Helicobacter pylori is a ubiquitous gram-negative bacterium infecting half the world's population[1,2] and causing chronic active gastritis in virtually all infected individuals. The majority of individuals who acquire chronic H pylori gastritis will exhibit mild gastritis, more prominent in the antrum compared with the corpus. A minority of infected patients develop marked chronic inflammation in the antrum, with mild inflammation in the oxyntic mucosa (antral-predominant gastritis), and are prone to develop duodenal ulcer. Infrequently, some individuals show a corpus-predominant pattern that overlaps with autoimmune gastritis. Recently, epidemiologic and laboratory studies in animals as well as interventional studies in humans strongly suggested that H pylori may play a pathogenic role in the development of adenocarcinoma of the distal stomach.[5,6,7] In particular, individuals with corpus-predominant gastritis seem more susceptible to development of adenocarcinoma of the distal stomach.
The mechanisms whereby H pylori may cause gastroduodenal disease and contribute to gastric carcinogenesis are still hypothetical.[5,6,7,8] However, the production of specific virulence factors by the bacterium, the inflammatory response of the host, and the association with environmental factors may all play a contributory role.[5,6,8]
© 2004 Medscape
Cite this: Eradication of Helicobacter pylori: A Clinical Update - Medscape - Feb 18, 2004.