Background/Purpose: It is still difficult to completely prevent the progression of joint destruction with any of the currently available biologics. It has been reported that baseline CRP may predict early improvement of synovitis and bone erosion by TCZ therapy¹⁾. However, only a few reports have described whether TCZ may prevent joint destruction for a long period of time in clinical settings.

 TCZ was administered for 3 years to identify risk factors for the progression of joint destruction in clinical settings and utilize the data to build treatment plans in RA patients.

Methods: TCZ was administered at a dose of 8 mg/kg every 4 weeks in combination with DMARDs including methotrexate. The effect on joint destruction was assessed on the basis of X-ray findings at baseline and year 3 of treatment using the modified total Sharp score (mTSS). Statistical analysis was performed using chi-square tests and Wilcoxon tests.

Results and Conclusion: Among 57 patients registered, 51 patients evaluable with X-ray were assessed. At baseline, patients were 53.5 years in average, had suffered from RA for 10.9 years, and had a DAS28-ESR of 5.31 and an mTSS of 100.6. Biologic-experienced patients at baseline accounted for 66%, and PSL users 68.6%. One patient received TCZ as monotherapy. The mean DmTCC at year 3 was 1.0, and the structural remission rate (i.e., percentage of patients with DmTCC <1.5/3y) was 75%. A comparison of patients with and without progressive joint destruction revealed significant differences in CRP and ERS at baseline. Baseline CRP was 3.6 and 1.2 in patients with and without progressive joint destruction, respectively (p = 0.024). Logistic regression analysis revealed that the cut-off point of baseline CRP was 2.8 (specificity 92.1%; sensitivity 46.5%; p=0.003). The mean DmTSS values at year 3 in patients above and below the cut-off value were compared in groups of biologic-naïve patients and biologic-experienced patients. The mean DmTSS was -0.3 for biologic-naïve patients with CRP <2.8, and 0.3 for those with CRP ³2.8, indicating that TCZ prevented joint destruction regardless of inflammation status (P=0.739). In biologic-experienced patients, the mean DmTSS was 0.2 for those with CRP <2.8, and 8.0 for those with CRP ³2.8, with a significant difference between the two subgroups (p=0.011). This significantly higher score in the latter subgroup may be explained by the presence of severe inflammation not controlled with previous treatment as well as the higher DAS28-ESR, swollen joint count and ESR at baseline (p<0.05). 

 Long-term treatment with TCZ prevented joint destruction of RA patients, and a high structural remission rate was obtained. Our findings suggest that TCZ, if given to biologic-naïve patients, may strongly prevent the progression of joint destruction regardless of inflammation status.

Reference

1) ARTHRITIS AND RHEUMATISM Vol.62 No.10 Sup. P.S49-S50 (2010.10)

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/long-term-treatment-with-tocilizumab-tcz-strongly-suppresses-joint-destruction-in-biologic-naive-patients-with-rheumatoid-arthritis-ra-regardless-of-inflammation-status/