Abstract :
There is an increasing body of evidence implicating a causal association between Helicobacter pylori and the development of mucosa-associated lymphoid tissue (MALT) associated B-cell gastric lymphoma. Investigators have noted that almost all patients with H pylori-associated chronic gastritis develop lymphoid follicles. Some of these patients demonstrate infiltration of B cells and lymphoepithelial lesions typical of MALT lymphoma. When gastric tissue from patients with gastric B-cell lymphoma is analyzed for H pylori infection, the overwhelming majority of patients demonstrate this condition. Epidemiologic nested case-control studies have shown that patients with gastric non-Hodgkinʹs lymphoma are substantially more likely than matched controls to have H pylori infection. This situation may be analogous to the linkage between chronic Epstein-Barr virus and lymphoma. The mechanisms inducing the development of lymphoma are not clear, but it has been suggested that chronic infection with H pylori results in the stimulation of H pylori-responsive T cells which in turn activate B cells with the subsequent development of a mutation to a monoclonal B-cell population. Recent evidence indicates that cure of H pylori infection produces regression of MALT lymphoma within 3 to 12 months in approximately 75% of antibiotic-treated patients. Individual responsiveness remains unpredictable, however, and careful and prolonged endoscopic and histologic follow-up is needed. Large, well-controlled studies are necessary, however, to determine the duration of ‘cure’ and the appropriate setting for treatment.
