivo and to bind von Willebrand factor (vWF) in vitro. Aim: To investigate the role of the C1q-vWF interaction in human primary hemostasis.