Erythrocyte sedimentation rate, C-reactive protein level, and serum amyloid A protein for patient selection and monitoring of anti–tumor necrosis factor treatment in ankylosing spondylitis
Article first published online: 29 OCT 2009
Copyright © 2009 by the American College of Rheumatology
Arthritis Care & Research
Volume 61, Issue 11, pages 1484–1490, 15 November 2009
How to Cite
de Vries, M. K., van Eijk, I. C., van der Horst-bruinsma, I. E., Peters, M. J. L., Nurmohamed, M. T., Dijkmans, B. A. C., Hazenberg, B. P. C. and Wolbink, G. J. (2009), Erythrocyte sedimentation rate, C-reactive protein level, and serum amyloid A protein for patient selection and monitoring of anti–tumor necrosis factor treatment in ankylosing spondylitis. Arthritis & Rheumatism, 61: 1484–1490. doi: 10.1002/art.24838
- Issue published online: 29 OCT 2009
- Article first published online: 29 OCT 2009
- Manuscript Accepted: 23 JUN 2009
- Manuscript Received: 25 NOV 2008
- Investigation was facilitated by the Clinical Research Office of the Jan van Breemen Institute, which receives financial support from the Dutch Arthritis Foundation
To study the usefulness of erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and serum amyloid A (SAA) for response prediction and monitoring of anti–tumor necrosis factor (anti-TNF) treatment in ankylosing spondylitis (AS) patients.
Patients were included consecutively before starting etanercept or infliximab treatment. ASsessment in Ankylosing Spondylitis (ASAS) response, defined as a 50% improvement or an absolute improvement of 2 points of the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI; 0–10 scale), was assessed at 3 months. Inflammatory markers and the BASDAI were collected at baseline and 1 and 3 months. Longitudinal data analysis was performed to compare associations between inflammatory markers and the BASDAI over time by calculating standardized betas. Predictive values of baseline levels of inflammatory markers for ASAS response were calculated.
In total, 155 patients were included, of whom, after 3 months of treatment, 70% in the etanercept cohort and 71% in the infliximab cohort responded. All markers, notably SAA, decreased significantly (P < 0.0001). Standardized betas were 0.49 for ESR, 0.43 for CRP, and 0.39 for SAA. Normal baseline levels of CRP and SAA were significantly associated with nonresponse. A combination of elevated CRP and SAA levels at baseline revealed the highest predictive value (81%) for ASAS response.
ESR, CRP, and SAA were significantly associated with the BASDAI over 3 months, and the association with ESR was the strongest. Elevated baseline CRP and SAA levels revealed the highest predictive value for response. Together, this study demonstrates that inflammatory markers, and notably CRP and SAA, may facilitate patient selection and monitoring of efficacy of anti-TNF treatment in AS, and could be added to response criteria.