Relationship between antral lymphocyte density and basel gastrin levels in patients with Helicobacter pylori infection

Background. The mechanism by which Helicobacter pylori causes hypergastrinaemia is not completely understood. Aim. To evaluate whether antral lymphocyte density could play a role in this alteration. Methods. A total of 12 patients with active duodenal ulcer and 10 with non-ulcer dyspepsia were enrolled upon detection of Helicobacter pylori infection at endoscopy. Enrolled as controls were 7 matched dyspeptic patients without Helicobacter pylori infection. Biopsy specimens were collected for Helicobacter pylori and histological assessments, and for antral lymphocyte density assessment by a histomorphometric method. A blood sample was obtained from each patient to determine basal gastrin levels. All patients were controlled by a further endoscopy 4 weeks after the end of Helicobacter pylori treatment. Results. Antral lymphocyte density (5464+/-1328 and 5635+/-1186 vs 2267+/-557 lymphocytes/mm(2); p<0.001 and p<0.001, respectively) and gastrin levels (66.7+/-14.1 and 60.4+/-21.7 vs 40.7+/-7.8 pg/dl; p=0.004 and p=0.02, respectively) were higher in duodenal ulcer and non-ulcer dyspepsia patients than in controls, while no significant differences emerged between duodenal ulcer and non-ulcer dyspepsia patients. There was a significant direct correlation between antral lymphocyte density and gastrin levels both in duodenal ulcer (r=0.77; p=0.003) and in non-ulcer dyspepsia (r=0.75; p=0.03) patients, while no correlation was found in controls (r=0.12; p=0.8). After treatment, this correlation persisted in 10 eradication failure patients (r=0.68; p=0.027), but disappeared in those successfully cured. Conclusions. These data suggest that lymphocyte density in the antral mucosa could play a role in the impaired gastrin production occurring in patients with Helicobacter pylori infection.