Effect of Sucralfate onHelicobacter pyloriand Severity of Gastritis in Patients with Duodenal Ulcer

Sucralfate and <i>Helicobacter pylori</i>

“…Hui et al [35] were the first to report a decreased density of antral H. pylori colonisation on sucralfate treatment. This theme was developed further by Winter et al [36] who showed that while sucralfate treatment decreased the density of H. pylori colonisation in the antrum, the density in the corpus tended to increase -the urease tests used in this study (both the CLO test and the 14 C-urea breath test) were again uninfluenced by sucralfate therapy. On the other hand, Barbara et al [37] were unable to show any effect of sucralfate, 3 g/day, on gastric colonisation scores despite a significant improvement in gastritis scores.…”

Efficacy of sucralfate for Helicobacter pylori eradication triple therapy in comparison with a lansoprazole‐based regimen

“…In addition, it also suppresses H. pylori ‐related toxic substances that may aggravate duodenal mucosal injury 7 . In vivo studies have confirmed that sucralfate reduces the density of H. pylori in the stomach 8 –10 . Sucralfate is also reported to enhance the anti‐ H. pylori activity of metronidazole, erythromycin, tetracycline, and amoxycillin 11 .…”

“…A recent trend in curative therapy has been so‐called triple therapy, using a proton pump inhibitor and two different antimicrobials 1 . Sucralfate, which is a widely used cytoprotective agent for the gastric mucosa, is reported to inhibit several of the activities of H. pylori and to enhance the anti‐ H. pylori activity of antimicrobial agents 2 –11 . Therefore, several studies of sucralfate‐based eradication therapy have been reported recently 12 –18 .…”

Effect of Sucralfate on Gastric Mucosal Inflammatory Responses Induced byHelicobacter pyloriLipopolysaccharide

“…The ability of sucralfate to affect the downregulation of proinflammatory cytokine production may account for the relative therapeutic effectiveness of the agent in the treatment of gastric disease associated with H. pylori infection (37)(38)(39)(40). Such an interpretation of the above finding is further supported by the results obtained in the presence of sucralfate, which showed that a reduction in the lipopolysaccharide-induced gastritis on sucralfate administration shows a direct inverse relationship (r = ÿ 0.80) with the extent of induced enhancement in mucosal IL-4 expression, and that the increase in the regulatory cytokine level is also reflected in a marked reduction in TNF-a and epithelial cell apoptosis.…”