Helicobacter pylori and the risk and management of associated diseases: gastritis, ulcer disease, atrophic gastritis and gastric cancer

Abstract

This review addresses the role of H. pylori and the effect of H. pylori eradication on gastritis, peptic ulcer disease, atrophic gastritis and gastric cancer. Specific emphasis is given to various factors that influence the clinical course of this infection. H. pylori induces chronic gastritis in virtually all infected subjects. This inflammation can lead to peptic ulceration and atrophic gastritis in a considerable number of infected subjects. A minority eventually develops gastric cancer. The risk of such complications depends upon the severity of gastritis, which is determined by various host- and bacteria-related factors. Among bacterial factors, most of the evidence addresses the cagA pathogenicity island, the presence of which has been associated with more severe gastritis, peptic ulceration, atrophic gastritis and gastric cancer. Among host factors, most of the evidence focuses on acid production in response to H. pylori infection. An increase in acid secretion limits H. pylori gastritis to the antrum at the risk of duodenal ulcer disease; a reduction allows more proximal inflammation at the risk of atrophic gastritis, gastric ulcer disease, and gastric cancer. Gastritis and atrophy negatively influence acid secretion. H. pylori eradication is required in peptic ulcer disease and may be advocated in patients on profound acid suppressive therapy; it has been shown to cure gastritis and prevent ulcer recurrence. Further study is required to determine the efficacy of H. pylori eradication in the primary and secondary prevention of atrophic gastritis and gastric cancer.

Helicobacter pylori antibiotic susceptibility patterns in Bangladesh: Emerging levofloxacin resistance

“…Successful treatment of Helicobacter pylori, the Gram-negative bacterium responsible for infections affecting more than half of the world's population, results in pathogen eradication and often also cures and prevents development of associated diseases, including chronic gastritis, peptic ulcer diseases, gastric cancer, and mucosa-associated lymphoid tissue lymphoma [1]. First-line, alternative first-line, second-line, and even third-line therapies for H. pylori eradication have been proposed.…”

A comparative study of rapid urease test and dilute carbol fuchsin staining technique for diagnosis of Helicobacter pylori infection

“…Approximately 80% of gastric ulcer and 95% of duodenal ulcer were caused by H. pylori. 5 An array of invasive and noninvasive tests like endoscopy biopsy based tests viz RUT, HPE, PCR, Giemsa, Warthin starry staining and serological tests for demonstration of antibodies are available for diagnosis of H. pylori infection each with its own advantage and disadvantage. A combination of more than one test usually gives a higher rate of sensitivity and specificity for diagnosis.…”

The Helicobacter pylori cytotoxin CagA is essential for suppressing host heat shock protein expression

“…Infection with this bacterium is the strongest known individual risk factor for gastric cancer, which is the third leading cause of cancer-related death worldwide (Ferlay et al 2012;Herrera and Parsonnet 2009). In addition to gastric cancer, H. pylori infection is also a major risk factor for the development of chronic gastritis, mucosa associated lymphoid tissue lymphoma (MALT) as well as gastric and duodenal ulcers (Bayerdorffer et al 1997;Kuipers 1997). One of the major virulence factors of H. pylori strains is a 40-kb cytotoxin associated gene pathogenicity island abbreviated to cagPAI, which encodes a type IV secretion system (T4SS).…”