THU0186 Infliximab VS Etanercept: the Importance of Immunogenicity and Serum Drug Monitoring in Clinical Practice

Background Treatment with tumor necrosis factor (TNF) inhibitors in rheumatoid arthritis (RA) patients is based on the principle 'one size fits all', but different immunogenicity of these drugs has a profound effect on pharmacokinetics and clinical response [1]. Objectives To measure infliximab (INF) and etanercept (ETA) drug level and presence of antidrug antibodies (ADAb) and to investigate clinical response and its relationship to drug immunogenicity and disease modifying anti-rheumatic drug (DMARD) association. Methods Thirty nine patients with moderate or high disease activity RA, treated with INF or ETA were evaluated for 6 months. Their clinical characteristics, DMARD association and serum drug and ADAb level were measured at baseline. Clinical activity and improvement at 4 months were measured using DAS28 score and EULAR response criteria. Results Ninety percent of patients treated with INF had concomitant DMARD, compared to 73.6% in ETA group. Eleven (45%) out of 20 patients treated with INF had ADAb: 7 patients had undetectable INF level, and 2 patients - subtherapeutic INF drug level. The presence of ADAb has correlated negatively with DMARD association in INF group (r=-0.492, P=0.027). In ETA treated patients, no ADAb were found. For both biologics, detectable drug level correlated with EULAR response at 4 months (for INF: r=0.701, P=0.001; for ETA: r=0.550, P=0.018). The association of a DMARD correlated with detectable serum INF (r=0.459, P=0.042) and a better EULAR response in patients treated with INF (r=0.468, P=0.038). Conclusions Our study confirms the difference in anti TNF drug's immunogenicity and the importance of adding a DMARD to INF therapy. Also, therapeutic drug monitoring can be used to predict further clinical response. References Meghna Jani, Anne Barton RBW et al. The role of DMARDs in reducing the immunogenicity of TNF inhibitors in chronic inflammatory diseases. Rheumatol. (Oxford, England) Augv14. 2013; Disclosure of Interest : None declared DOI 10.1136/annrheumdis-2014-eular.4828