There were significant differences between both groups regarding liver decompensation (<i>P</i> = 0.001), red color sign over gastric varices (<i>P</i> = 0.0011), prevalence of <i>H. pylori</i> infection (<i>P</i> = 0.0049), histological patterns of gastritis (<i>P</i> = 0.0069), and serum gastrin level (<i>P</i> = 0.0200).
Only ~10% of chronically infected patients, mainly the young, manifest an antral predominant gastritis with increased acid secretion due to a decrease in somatostatin and increase in gastrin secretion; these patients are predisposed to develop peptic ulcer disease.
Immunohistochemical markers (p53, Ki-67, and BCL10), microsatellite instability, loss of heterozygosity, serum levels of antibodies (anti-H. pylori and anti-CagA), and markers for gastritis (gastrin and pepsinogens) were examined, and the results were compared between patients whose tumors regressed completely after eradication therapy (responders) and patients whose tumors did not regress (non-responders).
Gastritis scores and plasma gastrin and anti-H. pylori immunoglobulin G titers reached levels observed in naturally colonized animals by 4 months after the challenge; however, no plasma immunoglobulin A response was observed up to 10 months.
In order to study the association between gastrin and H. pylori infection the density of antral G cells was evaluated by transcriptional expression of gastrin mRNA using a sensitive cold probe labelled with digoxigenin. the study group included 22 patients with symptomatic H. pylori positive gastritis and/or duodenal ulcer, 12 of whom were re-evaluated after eradication of H. pylori and 6 controls.