Comparison of meal-stimulated serum gastrin response in Helicobacter pylori-positive duodenal ulcer and asymptomatic volunteers with and without H. pylori infection.

BACKGROUND

Duodenal ulcer (DU) patients exhibit raised postprandial gastrin release as compared to that in healthy controls. It is believed that serum pepsinogen I (PG I) concentration reflects the chief cell mass and that hyperpepsinogenemia I plays an important role in the pathogenesis of DU. Currently, strong evidence suggests that Helicobacter pylori (H. pylori) infection plays an important role in the pathogenesis of DU.

MATERIALS AND

METHODS

Subjects consisted of 15 patients with H. pylori-positive DU, 10 H. pylori-positive volunteers, and 35 H. pylori-negative volunteers. Blood samples were taken before and at 15, 30, and 60 minutes after eating the test meal, which consisted of 100 gm rice, 130 gm chicken, and 1 egg. The 1-hour integrated gastrin response (IGR) was taken as the area under the serum gastrin time curve, calculated by the trapezoid method. Serum gastrin (SG) and fasting serum PG I concentrations were measured by radioimmunoassay.

RESULTS

Meal-stimulated SG response and fasting PG I concentration were significantly higher in DU patients than in H. pylori-positive and -negative volunteers. The DU patients were divided into two groups in accordance with their IGR levels as follows: hyper-IGR and normo-IGR. Serum PG I concentration was significantly higher in the hyper-IGR than in the normo-IGR group.

CONCLUSIONS

The DU patients differed in some way (other than H. pylori infection) from the H. pylori-positive healthy volunteers. The fact that hyper-IGR DU patients had higher serum PG I concentrations suggests that patients in this group may be acid hypersecretors.