GASTRIC B-CELL CLONAL EXPANSION AND HELICOBACTER-PYLORI INFECTION IN PATIENTS WITH AUTOIMMUNE-DISEASES AND WITH DYSPEPSIA - A FOLLOW-UP-STUDY

Citation
D. Sorrentino et al., 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, 32(12), 1997, pp. 1204-1208
Citations number
22
ISSN journal
00365521
Volume
32
Issue
12
Year of publication
1997
Pages
1204 - 1208
Database
ISI
SICI code
0036-5521(1997)32:12<1204:GBCEAH>2.0.ZU;2-P
Abstract
Background: It is not clear whether gastric B-cell clonal expansion, a possible precursor of mucosa-associated lymphatic tissue (MALT) lymph oma, is exclusively linked to Helicobacter pylori infection and virule nce. Methods: In this study we followed up, for up to 33 months, 16 VD J polymerase chain reaction-positive patients (4 with dyspepsia, 9 wit h Sjogren's syndrome, and 3 with other autoimmune diseases). Of these, 12 were H. pylori-positive. In addition, in H. pylori-positive patien ts we tested whether the serum anti-cag-A (a potential marker of virul ence) was preferentially associated with B-cell clonality. Results: In all but one patient clonality appeared temporally unrelated to H. pyl ori infection. The prevalence of anti-cagA was not higher in H. pylori /VDJ-positive patients than in controls. Conclusions: These data indic ate that, in addition to H. pylori, gastric B-cell clonality may be su stained by other agents/mechanisms. Anti-cag-A does not appear to be i nvolved in the pathogenesis of clonality.