Helicobacter pylori, gastric MALT and B-cell clonality

MALT, or mucosa associated lymphoid tissue, is normally not present in gastric tissue. Its presence is often associated with persistent antigenic stimulation. MALT is a precursor of gastric MALT lymphoma, a low-grade lymphoma whose incidence recently appears to have increased. Although much epidemiologic and clinical evidence has linked both MALT and MALT lymphoma to Helicobacter pylori infection, it is not known whether other agents and or mechanisms may also play a role and whether there is a clearly defined pre-neoplastic lesion. In particular the clinical significance of B-cell clonality remains unknown. In a recent study we attempted to define the role of H. pylori and MALT in the genesis of B-cell clonality in a northern Italian patient population referred to us for simple dyspepsia. The results show that B-cell clonality is unexpectedly frequent in these patients regardless of the presence of H. pylori infection. These observations raise the possibility that agents and mechanisms other than H. pylori may be involved in the genesis of MALT lymphoma. Indeed, other studies conducted by our group inpatients with Sjogren's syndrome indicate that genetic/immunologic factors and possibly viruses may play a role. The high prevalence of B-cell clonality in an otherwise healthy population suggests either that most of these patients are at risk of developing MALT lymphoma (in which case this condition at the moment may be greatly underdiagnosed) or that B-cell clonality is a very early step in the development of neoplasia, which requires several other factors and which will occur only in a restricted fraction of these patients. Careful follow-up studies will provide an answer to this question

Gastric B-Cell clonal expansion and Helicobacter pylori infection in patients with autoimmune diseases and with dyspepsia - A follow-up study

Background: It is not clear whether gastric B-cell clonal expansion, a possible precursor of mucosa-associated lymphatic tissue (MALT) lymphoma, is exclusively linked to Helicobacter pylori infection and virulence. Methods: In this study we followed up, for up to 33 months, 16 VDJ polymerase chain reaction-positive patients (4 with dyspepsia, 9 with Sjogren's syndrome, and 3 with other autoimmune diseases). Of these, 12 were H. pylori-positive. In addition, in H. pylori-positive patients we tested whether the serum anti- cag-A (a potential marker of virulence) was preferentially associated with B- cell clonality. Results: In all but one patient clonality appeared temporally unrelated to H. pylori infection. The prevalence of anti-cagA was not higher in H. pylori/VDJ-positive patients than in controls. Conclusions: These data indicate that, in addition to H. pylori, gastric B-cell clonality may be sustained by other agents/mechanisms. Anti-cag-A does not appear to be involved in the pathogenesis of clonality