Forty percent of people who develop venous thromboembolism don’t know what caused it.
In a new study, researchers further explored inflammation’s role in this dangerous blood clot disease.
Their findings may help solve the mystery of how to detect and deal with higher-than-usual clot risk in patients’ veins.
The research was conducted by Michigan Medicine scientists.
It’s the third deadliest cardiovascular diagnosis, but doctors are still often stumped to explain why 40% of patients experience unprovoked venous thromboembolism (VTE).
And after a patient has dealt with these dangerous blood clots once, a second clot becomes much more likely.
In the study, the team focused on clots’ relationship to the body’s defense and repair system, which causes inflammation.
Their work aimed to identify and block a previously unrecognized pathway linking inflammation and thrombosis.
Some combination of coagulation and inflammation triggers VTE.
But current treatments come up short because they only focus on one side of the equation: anticoagulation. After VTE, patients have often prescribed blood thinners for life.
The team instead examined inflammation’s role in the development of deep vein thrombosis.
They found an enzyme called CD39 diffused circulating “danger” signals and inflammatory cytokines in blood during thrombosis.
FDA-approved drugs already exist for other conditions that are affected by the same pathway, and in particular, the paradigmatic inflammatory cytokine molecule called interleukin-1 beta.
In fact, when the researchers inhibited those interleukin-1 signals in their study, they reduced the number and size of venous blood clots the animals formed.
This means that blocking interleukin 1 signals was a powerful means to stop dangerous clotting.
According to the team, treatment guidelines recommend lifelong blood thinners for people who have had an unprovoked clot, but anticoagulation carries other risks, like bleeding and can be burdensome for patients.
Some of the people at the highest risk have underlying disorders that tend to cause inflammation, including autoimmune disorders like lupus or Crohn’s disease.
One author of the study is Yogen Kanthi, M.D., a vascular cardiologist at U-M’s Frankel Cardiovascular Center.
The study is published in the Journal of Clinical Investigation.
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