Helicobacter pylori in ulcerogenesis

Patients with peptic ulcer disease have elevated gastric acid secretion, hyperfunction of G cell, impaired bicarbonate secretion, increased levels of pepsinogen I and the presence of inflammatory mediators as well as Helicobacter pylori-induced gastroduodenitis and gastric metaplasia in the duodenum (in duodenal ulcer patients). Non-H. pylori-associated ulcers include those due to non-steroidal anti-inflammatory drugs, Zollinger-Ellison syndrome, and those related to other forms of gastritis. Evidence of H. pylori in ulcerogenesis includes the higher prevalence of H. pylori in gastritis and peptic ulcer patients plus the important observation that H. pylori eradication results in healing and long-term cure of ulcer disease. The precise mechanism of mucosal injury and ulceration is unclear. Bacterial and inflammatory factors are involved as well as host changes in hormones and gastric acid secretion.