Genes might explain why some patients with rheumatoid arthritis respond better to anti-TNF therapy than others, according to research presented this week at the American College of Rheumatology Annual Scientific Meeting in San Francisco, Calif.
Rheumatoid arthritis is a chronic disease that causes pain, stiffness, swelling, and limitation in the motion and function of multiple joints. Though joints are the principal body parts affected by RA, inflammation can develop in other organs as well. An estimated 1.3 million Americans have RA, and the disease typically affects women twice as often as men.
Drugs known as tumor necrosis factor, or TNF, inhibitors are often prescribed to individuals with rheumatoid arthritis. They work by targeting and blocking the inflammation, and can help reduce pain, morning stiffness, tender and swollen joints, limit damage to the joints and improve function.
Treatment strategies used in blocking tumor necrosis factor have been very successful in treating patients with RA. For reasons that are unknown, significant numbers of these patients do not respond to this type of treatment, and there are currently no means by which to identify these patients in advance of treatment.
While all cells in an individual contain the same genetic material, different cells may produce, or express, differing amounts of individual genes.
Researchers analyzed the gene expression in the white blood cells of 42 Dutch patients with RA prior to starting TNF inhibitor therapy. They identified patterns in gene expression levels in a group of 34 genes that were associated with responsiveness to anti-TNF therapy. These genes included the inflammatory genes PTGS2, EGR1, IL8 and IL28A. Researchers also identified a gene that showed a decrease in expression of two particular gene components, called exons, in patients who did not respond to anti-TNF medications, in comparison to those who did.
This gene expression analysis was also studied in 30 U.S. patients with RA, confirming that lack of response to anti-TNF treatment is associated with a low expression of these two exons. This suggests that the particular gene expression patterns in RA patients may serve as new biomarkers for predicting response to therapy with anti-TNF drugs.
“Patients with rheumatoid arthritis are often treated with medication directed to tumor necorsis factor alpha, anti-TNF therapy,” explains Marieke Coenen, PhD; Nijmegen Centre for Molecular Life Sciences and Institute of Genetic and Metabolic Disease, research lab for multifactorial diseases, division of DNA-diagnostics, department of human genetics, Radboud University Nijmegen Medical Centre, Nijmengen, The Netherlands, and lead investigator in the study. “Given the extremely high costs of anti-TNF therapy and the risk of adverse effects, it would be beneficial to predict whether an individual patient will benefit from this treatment, beforehand. In this study we identified a gene that might be used to determine which patients will respond to anti-TNF treatment.”
Patients should talk to their rheumatologists to determine their best course of treatment.
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