Ramot Y, Nyska A, Spectre G, et al.
Drug safety. Date of publication 2013 Aug 1;volume 36(8):585-603.
1. Drug Saf. 2013 Aug;36(8):585-603. doi: 10.1007/s40264-013-0054-6.
Drug-induced thrombosis: an update.
Ramot Y(1), Nyska A, Spectre G.
Author information:
(1)Hadassah-Hebrew University Medical Center, P.O. Box 12000, 91120, Jerusalem,
Israel. yramot@gmail.com
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.
DOI: 10.1007/s40264-013-0054-6
PMID: 23640658 [Indexed for MEDLINE]
