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

Scandinavian Journal of Gastroenterology
D SorrentinoE Bartoli

Abstract

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. In this study we followed up, for up to 33 months, 16 VDJ polymerase chain reaction-positive patients (4 with dyspepsia, 9 with Sjögren'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. 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. 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.

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Citations

Mar 4, 1999·Histopathology·H BouzoureneE Saraga
Jul 12, 2002·Journal of Gastroenterology·Francesco FranceschiAntonio R Sepulveda
Jul 13, 2002·Expert Review of Anticancer Therapy·M Raderer, P G Isaacson

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