[Frontiers in Bioscience 6, e213-226, December 1, 2001]


Robert G. Jones, David B. Trowbridge, Mae F. Go

Gastrointestinal Section, VA Salt Lake City Health Care System and the Division of Gastroenterology, University of Utah School of Medicine, Salt Lake City, Utah


1. Abstract
2. Introduction
3. Pathophysiology of Helicobacter pylori and Peptic Ulcer Disease
4. Diagnostic Tests
4.1 Endoscopic Tests
4.1.1. Rapid Urease Test (RUT)
4.1.2. Histology
4.1.3. Culture
4.2. Non-endoscopic tests
4.2.1. Urea Breath Test
4.2.2. Serology
4.2.3. Stool Antigen
5. Therapies
5.1. First Line Therapies
5.2. Second Line Therapies
6. NSAIDS and Helicobacter pylori
7. Helicobacter pylori and Nonulcer Dyspepsia
8. Helicobacter pylori and Gastric Malt Lymphoma and Gastric Adenocarcinoma 8.1. Malt Lymphoma
8.1.1.Clinical and Endoscopic Presentation of Gastric Malt Lymphoma
8.1.2.Pathogenesis of MALT Lymphoma
8.1.3. Histological Features of Gastric MALT Lymphoma
8.1.4.Evaluation of Gastric MALT Lymphoma
8.1.5. Treatment of Gastric MALT Lymphoma
8.2. Gastric Carcinoma
8.2.1.Clinical and Endoscopic Presentation of Gastric Carcinoma
8.2.2.Pathogenesis of Gastric Adenocarcinoma
8.2.3. Animal Model of Gastric Cancer
8.2.4.Management of Intestinal Metaplasia
8.2.5. Cost Effectiveness of Screening for Gastric Cancer
9. Perspective
10. References


Helicobacter pylori infection is the world's most common chronic infection in humans and is the cause of most gastritis cases. This infection is accepted as the etiology of the majority of peptic ulcers. It has been implicated as a significant contributing factor in the development of gastric malignancy - both gastric MALT lymphoma and gastric adenocarcinoma. Both endoscopic and non-endoscopic tests are available for accurate diagnosis of the infection. Several multi-drug regimens are useful for effective eradication of the infection. Strategies have been developed for managing patients with gastric MALT lymphoma. Criteria to identify populations with increased risk for gastric malignancy are being developed. H. pylori induces gastritis; it is also involved in both apoptosis and cellular proliferation. The role of H. pylori infection in the pathogenesis of premalignant lesions, altered gastric acid secretion, and significant clinical presentations is the subject of numerous studies worldwide.