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FRI0204 Comparison the long-term clinical outcomes between nontnf-inhibitors versus tnf-i in ra patients who failed to a first tnf-i
  1. P Bogas1,
  2. C Plasencia1,
  3. D Pascual-Salcedo2,
  4. G Bonilla1,
  5. E Moral1,
  6. C Tornero1,
  7. L Nuño1,
  8. A Villalba1,
  9. D Peiteado1,
  10. A Martinez2,
  11. B Hernandez2,
  12. A Balsa1
  1. 1Rheumatology
  2. 2Immunology, Hospital Universitario la Paz, Madrid, Spain

Abstract

Background There are many biological therapies for Rheumatoid Arthritis (RA) with different mechanisms of action and good efficacy rate; however, up to 40% of patients (pts) fail to respond to the 1st biologic agent, and it is still not clear what strategy to follow after showing inadequate response to tumor necrosis factor α inhibitors (TNF-i)

Objectives To assess the clinical response and survival (SVV), in our cohort of RA pts that discontinued the 1st TNF-i, of a 2nd TNF-i vs a nonTNF-i, both in the global cohort and in the subpopulation that dropped out the 1st TNF-I due to inefficacy

Methods This observational study included 110 pts in the RA-Paz cohort who previously suspended Ifx (68%) or Ada (32%) between 1999–2016. Two groups were established as they switched to a TNF-i or nonTNF-i. Clinical response was evaluated by DAS28, Delta-DAS28 (ΔDAS28) and EULAR response (E-resp). The assessments were performed at 6 (v-6) and 12 months (v-12) since initiating 2nd biological agent and during the last visit prior to drug discontinuation or ending of the study for those who did not interrupt the drug (v-end). Statistical analysis was performed using SPSS version 20.0

Results Of the 110 pts who had stopped Ifx or Ada as 1st TNF-i, 65% changed to a 2nd TNF-i. The 84% of the overall pts were women. The mean age was 64±14 years and the mean time of 2nd biologic drug was 3.71±3.51 years. 61% associated methotrexate at the beginning of 2nd biologic agent and 56% at the v-end, without differences between those who switched to TNF-i and those who did to nonTNF-i. At v-6 and v-12, there was no difference in ΔDAS28 [at v-6:1.3±1.4 in TNF-i and 1.2±1.2 in nonTNF-i (p=0.919), at v-12: 1.3±1.5 in TNF-I and 1.2±1.1 in nonTNF-i (p=0.852)]. In contrast, at v-end, pts with nonTNF-i showed a higher clinical improvement (ΔDAS28: 0.68±1.7 in TNF-i, 1.8±1.1 in nonTNF-i, p=0.002). At v-6, the TNF-i group achieved higher good E-resp rate (41% vs 18%, p=0.035), but there was no difference at v-12 (36% in TNF-I vs 23% in nonTNF-i, p=0.435). However, at v-end, the nonTNF-I group achieved better E-resp (good resp: 38% in nonTNF-i vs 25% in TNF-I, no resp 18% in nonTNF-i vs 50% in TNF-i, p=0.01). Likewise, 100% (n=7) of the pts that finished 2nd biologic agent by remission, had changed to a nonTNF-i (p<0.00001). There were no differences regarding 2nd biologic drug SVV (mean SVV time of 5.7±0.66 in TNF-I, 4.3±0.59 in nonTNF-i, p=0.797). When analyzing the cohort that discontinued 1st TNF-I because of inefficacy, at v-6 and v-12 there were no differences between switchers to TNF-I and nonTNF-i in ΔDAS28 [v-6: 1.4±1.4 vs 0.9±1 p=0.164); v-12: 1.5±1.4 vs 1±1, p=0.192)], but at v-end, the nonTNF-i group reached a higher ΔDAS28 (0.9±1.5 in TNF-i, 1.6±1 in nonTNF-i, p=0.031)

Conclusions In our sample of RA patients who suspended Ifx/Ada as 1st TNF-i, switching to a 2nd biologic agent did not show relevant clinical differences between a TNF-i and a nonTNF-i within the 1st year of treatment. However, in the long-term, switching to a nonTNF-i shows enhanced clinical benefits with no impact on survival vis-à-vis a 2nd TNF-i. Despite the efficacy of TNF-i, new therapeutic targets are needed for those who fail to respond to these biological agents

Disclosure of Interest None declared

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