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The aim of our study was to identify PCR- detectable clonal B- cell population in Helicobacter pylori gastritis and assess their relation to the Wotherspoon- Isaacson (W- I) grade for gastric lymphoid infiltrates. Amplified DNA was obtained from thirty four H. pylori positive gastritis dyspeptic patients and thirty four H. pylori negative matched controls. Clonal bands were observed in 6 (2/17 W- I Grade 1, 2/13 W- I Grade 2, and 2/4 W- I Grade 3 lesions) and polyclonal smears in 24 cases (15 W- I Grade 1, 7 W- I Grade 2, and 2 W- I Grade 3). Four additional W- I Grade 2 samples with clonal bands were associated with background polyclonal smear and were not reproducible. Clonal bands were not recorded in controls. B- cell clonality was not related to W- I grades. We conclude that certain H. pylori positive gastritis patients show PCR- detectable monoclonality, which is independent of the W- I grade of gastritis and cannot be taken as evidence of an existing neoplastic lesion.
The aim of our study was to identify PCR-detectable clonal B-cell population in Helicobacter pylori gastritis and assess their relation to the Wotherspoon-Isaacson (W- I) grade for gastric lymphoid infiltrates. Amplified DNA was obtained from thirty four H. pylori positive gastritis dyspeptic patients and thirty four H. pylori negative matched controls. Clonal bands were observed in 6 (2/17 W- I Grade 1, 2/13 W- I Grade 2, and 2/4 W- I Grade 3 lesions) and polyclonal smears in 24 cases (15 W-I Grade 1, 7 W-I Grade 2, and 2 W-I Grade 3). Four additional W-I Grade 2 samples with clonal bands were associated with background polyclonal smear and were not We conclude that certain H. pylori positive gastritis patients show PCR-detectable monoclonality, which is independent of the W- I grade of gastritis and can not be taken as evidence of an existing neoplastic lesion.