AI Article Synopsis
- Anti-TNF-alpha therapies are commonly used for rheumatoid arthritis (RA), but around 40% of patients do not respond effectively to the treatment, prompting this study.
- Researchers examined two specific genetic variations to see if they were linked to RA susceptibility and treatment response among 78 RA patients and 70 healthy individuals.
- The study found no link between these genetic variations and RA risk, but identified a significant connection between one genetic variant (TNFRSF1B-M196R) and a poorer response to infliximab therapy, suggesting further research is required to validate these findings.
Article Abstract
Objective: Anti-TNF-alpha therapies are widely used in rheumatoid arthritis (RA) patients. Despite their clearly proven efficacy, some discrepancies were observed in the treatment response with 40% of non-responder patients. The aim of this study is to determine whether two functional single-nucleotide polymorphisms, V212F in the FCGR3A, and M196R in the TNFRSF1B genes correlate with rheumatoid arthritis susceptibility and response to anti-TNF-alpha therapy.
Methods: The population study was composed of a French cohort of 78 RA patients and 70 healthy controls. Allele and genotype frequencies were compared between patients and controls, according to their response to infliximab therapy, using the American College of Rheumatology (ACR) response criteria.
Results: No association was found between these two SNPs and RA susceptibility. A significant correlation was found between 196R allele carriers and low response to infliximab therapy.
Conclusion: This is the first report of a statistically significant association between the TNFRSF1B-M196R SNP and response to infliximab in a French cohort. Larger studies are needed to confirm the relevance of this association.
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