FCGR2A/CD32AandFCGR3A/CD16AVariants and EULAR Response to Tumor Necrosis Factor-α Blockers in Psoriatic Arthritis: A Longitudinal Study with 6 Months of Followup

Abstract

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 relevantFCGR2A/CD32A(H131R) andFCGR3A/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 andFCGR3A-F158V polymorphisms were genotyped. Potential correlations between clinical response and theFCGR2A-R131H andFCGR3A-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-affinityFCGR2Agenotypes (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 < 0.025). This association was due mainly to the group of patients treated with etanercept. No correlation was found for theFCGR3Apolymorphism. Similarly, no effect of C-reactive protein levels was observed.Conclusion.Our data indicate thatFCGR2Apolymorphism 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.