The University of North Carolina has revealed results from a study on Pradaxa. The study finds that Pradaxa may give patients an increased risk of viral infections such as the flu and myocarditis. Myocarditis is a potentially fatal infection that has caused death in children and young adults. In addition to increased risk of developing viral infections, Pradaxa patients may also suffer increased severity after infected.
A number of research teams collaborated on the study, including the Charité – Universitätsmedizin in Berlin, Germany. The teams did not anticipate discovering Pradaxa’s role in increasing viral infection risk. The finding was discovered during an investigation of the body’s response to viruses as seen on a cellular level.
Pradaxa and the Blood
Pradaxa is an anticoagulant drug used to treat patients with a condition called atrial fibrillation that affects the heart’s ability to pump blood. By thinning the blood, Pradaxa helps to improve blood flow for these patients. Pradaxa works by inhibiting a substance called thrombin. Thrombin is an enzyme that significantly contributes to blood clotting.
Senior author Nigel Mackman, PhD states: “Our findings show that blocking thrombin reduces the innate immune response to viral infection.” By blocking thrombin, Pradaxa essentially also blocks the body from its full potential of fighting infections.
Clotting’s Role in Fighting Infection
Mackman explained that viral infections trigger coagulation of the blood. Coagulation is the body’s process used to form blood clots. At first, researchers assumed that this bodily reaction was problematic. However, further investigation shows that this coagulation process gives the immune system a helpful boost. Additional studies on bacterial infections show evidence of clotting proteins’ benefits for the immune system.
Fibrin, a clotting protein that is formed by thrombin, was believed to activate special cells in the immune system. These cells help to attack and digest bacteria, viruses, and other pathogens that can cause harm to the body. However, studies later showed that thrombin was responsible for this antiviral action, not fibrin. Evidence shows that thrombin triggers the body’s immune response because it activates a cell receptor called PAR-1.
Pradaxa Clinical Studies
Mackman’s team deactivated PAR-1 in mice to investigate the findings. After infecting the mice with the myocarditis virus, the virus showed increased buildup in the heart. Additionally, the heart function of the mice showed increased impairment. The absence of PAR-1 also suggested a slower immune response following infection. Mackman states: “Pradaxa might not only facilitate significant lifesaving effects in reducing cardiac death, but may also interfere with other processes in the body.”
These findings contribute to the already-troublesome list of Pradaxa risks. In 2011, roughly 4,000 patients reported severe side effects from Pradaxa use. Additionally, hundreds of lawsuits have been filed against manufacturer Boehringer Ingelheim.