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

Abstract: 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.