Role of Helicobacter pylori in gastric cancer following partial gastrectomy for benign ulcer.

During the 1970s, Correa (1) formulated his theory on the sequence of histological changes from type B chronic gastritis to gastric cancer, through intermediate atrophic gastritis, intestinal metaplasia, and dysplasia stages. Based on epidemiological studies, it was suggested that the initial stage in this process, that is, initial gastritis, could result from environmental factors such as diets rich in salt and nitrates, and poor in vegetables and fresh fruits. In 1983, Marshall and Warren (2) demonstrated that mucosal inflammation was caused by the organism Helicobacter pylori (Hp), and thus they first related gastric cancer to Hp, a view that was supported by case-control studies and meta-analyses (3-5) showing a 2 to 4-fold increase in the risk for gastric cancer among the infected population when compared to the noninfected population. In 1994, IARC (International Agency for Research on Cancer dependent of the World Health Organization) defined Hp as a type I carcinogen (6), matching it, for instance, with the association between smoking and lung cancer. All studies suggest that cancer development requires the presence of Hp for many years; in other words, it is required that infection be initiated at an early age. Furthermore, some studies suggest that the association between Hp and cancer is more obvious in early versus advanced cancer (7). Similarly, this correlation is more apparent if infection was diagnosed years before the diagnosis of cancer (4,8), which suggests that their relationship may be underestimated because of potential infection clearance during disease development. A recent German study (9) compared 68 patients with gastric cancer (excluding cardia cases) versus 360 control individuals; a serology performed a few years before had shown that 78% of patients with cancer were infected versus 63% among controls, which represented an odds ratio (OR) of 3.7 that may reach 5.7 in patients with Hp CagA + infection. A Spanish study (10) demonstrated that the prevalence of infection was not different for intestinal-type and diffuse-type gastric carcinoma (incidence, 69%), but significant differences were found in the prevalence of Hp for distal cancer, which was of 73.6% versus only 48.6% for cardial cancer, the latter with no differences versus the prevalence of infection in the control population. While infection is present in more than 80% of patients with gastric cancer, most infected persons will not develop the latter condition, which suggests that Hp is a nearly necessary but insufficient factor. In fact, the prevalence of gastric cancer does not always correlate with the prevalence of infection; for example, areas with a high (Japan) or low (sub-saharian Africa) incidence of gastric cancer have a similar prevalence of infection. Even in regions with a high incidence of Hp and cancer, the latter will only develop in 2% of infected individuals. It is widely accepted that less Role of Helicobacter pylori in gastric cancer following partial gastrectomy for benign ulcer 1130-0108/2005/97/11/767-777 REVISTA ESPAÑOLA DE ENFERMEDADES DIGESTIVAS Copyright © 2005 ARÁN EDICIONES, S. L. REV ESP ENFERM DIG (Madrid) Vol. 97, N. ° 11, pp. 767-777, 2005