PT - JOURNAL ARTICLE AU - Julio Ramírez AU - José Luis Fernández-Sueiro AU - Raquel López-Mejías AU - Carlos Montilla AU - Maite Arias AU - Concepción Moll AU - Mercé Alsina AU - Raimon Sanmarti AU - Francisco Lozano AU - Juan D. Cañete TI - <em>FCGR2A/CD32A</em> and <em>FCGR3A/CD16A</em> Variants and EULAR Response to Tumor Necrosis Factor-α Blockers in Psoriatic Arthritis: A Longitudinal Study with 6 Months of Followup AID - 10.3899/jrheum.110980 DP - 2012 Apr 01 TA - The Journal of Rheumatology PG - jrheum.110980 4099 - http://www.jrheum.org/content/early/2012/03/25/jrheum.110980.short 4100 - http://www.jrheum.org/content/early/2012/03/25/jrheum.110980.full AB - Objective The efficacy of antibody-based biological therapies currently used in psoriatic arthritis (PsA) depends not only on their blocking effect on the targeted molecule but also on their binding affinity to genetically defined variants of cell-surface Fc-γ receptors. Our objective was to assess the potential influence of functionally relevant FCGR2A/CD32A (H131R) and FCGR3A/CD16A (V158F) genetic polymorphisms on the EULAR response to tumor necrosis factor-α (TNF-α) blocker therapy in PsA. Methods In total 103 patients with PsA starting anti-TNF-α therapy were included. The efficacy of therapy was evaluated according to EULAR response criteria at 3 and 6 months. FCGR2A-R131H and FCGR3A-F158V polymorphisms were genotyped. Potential correlations between clinical response and the FCGR2A-R131H and FCGR3A-F158V polymorphisms were evaluated. Results EULAR response (moderate plus good) was 85.4% at 3 months and 87.4% at 6 months, while good EULAR response was 61.2% and 62.1%, respectively. More patients with high-affinity FCGR2A genotypes (homozygous or heterozygous combinations) achieved a EULAR response at 6 months compared to patients with the low-affinity genotype (RR; p = 0.034, adjusted comparison error rate &lt; 0.025). This association was due mainly to the group of patients treated with etanercept. No correlation was found for the FCGR3A polymorphism. Similarly, no effect of C-reactive protein levels was observed. Conclusion Our data indicate that FCGR2A polymorphism may influence the response to TNF-α blockers (namely etanercept) in PsA in a direction opposite to that previously found in patients with rheumatoid arthritis.