H.pylori gastritis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]

Pathophysiology

The H.pylori induced gastritis includes the following stages: They are

• The acute phase
• Active chronic gastritis
• Atrophy
• Intestinal metaplasia

The acute phase

In majority of patients, the initial acute phase of gastritis is subclinical.

• Following transmission, H.pylori penetrates the mucous layer of stomach and multiplies close to the surface epithelial cells.
• Following adhesion to epithelial cells, the bacteria releases lipopolysaccharides and chemotactic mediators which penetrate the surface epithelial cells.Crabtree, J. E. "Gastric mucosal inflammatory responses to Helicobacter pylori." Alimentary pharmacology & therapeutics 10.Sup1 (1996): 29-37.
• These bacterial factors attract the polymorphonuclear leukocytes to the site of infection and also caused mast cell degranulation, which releases acute inflammatory mediators. MAst cell degranulation leads to:

• Increased vascular permeability
• Increased polymorph emigration
• Increased expression of leukocyte adhesion molecules

• The macrophages release IL-1 and tumor necrosis factor alpha (TNF-α) which stimulates gastric epithelium to produce IL-8.
• The acute phase is associated with profound hypochlorhydria and a decreased ascorbic acid secretion into the gastric juice.
• The acid output reaches pre-infection levels after several weeks but the ascorbic acid remains lower than normal for the duration of chronic gastritis, indicating that it is due to persisting inflammation rather than hypochlorhydria.