- H. pylori is a gram-negative, motile, spiral-shaped bacterium.
- The prevalence of H. pylori infection is decreasing.
- Previous studies suggested that 90% of duodenal ulcers and 70% of gastric ulcers are associated with H. pylori infection. This is also thought to be falling [3].
H. pylori pathophysiology
- H. pylori lives in the mucous layer above the gastric epithelial cells.
- H. pylori multiplies optimally at a pH of 6.0 to 8.0. To survive in the acidic stomach, H. pylori produces a urease enzyme. This converts the urea produced by gastric epithelial cells into ammonia and bicarbonate, thereby buffering gastric acid and allowing survival.
- In health, a low antral pH stimulates the release of somatostatin from D cells. This inhibits gastrin release from adjacent G cells, and so increases pH.
- The ammonia produced by H. pylori prevents the D cells from sensing the true pH. The negative feedback loop is lost, causing ongoing inappropriate gastrin release and excess acid production.
- H. pylori also impairs neural pathways which would otherwise down-regulate acid production.
- H. pylori can only colonise gastric epithelial cells. However, excess acid secretion can provoke gastric metaplasia of duodenal cells, allowing colonisation.
- Infected cells become more susceptible to erosion and ulceration (11).
- In addition to acid hypersecretion, the immune response provoked by H. pylori impairs mucosal defences and can lead to ulceration through a complex interplay between epithelial-derived cytokines, neutrophils, macrophages, leukotrienes, and B- and T-lymphocytes.
Learning Bite
The urease enzyme produced by H. pylori allows its survival and leads to inappropriate gastrin release and excess acid production.