 |
|
|
 |
14 Day Endoscopy Study Comparing Risedronate and Alendronate in Postmenopausal Women Stratified by Helicobacter pylori Status
ALAN B.R. THOMSON, JOHN K. MARSHALL, RICHARD H. HUNT, J. MARK PROVENZA, FRANK L. LANZA, MARY G. ROYER, ZHENGQING LI, and MARION A. BLANK, for the Risedronate Endoscopy Study Group
ABSTRACT.
Methods. Subjects were randomized to receive risedronate 5 mg (n = 318) or alendronate 10 mg (n = 317) daily for 14 days. Endoscopy and evaluator-blind assessments of the esophageal, gastric, and duodenal mucosa were performed at baseline and on Days 8 and 15. Results. Overall, gastric ulcers ³ 3 mm were observed in 18 (6.0%) of 300 evaluable subjects in the risedronate group and 36 (12.1%) of 297 in the alendronate group during treatment (p = 0.013). On Day 8, the incidences of gastric ulcers in the risedronate and alendronate groups were 3.6% and 6.6%, respectively (p = 0.133), and on Day 15, they were 3.3% and 8.7% (p = 0.008). The incidence of gastric ulcers was not affected by H. pylori status. Mean gastric endoscopy scores at Days 8 and 15 were significantly lower in the risedronate group than in the alendronate group (p < 0.001). Mean esophageal and duodenal endoscopy scores were similar in the 2 groups at Days 8 and 15. When the treatment groups were combined, gastric endoscopy scores were significantly higher among H. pylori negative than H. pylori positive subjects at Days 8 and 15 (p < 0.05). Upper GI adverse events were reported by 18 (5.7%) subjects in the risedronate group (19 events) and 28 (8.8%) subjects in the alendronate group (32 events). Symptoms did not predict the presence of mucosal damage. Conclusion. Risedronate was associated with a significantly lower incidence of gastric ulcers than alendronate. H. pylori infection did not increase the incidence of bisphosphonate related gastric ulcers. The findings from this 14 day study in healthy volunteers support the hypothesis that bisphosphonates may differ from one another in their potential to produce upper GI mucosal damage. (J Rheumatol 2002;29:1965-74) Key Indexing Terms:
OSTEOPOROSIS
From University of Alberta, Edmonton, Alberta; McMaster University, Hamilton, Ontario, Canada; Gastrointestinal Specialists, Shreveport, Louisiana; Houston Institute for Clinical Research, Houston, Texas; and Procter & Gamble Pharmaceuticals, Mason, Ohio, USA. Supported by Procter & Gamble Pharmaceuticals, Mason, Ohio, and Aventis Pharma, Bridgewater, New Jersey. A.B.R. Thomson, MD, PhD, FRCPC, FACP, Professor of Medicine, Division of Gastroenterology, University of Alberta; J.K. Marshall, MD, MSc, FRCPC, Assistant Professor; R.H. Hunt, MD, FRCP, FRCPC, Professor, Division of Gastroenterology, McMaster University; J.M. Provenza, MD, Gastrointestinal Specialists; F.L. Lanza, MD, Clinical Professor of Medicine, Section of Gastroenterology, Baylor College of Medicine, Houston, Texas; M.G. Royer, MS; Z. Li, PhD; M.A. Blank, PhD, Procter & Gamble Pharmaceuticals. Address reprint requests to Dr. A.B.R. Thomson, 519 Robert Newton Research Building, University of Alberta, Edmonton, Alberta T6G 2C2, Canada. Submitted July 9, 2001; revision accepted February 22, 2002.
|