Kamada T, Haruma K, Komoto K, Mihara M, Sumii K, Kajiyama G
Gastrointestinal Unit, First Department of Internal Medicine, Hiroshima University School of Medicine, Japan.
Helicobacter. 1999 Sep;4(3):170-7. doi: 10.1046/j.1523-5378.1999.99276.x.
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.
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.
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.
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.
