Clinical responses to tumor necrosis factor α antagonists do not show a bimodal distribution: Data from the Stockholm Tumor Necrosis Factor α Followup Registry
Article first published online: 3 JUN 2003
Copyright © 2003 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 48, Issue 6, pages 1500–1503, June 2003
How to Cite
van Vollenhoven, R. F. and Klareskog, L. (2003), Clinical responses to tumor necrosis factor α antagonists do not show a bimodal distribution: Data from the Stockholm Tumor Necrosis Factor α Followup Registry. Arthritis & Rheumatism, 48: 1500–1503. doi: 10.1002/art.11027
- Issue published online: 3 JUN 2003
- Article first published online: 3 JUN 2003
- Manuscript Accepted: 24 FEB 2003
- Manuscript Received: 28 OCT 2002
- Swedish Rheumatism Association
To study the distribution of clinical responses to treatment with the tumor necrosis factor α (TNFα) antagonists etanercept and infliximab, and in particular, to determine whether there is a biologically meaningful distinction between responders and nonresponders.
Among patients in the Stockholm TNFα Followup Registry, we analyzed the clinical responses to etanercept and infliximab, using the American College of Rheumatology (ACR) core set of outcome measures. For each parameter, the absolute change (value at baseline − current value) and the percentage change ([absolute change]/[value at baseline] × 100) from baseline were calculated. The results were plotted as histograms and inspected visually, and the distributions were statistically compared with computer-generated normal distributions.
Absolute and relative changes in outcomes on the ACR core set of measures in 406 patients receiving etanercept or infliximab were studied. All but a few of these analyses yielded normal or somewhat skewed distributions. The statistical analyses did not detect any non-normal distributions, and visually, the distributions did not appear to be bimodal.
The clinical response to TNFα blockade displays a normal or skewed, but not bimodal, distribution. The frequently encountered perception that a clear distinction can be made between responders and nonresponders is not borne out. These relatively straightforward findings imply that the biologic mechanisms determining responsiveness to TNFα blockade are multifactorial and may also have important implications for regulatory guidelines pertaining to treatment with these biologic agents.