Share on Facebook
Share on Twitter
Share on LinkedIn
Share by Email
Print
At the European League Against Rheumatism Annual Congress (EULAR 2014), a potential biomarker of response to anti-TNF therapies in patients with rheumatoid arthritis (RA) has been identified, which could lead to the personalization of RA treatment.
Participants from the Biologics in Rheumatoid Arthritis Genetics and Genomics Study Syndicate (BRAGGSS) longitudinal cohort with an extreme response phenotype after 3 months of treatment with etanercept or adalimumab were included in this study. Patients with an endpoint of DAS28 <2.6 were considered good responders, while those with an improvement of <0.6 or between 0.6–1.2 with an endpoint DAS28 >5.1 were considered poor responders to treatment.
RELATED: Arthritis Treatments: DMARDS and Other Immune Modulators
Prior to therapy initiation, DNA was sampled from each patient. Unmethylated vs. methylated cytosines in the DNA were evaluated. The most differentially methylated position in etanercept patients mapped to the LRPAP1 gene (P=1.46×10-8) and the PDZD8 gene in adalimumab patients. In analyzing the drugs together, a differentially methylated region overlapping the CRYZ and TYW3 genes was noted; this has been previously associated with inflammation and type 2 diabetes.
Only 20–40% of patients with RA achieve a good response to anti-TNF therapies, but the discovery of the biomarker DNA methylation can assist in identification of optimal response treatments in the future.
For more information visit EULAR.org.
