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 anti genic stimulation. MALT is a precursor of gastric MALT lymphoma, a low -grade lymphoma whose incidence recently appears to have increased. Al though much epidemiologic and clinical evidence has linked both MALT a nd MALT lymphoma to Helicobacter pylori infection, it is not known whe ther other agents and or mechanisms may also play a role and whether t here is a clearly defined pre-neoplastic lesion. In particular the cli nical significance of B-cell clonality remains unknown. In a recent st udy we attempted to define the role of H. pylori and MALT in the genes is of B-cell clonality in a northern Italian patient population referr ed 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 gene sis of MALT lymphoma. Indeed, other studies conducted by our group inp atients with Sjogren's syndrome indicate that genetic/immunologic fact ors and possibly viruses may play a role. The high prevalence of B-cel l clonality in an otherwise healthy population suggests either that mo st of these patients are at risk of developing MALT lymphoma (in which case this condition at the moment may be greatly underdiagnosed) or t hat B-cell clonality is a very early step in the development of neopla sia, which requires several other factors and which will occur only in a restricted fraction of these patients. Careful follow-up studies wi ll provide an answer to this question.