Background Treatment of rheumatoid arthritis (RA) has been revolutionized by the introduction of tumor necrosis factor inhibitors (TNFi). Nonetheless a significant proportion of patients fails to respond (primary failure) or may lose the initial response over time (secondary failure). Subsequent treatment for the patients who experienced secondary failure yet needs to be defined, particularly, as to whether a second TNFi or an alternative biological agent (non- TNFi), should be used.
Objectives With the aim to assess and compare the efficacy of second TNFi versus non-TNFi after secondary failure to the first TNFi, we obtained data from patients with secondary failure who had started treatment with biologics from 2010 to 2015.
Methods A pro-forma has been given to patients with secondary failure who were on either second TNFi or non-TNFi either in clinic or sent by post. Patients were excluded if they had missing or incomplete data, if the nature of the failure was unclear or if the treatment was changed due to infection, cancer, hepatitis, tuberculosis (TB) or Multiple Sclerosis (MS). Response was assessed by ACR20. Additionally, the clinical notes were reviewed and scrutinised aiming to gather as accurate as possible information on patients' clinical assessments. The response to treatment following secondary failure was further analysed according to the presence or absence of Rheumatoid Factor (RF) and Anti-CCP Antibodies (aCCP).
Results Data from a total of 109 patients were obtained. 43 patients (M:F =1:3) were included in the analysis. Patient's mean age was of 61 years (SD ±10). From those patients excluded, 16 patients had incomplete data, 13 had unclear data, 19 patients had infection, 11 had cancer, 4 had hepatitis, 2 had TB, and 1 had MS. From the 43 patients analysed 20 were on a second TNFi [6 on Adalimumab (ADA), 5 on Certolizumab (CZP), 5 on Etanercept (ETA), 4 on Golimumab (GLM)] while 23 were on non-TNFi [12 on Rituximab (RTX), 6 on Tocilizumab (TCZ), 5 on Abatacept (ABT)].
A total of 24 of 43 patients (46.5%) responded to treatment after secondary failure. Of these, 8 patients (of 20; 40%) were from the TNFi group and 16 (of 23; 70%) from the non- TNFi group (p=0.05). Among the TNFi group, the response rate was 16% (1/6) for ADA, 60% (3/5) for CZP, 40% (2/5) for ETA, 50% (2/4) for GLM. In the non-TNFi group, the response rate was 75% (9/12) for RTX, 67% (4/6) for TCZ and 60% (3/5) for ABT.
When stratifying the response according to the presence or absence of RF or aCCP, seropositive patients showed significantly better response to non-TNFi compared to TNFi (70% vs 33%; p=0.03). Looking at responses according to drugs used after secondary failure, all patients who were seronegative responded to CZP and ABT (100% response) while seropositive patients showed 90% response to RTX.
Conclusions Secondary failures to TNFi overall respond better to non-TNFi compared to second TNFi, especially if they are seropositive.Further studies are needed in order to guide the accurate pharmacological interventions.
Disclosure of Interest None declared
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