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Study: Pradaxa May Up the Risk, Severity of Viral Infections

Filed April 3rd, 2013 edlieber1

The blood thinner Pradaxa may increase the risk and severity of viral infections, including the flu, a new study suggests.

Researchers at the University of North Carolina also found that Pradaxa can lead to an increased risk of myocarditis, an infection that can cause sudden death in young children, said.

Pradaxa was recently approved by the U.S. Food and Drug Administration (FDA) as competition for warfarin, which had the run of the blood-thinning market for 50 years.

Pradaxa works by inhibiting the body’s central coagulation activator of the blood clotting system. By blocking thrombin activity, the drug disturbs the protease cascade of molecular events that normally occurs in coagulation, said. Although clot formation is condensed, the study revealed it may also reduce the innate immune response to viral infection.

For the study, researchers used mice in which the PAR-1 gene was deleted and subjected to infection with a virus that causes myocarditis, said. They found that “loss of PAR-1 mediated signaling after infection with the cardiotrophic virus resulted in increased viral buildup in the heart, cardiac injury and, later, increased impairment of heart function,” said.

The researchers then treated normal mice with Pradaxa. Results showed that thrombin inhibition amplified cardiac virus load and cardiac injury after viral infection in a similar manner to a deficiency of PAR-1, said. In addition, they infected the PAR-1 deficient mice with the flu and found that PAR-1 signaling was key in controlling the virus load in the lung during the early stages after infection. These results indicate that thrombin and PAR-1 arbitrate important early antiviral signals after infection, said


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