Thromboembolism in patients with malignancy.

摘要

It is well known that malignancy is often associated with a hypercoagulable state. Malignant cells may express procoagulant activity, such as cancer procoagulant and tissue factor, which can unswervingly trigger thrombin production. Additionally, normal host cells (monocytes, platelets, and endothelial cells) may also express or release procoagulants in response to the tumour. Cell adhesion moiety p-selectm, is an important activator of haemostatic mechanisms, which is originated in the alpha granules of platelets and the Weibel-Palade bodies of endothelial cells. Studies in animal models have demonstrated that high plasma levels of p-selectin exhibit prothrombotic activity and also represent an independent predictor of venous thromboembolism in cancer patients. Although mononuclear phagocytes are essentially lacking of any procoagulant activity, they may be triggered by tumour necrosis factor (TNF) and produce tissue factor (TF) and other direct factor X activators, which may modulate immunologic, inflammatory, and haemostatic processes but also promote tumour growth and dissemination.