WEDNESDAY, SEPTEMBER 28, 2016

Pradaxa could increase risk of viral infections

Researchers at the University of North Carolina have recently found that the newly approved blood thinner Pradaxa, which blocks a key component of human blood clotting, could increase the risk of some viral infections.

The U.S. Food and Drug Administration recently gave approval to the drug Dabigatran etexilate, known as Pradaxa. The drug inhibits thrombin, which is the body's coagulation activator.

In blocking thrombin, Pradaxa disturbs the protease cascade of molecular events that would naturally happen in coagulation. This has been shown to have an unintended consequence.

"Our findings show that blocking thrombin reduces the innate immune response to viral infection," Nigel Mackman, the John C. Parker distinguished professor of medicine in the division of hematology and director of the UNC McAllister Heart Institute, said. "The use of the new generation of blood thinners might increase the risk and severity of flu and myocarditis."

Viral infections like dengue fever trigger the coagulation system, which has previously been thought to be harmful. This effect, however, helps the body activate immune cell macrophages, which boosts the immune system.

"The results we generated were completely unexpected and in fact our hypothesis was that PAR-1 deficient mice would be protected from viral myocarditis because they would have reduced inflammation," Mackman said. "We are now determining if the traditional long term anticoagulant warfarin has the same effect on viral infection or is this specific to the new blood thinner."

The study was a collaboration between the Mackman group at UNC and Charité - Universitätsmedizin in Berlin, Germany, along with other groups at UNC.