Scientists from Hospital for Special Surgery and University of Southern California have identified a biomaker that may help personalise rheumatoid arthritis treatment for patients.
While tumour necrosis factor (TNF)-antagonist drugs such as Enbrel has brought relief to thousands of people with rheumatoid arthritis, the drugs are not highly effective in 30 percent to 50 percent of patients.
Clinicians thus run the risk of providing a therapy to patients that doesn't work well, is expensive and is potentially toxic. Patients taking TNF antagonists, which have been available for roughly ten years, can run the risk of developing bacterial or fungal infections.
In the new study, researchers focused on type I interferon proteins, specifically a type called interferon beta (IFN-beta).
Previous studies have revealed that levels of IFN-beta, a protein that can limit cell division, is present in the joint tissue of some patients with rheumatoid arthritis.
The researchers sought to determine if variable levels of this protein could play a role in how patients respond to TNF-antagonist drugs.
They studied the relationship between levels of type I interferon activity in the blood prior to beginning therapy and the ability of the drug to control rheumatoid arthritis in patients.
They studied the role of IFN-beta, and because they knew that IFN-beta induces interleukin-1 receptor antagonist (IL-1Ra), another protein, they also tested levels of IL-1Ra.
The investigators found that patients with higher baseline levels of type I IFN were more likely to respond to therapy with TNF antagonists.
Patients, who had an increased IFN-beta/alpha ratio, meaning they had more IFN-beta, were also more likely to respond to therapy.
They also observed significantly higher baseline levels of IL-1Ra in plasma samples from good responders as compared with those from nonresponders or moderate responders.
"We have drawn attention to a potential biomarker that, if our results are supported by additional future studies in other patient populations, might provide a tool to predict who might be a responder to this class of biologic rheumatoid arthritis therapies, the TNF antagonists, and who might be less likely to be a responder," said Dr Mary K. Crow, director of Rheumatology Research and co-director of the Mary Kirkland Center for Lupus Research at Hospital for Special Surgery.