A strong initial systemic inflammatory response is associated with higher corticosteroid requirements and longer duration of therapy in patients with giant-cell arteritis
Article first published online: 7 FEB 2002
Copyright © 2002 by the American College of Rheumatology
Arthritis Care & Research
Volume 47, Issue 1, pages 29–35, February 2002
How to Cite
Hernández-Rodríguez, J., García-Martínez, A., Casademont, J., Filella, X., Esteban, M.-J., López-Soto, A., Fernández-Solà, J., Urbano-Márquez, Á., Grau, J. M. and Cid, M. C. (2002), A strong initial systemic inflammatory response is associated with higher corticosteroid requirements and longer duration of therapy in patients with giant-cell arteritis. Arthritis & Rheumatism, 47: 29–35. doi: 10.1002/art1.10161
- Issue published online: 7 FEB 2002
- Article first published online: 7 FEB 2002
- Manuscript Accepted: 19 JUL 2001
- Manuscript Received: 23 MAR 2001
- Fondo de Investigación Sanitaria. Grant Numbers: (FIS 98/0443, FIS 00/0689)
- Fundació Pedro Pons
- Inflammatory response;
- Giant-cell arteritis;
To assess whether the intensity of the initial systemic inflammatory response is able to predict response to therapy in patients with giant cell arteritis (GCA).
Retrospective review of 75 patients (49 women and 26 men) with biopsy-proven GCA who had regular followup and were treated according to uniform criteria. Four parameters were used to evaluate the baseline inflammatory response at diagnosis: fever, weight loss, erythrocyte sedimentation rate ≥ 85 mm/hour, and hemoglobin < 110 gm/liter. Patients were considered to have a weak inflammatory response if they had 2 or fewer inflammatory parameters (group 1) and a strong inflammatory response if 3 or 4 parameters were present (group 2). Time required to achieve a maintenance dose of less than 10 mg prednisone/day was recorded and analyzed by the Kaplan–Meier survival analysis method. Tumor necrosis factor α (TNFα) and interleukin 6 (IL-6) serum levels were also determined in 62 patients and 15 controls.
Forty patients had a weak (group 1) and 35 had a strong (group 2) initial inflammatory response. Patients in group 2 had significantly higher levels of circulating TNFα (31.9 ± 16.8 versus 22.3 ± 9 pg/ml; P = 0.01) and IL-6 (28.2 ± 17.4 versus 16.6 ± 13 pg/ml; P = 0.004) than patients in group 1. In group 1, 50% of patients required a median of 40 weeks (95% CI 37–43) to reach a maintenance dose of <10 mg, whereas in group 2 a median of 62 weeks (95% CI 42–82) was necessary (P = 0.0062). Patients in group 2 experienced more flares than patients in group 1 (P = 0.01) and received higher cumulative steroid doses (8.974 ± 3.939 gm versus 6.893 ± 3.075 gm; P = 0.01).
GCA patients with a strong initial systemic inflammatory reaction have more elevated circulating levels of IL-6 and TNFα, have higher and more prolonged corticosteroid requirements, and experience more disease flares during corticosteroid therapy than patients with a weak systemic acute phase response.