Lack of response to anakinra in rheumatoid arthritis following failure of tumor necrosis factor α blockade

MH Buch, SJ Bingham, Y Seto… - Arthritis & …, 2004 - Wiley Online Library
MH Buch, SJ Bingham, Y Seto, D McGonagle, V Bejarano, J White, P Emery
Arthritis & Rheumatism, 2004Wiley Online Library
Objective. In patients with rheumatoid arthritis (RA) treated with tumor necrosis factor α
(TNFα)–blocking therapy, there is heterogeneity of response. This raises the possibility that
in certain circumstances, cytokines such as interleukin‐1 (IL‐1) may dominate the drive
toward joint inflammation. This study was undertaken to investigate whether blocking the
action of IL‐1 with an IL‐1 receptor antagonist (IL‐1Ra) is efficacious in patients with
disease that did not respond to TNFα blockade. Methods. We identified 26 RA patients …
Objective
In patients with rheumatoid arthritis (RA) treated with tumor necrosis factor α (TNFα)– blocking therapy, there is heterogeneity of response. This raises the possibility that in certain circumstances, cytokines such as interleukin‐1 (IL‐1) may dominate the drive toward joint inflammation. This study was undertaken to investigate whether blocking the action of IL‐1 with an IL‐1 receptor antagonist (IL‐1Ra) is efficacious in patients with disease that did not respond to TNFα blockade.
Methods
We identified 26 RA patients whose disease had failed to respond to TNFα‐blocking therapy, defined as failure to achieve or sustain a 20% improvement in disease activity according to the criteria of the American College of Rheumatology (ACR20 response). These patients were then treated with anakinra (100 mg/day subcutaneously) for 12 weeks, and their levels of response were assessed.
Results
After 3 months of anakinra therapy, only 2 of 26 patients (8%) achieved an ACR20 response; none achieved an ACR50 or ACR70 response. A rise in the mean C‐reactive protein level and an increase in the mean swollen joint count were noted during the study period.
Conclusion
This study demonstrates that patients with disease that fails to respond to TNFα blockade also do not respond to IL‐1Ra. These data do not provide evidence of a dominant role for IL‐1 in patients who do not respond to TNFα blockade, but they do not exclude a role for other proinflammatory mediators.
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