Helicobacter pylori, gastric cancer and gastric lymphoma

From several recent epidemiological studies and the WHO report (1994) on this topic, it has become very clear that H. pylori is responsible for the large majority of gastric cancers. The acquisition of H. pylori in childhood is associated with progressive atrophy of the gastric mucosa and most countries with a poor socio-economic status have an increased incidence of gastric cancer. The longer the process of chronic gastritis continues, the larger the chance that mucosal atrophy and dysplasia may indeed occur, as precursor of gastric carcinoma. Alternatively, the incidence of gastric cancer in countries with improvement of their social and economic infrastructure is declining, partly to be attributed to a decline in infection rates of H. pylori. Several factors are important in the mechanism of development of gastric cancer; such as dietary factors, smoking, genetic factors of the host, different aggressivity of H. pylori strains (heterogeneity, e.g. cagA). The presence of nitrosocompounds and free radicals is important; increased cellular proliferation and epithelial turnover as well as apoptosis may all lead to final mutation. While life-style improvement (diet, smoking) may be of benefit, eradication of H. pylori in selected patients may contribute to halting the process of progressive atrophic gastritis and atrophy. H. pylori has also been associated with gastric lymphoma, although the mechanisms have not been clarified yet. Eradication of H. pylori in low-grade gastric lymphoma has led to impressive improvement, however long-term results are not yet available.