Researchers in Australia have identified a potentially important link between the excess production of inflammatory proteins that cause rheumatoid arthritis and the development of heart valve disease.
The Walter and Eliza Hall Institute team were able to identify critical regions of DNA that control production of the inflammatory protein TNF (tumour necrosis factor), the overproduction of which has been known for years to contribute to the development of rheumatoid arthritis.
Excess TNF causes immune cells to damage the joints and keeps the body in a perpetual state of inflammation. This new study – published in the Proceedings of the National Academy of Sciences – showed the same process also leads to inflammation and disease of the heart valves, including aneurysms.
In addition, the researchers identified a previously unknown way in which the body destabilises molecules during the process of TNF production, potentially opening the door for new agents to be created that can prevent excess TNF levels from building up.
This could be a viable alternative to current anti-TNF therapies, which have proven a hugely effective way of treating arthritis, but can sometimes lose efficacy as patients develop immunity.
Study leader Dr Philippe Bouillet, a researcher from the Walter and Eliza Hall Institute, said: “This is the first time that we have linked the overproduction of TNF to heart valve disease.
“While it seems that genetics makes a substantial difference to the severity of the heart disease in our models, it does suggest that in humans we may be able to better diagnose heart valve disease in people with rheumatoid arthritis in the future.”
A spokesman for Arthritis Research UK, which pioneered and developed anti-TNF therapy for rheumatoid arthritis, said: “We know that people with rheumatoid arthritis have an increased risk of heart disease, and that anti-TNF therapy, although important, doesn’t work for everyone.
“This is an interesting new finding that requires further investigation to find to more about the link between TNF and this specific type of heart disease.”