@article {Fabris1847, author = {Martina Fabris and Barbara Tolusso and Emma Di Poi and Roberta Assaloni and Luigi Sinigaglia and Gianfranco Ferraccioli}, title = {Tumor necrosis factor-alpha receptor II polymorphism in patients from southern Europe with mild-moderate and severe rheumatoid arthritis.}, volume = {29}, number = {9}, pages = {1847--1850}, year = {2002}, publisher = {The Journal of Rheumatology}, abstract = {OBJECTIVE: To define the frequency of the exon 6 tumor necrosis factor-alpha (TNF-alpha) receptor II (TNFRII) gene polymorphism in severe and mild-moderate rheumatoid arthritis (RA) and its possible influence on anti-TNF-alpha treatment responsiveness. METHODS: Two cohorts of patients with RA, the first (n = 97) defined as methotrexate responders (MTX-R) with mild-moderate synovitis, and the second (n = 78) defined as nonresponders to combination therapy and receiving anti-TNF-alpha treatment because of their severe and aggressive disease (TNF-T), were studied retrospectively and compared to age, sex, and ethnically matched controls (n = 84). In the prospective study, 66 patients with severe RA were followed over the first 6 months of anti-TNF-alpha therapy and their response was examined according to genotype. RESULTS: We observed a trend towards an increased frequency of the GG genotype in patients with severe RA (6.4\%) in comparison with patients with mild-moderate disease (3.1\%) and controls (1.2\%). When looking at the response to anti-TNF-alpha therapy, we observed that after 12 weeks of treatment, 37.8\% of the TT versus 10.7\% of the TG/GG patients passed from high to medium-low disease activity (p = 0.03). CONCLUSION: In our cohorts of patients selected by response to the conventional therapy and by disease severity, our preliminary study results showed a trend towards a higher prevalence of the GG genotype for the exon 6 TNFRII polymorphism in the less responsive patients with more aggressive disease. We also found a lower degree of response to anti-TNF-alpha treatments in patients carrying the G allele.}, issn = {0315-162X}, URL = {https://www.jrheum.org/content/29/9/1847}, eprint = {https://www.jrheum.org/content/29/9/1847.full.pdf}, journal = {The Journal of Rheumatology} }