ERADICATION OF HELICOBACTER-PYLORI AND REGRESSION OF B-CELL LYMPHOMA

There is an increasing body of evidence implicating a causal associati on between Helicobacter pylori and the development of mucosa-associate d lymphoid tissue (MALT) associated B-cell gastric lymphoma. investiga tors have noted that almost all patients with H pylori-associated chro nic gastritis develop lymphoid follicles. Some of these patients demon strate 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-con trol studies have shown that patients with gastric non-Hodgkin's lymph oma are substantially more likely than matched controls to have H pylo ri infection. This situation may be analogous to the linkage between c hronic Epstein-Barr virus and lymphoma. The mechanisms inducing the de velopment of lymphoma are not clear, but it has been suggested that ch ronic infection with H pylori results in the stimulation of H pylori-r esponsive T cells which in turn activate B cells with the subsequent d evelopment of a mutation to a monoclonal B-cell population. Recent evi dence indicates that cure of H pylori infection produces regression of MALT lymphoma within 3 to 12 months in approximately 75% of antibioti c-treated patients. Individual responsiveness remains unpredictable, h owever, and careful and prolonged endoscopic and histologic follow-up is needed. Large, well-controlled studies are necessary, however, to d etermine the duration of 'cure' and the appropriate setting for treatm ent.