When and how to eradicate Helicobacter pylori: role of histamine receptor antagonists

Peptic ulcer is today frequently considered to be an infectious disease. The bacteria assumed to be the cause of gastric or duodenal ulcer was first called Campylobacter pyloridis and later C. pylori because of its structural similarity to other Campylobacter species. Later, unique characteristics were reported, and it was renamed Helicobacter pylori (Hp). In retrospect, it was presumably first described in man in 1938 (Doenges 1938), although the clinical significance was not established until 1983 (Warren 1983, Warren and Marshall 1983). It is a spiral-shaped, gram-negative bacteria with four to six flagella and dimensions of 0.5 x 3.0 micron. . With the help of these flagella, it moves into the mucous layer overlying the gastric epithelium where it colonizes at the interface of the mucous layer and the surface epithelial cells. It can be found in any part of the gastrointestinal tract demonstrating gastric epithelium, i.e. the stomach and metaplastic areas of the esophagus or the duodenum. One characteristic of this bacteria is the production of a urease enzyme that catalyzes urea to ammonium and bicarbonate. The production of ammonium causes the development of an alkaline microenvironment that protects it from the gastric acid. In the presence of urea, the organism will therefore replicate to a pH as low as 4.3 and survive without replication to a pH as low as 2.3. In Western countries, an increase in the prevalence of Hp infection is observed in the population with progressing age. In childhood, infection before the age of 20 years is rare. At the age of 60 years or older, however, the prevalence rate is on the order of 40% to 60% (Dooley et al. 1989, Perez-Perez et al. 1988, Marshall 1994). The seroconversion rate in adults is lower than 1% per year (Parsonnet et al. 1992). The infection seems to be stable, probably persisting for many years or even a lifetime.