Helicobacter pyloriinduced Ulcers

The majority of patients with peptic ulcers are infected with H. pylori (95-100% for DU; 75-85% for GU). Although only a small proportion of all H. pylori-positive individuals are found to have peptic ulcer disease (1-6%), this is a four- to tenfold increase of the number who are H. pylori-negative. The causal relationship between

H. pylori infection and ulcers is further supported by the reduction of ulcer recurrence after H. pylori eradication. It is generally accepted, however, that other factors contribute to the pathogenesis of ulcers. It is known that smoking reduces healing and is also associated with peptic ulcer disease. Variations in bacterial strain virulence and host immune response may also be determinants of pathogenicity.

Infection with H. pylori results in a chronic, active gastritis in the antrum or the entire stomach. Peptic ulcers have long been associated with a diffuse antral gastritis. Gastritis is not a predominant feature in other forms of peptic ulcer (e.g., NSAID-induced) unless H. pylori is also present. The gastritis is present in both gastric and duodenal ulcers, but it is more severe in the former where it is also associated with gastric atrophy and intestinal cell metaplasia.

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