Biomarker Could Help Doctors Tailor Treatment for Rheumatoid Arthritis
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Biomarker Could Help Doctors Tailor Treatment for Rheumatoid Arthritis

NEW YORK -- January 29, 2010 -- Investigators have identified a biomarker that could help doctors select patients with rheumatoid arthritis who will benefit from therapy with drugs such as etanercept. The study appears in the February issue of the journal Arthritis & Rheumatism.

“While our study was performed on a relatively small group of patients and will need to be confirmed in a larger cohort, the data are promising and may be clinically significant for the medical management of patients,” said Mary K. Crow, MD, Mary Kirkland Center for Lupus Research at Hospital for Special Surgery, New York, New York.

“Treatment with these drugs is very expensive … if you are going to use them, you would like to know that they are likely to work in your patient.”

While studies have identified factors associated with poor response to these drugs such as expression of certain genes, none of the factors has yet provided doctors with a tool that will help select patients who are likely to respond to the drugs or identify those less likely to respond.

Previous studies have shown that different levels of interferon beta (IFN-beta) are present in the joint tissue of some patients with rheumatoid arthritis. The researchers wondered if variable levels of this protein could play a role in how patients respond to treatment.

To test this hypothesis, Dr. Crow and colleagues set out to determine the relationship between levels of type 1 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), they also tested levels of IL-1Ra.

The study involved 3 cohorts of patients: patients who had rheumatoid arthritis and received a tumour necrosis factor (TNF) antagonist (n = 35), patients with rheumatoid arthritis who received no drug (n = 12), and healthy volunteers (n = 50).

Outcomes were evaluated during a window of therapy consisting of more than 3 months but fewer than 9 months, allowing for sufficient time for clinicians to determine clinical response. Researchers used the Disease Activity Score in 28 joints to deem whether patients had a moderate, good, or no response to the drug.

The investigators found that patients with higher baseline levels of type 1 IFN were more likely to respond to therapy with TNF antagonists. Patients who had an increased IFN-beta/alfa ratio 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 TNF antagonists and who might be less likely to be a responder,” said Dr. Crow. “For those who demonstrate low levels of blood interferon activity, that information might be useful to guide patients to alternative treatments that might be more likely to work for them.”

SOURCE: Hospital for Special Surgery

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