Drug-induced thrombosis: an update

Abstract

Drugs may play an important role in development of thrombosis, and in recent years there has been increased attention to the importance of this issue. Although drug-induced thrombosis usually causes venous thrombotic events, arterial events are also noted due to drug administration. Here we review the different mechanisms through which drugs can exert thrombosis. Drugs can cause direct endothelial damage and expose the underlying subendothelium thus leading to platelet adherence and subsequent thrombus formation. Such an effect is seen by contrast media and chemotherapeutic cytotoxic drugs. Drugs may also attenuate the secretion of pro- and anticoagulation mediators by the endothelial cells and may have prothrombotic effects on platelets by increasing adhesion and aggregation, as for example seen after heparin administration in an immune-mediated mechanism. Red and white cells can also be affected by drugs, by increasing their aggregation or adhesion to the endothelial wall. Some drugs, such as oral contraceptive pills, may promote thrombosis by altering the balance between the different coagulation factors, and many drugs can lead to decreased blood flow by increasing blood viscosity, as seen for example after intravenous immunoglobulin administration. Better understanding of the mechanisms through which drugs exert thrombosis may facilitate their safe use in patients. Additionally, awareness of the drugs that are known to induce thrombosis is important in order to stop their administration in case of a thrombotic event. This review further emphasizes the fact that drug administration is a risk factor that should always be considered together with additional known thromboembolic risk factors such as genetic predisposition or cancer.