Article first published online: 31 AUG 2011
Copyright © 2011 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 63, Issue 9, page 2834, September 2011
How to Cite
Klaasen, R., Wijbrandts, C. A., Gerlag, D. M. and Tak, P. P. (2011), Reply. Arthritis & Rheumatism, 63: 2834. doi: 10.1002/art.30461
- Issue published online: 31 AUG 2011
- Article first published online: 31 AUG 2011
- Accepted manuscript online: 25 MAY 2011 11:01AM EST
To the Editor:
We would like to thank Dr. Shin and colleagues for their interest in our work. Based on circumstantial evidence, they suggest that activation of T cells in response to leptin might result in diminished clinical improvement in obese patients treated with infliximab. It should be noted that leptin may also stimulate monocytes (1), and together, these may promote a proinflammatory state (2). We previously found that increased inflammation in RA synovial tissue is predictive of a better response to infliximab treatment (3–5). Based on these findings, we would not predict that a state of increased inflammation is related to a decreased clinical response, but we cannot exclude the possibility that results may be different in peripheral blood compared to the synovium. We can only resolve this interesting issue in future studies by directly examining the relationship of obesity, leptin, and sIL-2R with the clinical response to infliximab treatment.
Smoking can increase sIL-2R levels and has been associated with a diminished clinical response to anti- TNFα therapy, which led Dr. Shin and colleagues to question whether smoking was a possible confounder in our study. The percentages in each BMI group of patients who smoked were 26% in responders (Disease Activity Score in 28 joints [DAS28] ≥1.2) and 31% in nonresponders (DAS28 <1.2). When smoking status at baseline was included in the statistical analysis, no influence on our results was found.
Dr. Tak has received consulting fees from Abbott, Centocor, Schering-Plough, and Wyeth (less than $10,000 each).
- 1High-dose leptin activates human leukocytes via receptor expression on monocytes. J Immunol 2001; 167: 4593–9., , , , , , et al.
- 2Towards a pro-inflammatory and immunomodulatory emerging role of leptin. Rheumatology (Oxford) 2006; 45: 944–50., , , , , , et al.
- 3The relationship between synovial lymphocyte aggregates and the clinical response to infliximab in rheumatoid arthritis: a prospective study. Arthritis Rheum 2009; 60: 3217–24., , , , , , et al.
- 4Responsiveness to anti-tumour necrosis factor α therapy is related to pre-treatment tissue inflammation levels in rheumatoid arthritis patients. Ann Rheum Dis 2008; 67: 563–6., , , , , , et al.
- 5The clinical response to infliximab in rheumatoid arthritis is in part dependent on pretreatment tumour necrosis factor α expression in the synovium. Ann Rheum Dis 2008; 67: 1139–44., , , , , , et al.
Ruth Klaasen MD*, Carla A. Wijbrandts MD, PhD*, Danielle M. Gerlag MD, PhD*, Paul P. Tak MD, PhD*, * Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.