Helicobacter pylori

Helicobacter pylori is a spiral bacterium which specifically colonizes gastric mucosa. It is able to survive in a near neutral pH through the production of urease. H. pylori infection has been correlated with the formation of peptic ulcers. Several lines of evidence link H. pylori to peptic ulceration.

• First, eradication of H. pylori, without the suppression of acid, leads to ulcer healing rates that are similar to those of acid suppression therapy alone.

• Secondly, relapse of duodenal ulceration after antimicrobial treatment is preceded by reinfection of gastric mucosa.

• Additionally, the prevalence of H. pylori in patients with duodenal ulceration is near 100%. Patients with gastric ulcers have a prevalence of H. pylori in the range of 60-80%. Comparatively, Helicobacter colonizes approximately 20% of those without peptic ulcer disease.

Consequently, the evaluation for and the treatment of Helicobacter infection is an integral part of the treatment of peptic ulcer disease.

There are several other environmental factors which are associated with the development of peptic ulcers. Cigarette smoking has been associated with peptic ulcer disease in so far as it impairs healing, decreases the effectiveness of therapy, increases recurrence rates, and increases the likelihood of complications. Ethanol also has injurious effects on gastroduodenal mucosa. NSAID use has also shown ulcerogenic effects. Ulcer formation is promoted through the systemic effects of cyclooxygenase

inhibition and a direct toxic effect on mucosal cells. The use of NSAIDS is more strongly associated with gastric ulcers.

Finally, altered host defense mechanisms play a role in the pathogenesis of peptic ulcer formation. Surface epithelial cells produce bicarbonate and mucus. The generation of these substances allows for the creation of a pH gradient at the luminal interface such that there is a near neutral environment at the mucosal surface. Additionally, prostaglandins PGE2 and PGI2 have a protective effect on the mucosa through inhibition of acid secretion by the parietal cell. Patients with peptic ulcer disease have been shown to have decreased bicarbonate secretion and decreased production of mucosal prostaglandins. Motility disorders can also promote ulcerogenesis presumably through a mechanism of impaired clearance of noxious substances.

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