NSAIDs May Increase Risk of VTE
Researchers have found there is a statistical significance between NSAID use and VTE.
NSAID Use and the Risk of VTE
Medscape reports, nonsteroidal anti-inflammatory drugs (NSAIDs) may increase the risk two-fold for venous thromboembolism, or VTE. The risk includes deep venous thrombosis as well as pulmonary embolisms.
According to Patompong Ungprasert, MD, from the Bassett Medical Center and Columbia University College of Physicians and Surgeons, New York City, and colleagues, “The results of our meta-analysis demonstrate a statistically significantly increased VTE risk among NSAID users. Physicians should be aware of this association and NSAIDs should be prescribed with caution, especially in patients at high baseline risk of VTE”.
The research performed was the first systematic review and meta-analysis of published observational studies that examined the correlation between NSAIDs and VTE.
Researchers were unable to use randomized clinical trials for analysis because the complication is too rare, thus requiring use of observational studies instead. The studies were conducted between 2007 and 2013 in the United Kingdom, France, the Netherlands, Denmark, and Sweden.
Break Down of NSAID Analysis
In their final analysis, researchers used 6 out of 597 potential published studies, which represented 21,401 VTE incidents. The findings reported odds ratios, relative risks, hazard ratios, or standardized incidence ratios for VTEs in comparisons between NSAID users and nonusers.
1 cohort (n= 19,293; 215 events) and 5 case-controls studies (cases, 21,186; controls, 110,824) were used in the studies. NSAID users were found to have a pooled risk ratio of 1.8-fold based on 95% confidence interval ranging from 1.28-2.52. The pooled risk ratio in patients who used selective cyclooxygenase 2 (COX-2) inhibitors was 1.99 based on 95% confidence interval ranging from 1.44-2.75. Therefore, the two measures were statistically significant.
Aspirin, a COX-1 inhibitor, is shown to be effective in VTE prevention leading researchers to believe the increased VTE risk may come from COX-2 inhibitors. Researchers stated, “Inhibition of the COX-2 enzyme has been shown to inhibit the synthesis of prostacyclins, potent platelet activation inhibitors, while stimulating the release of thromboxane, a potent platelet aggregation facilitator, from the activated platelets. The activation and aggregation of platelets might, in turn, induce a coagulation cascade and clotting, with the widespread use of these medicines, this increased risk may have important public health implications”. However, the method of risk for VTE is still uncertain.
Factors that can affect the validity of the studies include a publication bias, heterogeneity among the studies, and inability to show cause and effect.