Dr. Townsend emphasized that the samples don’t fall neatly into discrete groups, but rather are described according to their place in the “continuum of pathophysiology.”
Researchers have found that synovial samples with the myeloid phenotype are elevated in those with an ACR50 response to anti-TNF-alpha (infliximab) therapy.
They then delved further and found that the ICAM-1 gene is associated with an enhanced response to anti-TNF-alpha therapy and the CXCL13 gene is linked with an enhanced response to anti-IL-6 (tocilizumab) therapy. Dr. Townsend added that this is just the beginning of the effort to find more specific markers.
“We don’t think that all the targeted therapies work in the same patients,” he said. “Different mechanisms may work optimally in different patients….This work’s ongoing to build better predictive marker profiles.”
These findings might show a way forward to improve upon the very similar response rates—most drugs tend to achieve ACR50 rates in the 40% range—that have been seen with biologic therapies, he said.
“Do we want to develop another drug that does the same as what is already there?”
Thomas R. Collins is a freelance medical writer based in Florida.
References
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- Van Nies JAB, Tsonaka R, Gaujoux-Viala C, et al. Evaluating relationships between symptom duration and persistence of rheumatoid arthritis: Does a window of opportunity exist? Results on the Leiden Early Arthritis Clinic and ESPOIR cohorts. Ann Rheum Dis 5 Jan 2015 [Epub ahead of print].
