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Efficacy and Safety of Willow Bark Extract in the Treatment of Osteoarthritis and Rheumatoid Arthritis: Results of 2 Randomized Double-Blind Controlled Trials
CLAUDIA BIEGERT, IRMELA WAGNER, RAINER LÜDTKE, INA KÖTTER, CLAUDIA LOHMÜLLER, ILHAN GÜNAYDIN, KATJA TAXIS, and LUTZ HEIDE
ABSTRACT. Methods. We studied 127 outpatients with hip or knee OA and a WOMAC pain score of at least 30 mm and 26 outpatients with active RA in 2 randomized, controlled, double-blind trials with followup for 6 weeks. OA trial: Patients were randomized to receive willow bark extract, corresponding to 240 mg of salicin/day, diclofenac 100 mg/day, or placebo (n = 43, 43, and 41, respectively). Main outcome measure was the pain subscore of the WOMAC OA Index. RA trial: Patients were randomized to receive willow bark extract, corresponding to 240 mg salicin/day (n = 13) or placebo (n = 13). Main outcome measure was the patient's assessment of pain rated on a 100 mm visual analog scale (VAS). Results. OA trial: WOMAC pain scores decreased by 8 mm (17%) in the willow bark group and by 23 mm (47%) in the diclofenac group, compared with 5 mm (10%) in the placebo group. The difference between willow bark extract and placebo was not statistically significant (–2.8 mm; 95% CI –12.1 to 6.4 mm; p = 0.55, ANCOVA), but the difference between diclofenac and placebo was highly significant (–18.0 mm; 95% CI –27.2 to –8.8 mm; p = 0.0002, ANCOVA). RA trial: The mean reduction of pain on the VAS was –8 mm (15%) in the willow bark group compared with –2 mm (4%) in the placebo group. The difference was not statistically significant (estimated difference –0.8 mm; 95% CI –20.9 to 19.3 mm; p = 0.93, ANCOVA). Conclusion. The OA study suggested that the willow bark extract showed no relevant efficacy in patients with OA. Similarly, the RA trial did not indicate efficacy of this extract in patients with RA. (J Rheumatol 2004;31:2121-30) Key Indexing Terms:
OSTEOARTHRITIS
From the Pharmaceutical Institute, Eberhard Karls-Universität, Tübingen; the Department of Internal Medicine II (Haematology, Oncology, Immunology, and Rheumatology), University Hospital, Tübingen; and the Karl and Veronica Carstens Foundation, Essen, Germany. Supported by Tübingen University and by Robugen GmbH, Esslingen, Germany. R. Lüdtke was supported by funding from the Karl and Veronica Carstens Foundation. C. Biegert, PhD; I. Wagner, PhD; K. Taxis, PhD; L. Heide, PhD, Pharmaceutical Institute, Eberhard Karls-Universität Tübingen; I. Kötter, MD; C. Lohmüller, MD; I. Günaydin, MD, Department of Internal Medicine II, University Hospital, Tübingen; R. Lüdtke, Dipl. Stat., Karl and Veronica Carstens Foundation. Dr. Biegert and Dr. Wagner contributed equally to this report. Address reprint requests to Dr. L. Heide, Pharmaceutical Institute, University of Tübingen, Auf der Morgenstelle 8, 72076 Tübingen, Germany. E-mail: heide@uni-tuebingen.de Submitted March 4, 2004; revision accepted May 21, 2004. |