FRI0095 CHANGES IN B CELL PROFILE AS INDICATOR OF CLINICAL REMISSION TO TNF INHIBITORS IN PATIENTS WITH RHEUMATOID ARTHRITIS
2019
Background Rheumatoid arthritis (RA) is a chronic inflammatory disease with the typical characteristic of synovitis of small-sized and medium-sized joints that leads to cartilage and bone damage. TNF inhibitors (TNFi) are widely used for the treatment of rheumatoid arthritis (RA) however, there are still no objective indicators of clinical response to TNFi therapy. Objectives To analyse the change of peripheral blood mononuclear cells (PBMC) profile after 6 months (m) of treatment with TNFi in order to find cellular indicators of response. Methods Prospective bi-center pilot study including 100 RA patients receiving TNFi therapy. PBMC were isolated from patients at baseline and 6m of treatment, and were analysed by flow-cytometry. Clinical activity at baseline and 6m of TNFi treatment was assessed by DAS28. Clinical remission (DAS28≤2.6) after 6m of treatment was considered as optimal response. The association between clinical remission and the percentage of change (Δ, 6m-0m) within each PBMC subset was analysed through univariate logistic regression model (odds ratio; 95% CI; β; p-value). All the analyses were adjusted by sex, age, disease duration, concomitant-methotrexate, seropositivity (ACPA and/or Rheumatoid factor) and baseline-DAS28. Results Demographic characteristics before starting TNFi therapy are shown in Table 1. After 6m of TNFi treatment, 40% patients achieved clinical remission. Decreased percentage of B cells (ΔCD19+) was found after 6m of TNFi treatment in optimal responders, while suboptimal responders did not show differences with the baseline (OR: 0.78; 95% CI: 0.63-0.97; β: -0.25; p: 0.027) (Figure 1). This effect was essentially owing to a reduction of naive B cells (OR: 0.76; 95% IC: 0.62-0.94; β: -0.27; p: 0.011) (Figure 1). No significant association was found between the other PBMC subsets (monocytes, NK cells, CD4+ T cells and CD8+ T cells) and clinical remission (Figure 1). Conclusion Our results suggest that B cells may be useful as a cellular indicator of response to TNFi in RA patients. Acknowledgement ISCIII (PI16/00474; PI16/01092) Disclosure of Interests Borja Hernandez-Breijo: None declared, Israel Nieto-Ganan: None declared, Cristina Sobrino: None declared, Victoria Navarro-Compan: None declared, ANA MARTiNEZ-FEITO: None declared, Carlota Garcia-Hoz: None declared, Paloma Lapuente-Suanzes: None declared, Javier Bachiller-Corral: None declared, Gemma Bonilla: None declared, Cristina Pijoan Moratalla: None declared, Garbine Roy: None declared, Monica Vazquez: None declared, Alejandro Balsa Grant/research support from: Abbvie, Pfizer, Novartis, BMS, Nordic, Sanofi, Consultant for: Abbvie, Pfizer, Novartis, BMS, Nordic, Sanofi, Sandoz, Lilly, Paid instructor for: Pfizer, Speakers bureau: Pfizer, Novartis, UCB, Nordic, Sanofi, Sandoz, Lilly, Luisa Maria Villar: None declared, DORA PASCUAL-SALCEDO Grant/research support from: Pfizer, Speakers bureau: Pfizer, Abbvie, Takeda, Eulalia Rodriguez-Martin: None declared, Chamaida Plasencia Speakers bureau: Pfizer, MSD
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