In the past five years 12 patients have been identified presenting with chronic duodenal ulcer (DU) disease and with no evidence of current or recent Helicobacter pylori (H pylori) infection. Four of them were taking regular non-steroidal anti inflammatory agents, one was subsequently found to have Crohn's disease of the duodenum, and one to have the Zollinger-Ellison syndrome. The remaining six patients with idiopathic DU disease were remarkable for their absence of the A1 blood antigen gene. Detailed studies of gastric function were performed in these six patients and compared with H pylon positive patients with DU and with healthy volunteers. The median integrated gastrin response in the patients with idiopathic DU (2810 (range 750-8750) ng/l min) was similar to that of the H pylori positive patients with DU (3355 (550-8725)) and higher than that of the H pylon negative healthy volunteers (560 (225-1125)). The median peak acid output in the patients with idiopathic DU (37 mmol/h, range 17-52) was similar to that of the H pylon positive patients with DU (40 (15-57)) and higher than that ofthe non-ulcer controls (22 (16-29)). The median percentage of a liquid meal retained in the stomach at 60 minutes was less in the patients with idiopathic DU (23 (15-33)) than in Hpyloni negative healthy volunteers (34 (30-53) p<0-01). The median percentage of a solid meal retained at 60 minutes was less in the patients with idiopathic DU (54 (9-83)) than in either H pylon negative healthy volunteers (87 (49-95) p<001) or H pylon positive patients with DU (79 (51-100) p<0-01). In conclusion, three abnormalities of gastric function are prevalent in patients with H pylon negative idiopathic DU disease -hypergastrinaemia, increased acid secretion, and the one feature distinguishing them from H pylon positive patients with DU -rapid gastric emptying of both liquids and solids. Each of these abnormalities will increase the exposure of the duodenal mucosa to acid and thus explain its ulceration. The absence of the blood group A1 antigen gene is consistent with a genetic basis for the disturbed gastric function linked to the ABO blood group antigen genes. (Gut 1993; 34: 762-768) More than 95% of patients with chronic duo-
Helicobacter pylon infection increases the serum concentration of gastrin, and this may be one of the mechanisms by which it predisposes to duodenal ulceration. Different forms of circulating gastrin were studied both basally and postprandially in 13 duodenal ulcer patients before and one month after eradication of H pylon. Three antisera that are specific for particular regions of the gastrin molecules were used. Gel chromatography indicated that >90% of the circulating gastrin consisted ofgastrin (G) 17 and G34 both before and after eradicating the infection. The basal median total immunoreactive gastrin concentration fell from 26 pmol/l (range 11-43) to 19 pmolIl (8-39) (p<0-05), entirely because of a fail in G17 from 6 pmol/l (<2.4-25) to <2-4 pmoil/ (<2.4-23) (p<0.001). The median (range) basal G34 values were similar before (15 pmol (2-36)) and after (10 pmol (2-30)) eradication. The median total immunoreactive gastrin concentration determined 20 minutes postprandially fell from 59 pmolll (38-114) to 33 pmol/ (19-88) (p<0 005), and again this was entirely the result of a fall in G17 from 43 pmol/l (9-95) to 17 pmolfl (<2-4-52) (p<0-001).The median postprandial G34 values were similar before (13 pmol/l, range 6-42) and after (15 pmolll, range 6-30) eradication. Eating stimulated a noticeable rise in G17 but little change in G34, both in the presence and absence of H pylori. The finding that H pylon infection selectively increases G17 explains why the infection causes mainly postprandial hypergastrinaemia. G17 is increased selectively because H pylon predominantly affects the antral mucosa which is the main source of G17 whereas G34 is mainly duodenal in origin. This study also indicates that the increased concentration ofgastrin in Hpylon infection is the result of an increase in one of the main biologically active forms of the hormone. (Gut 1993; 34: 757-761)
It has been proposed that the hypergastrinaemia in subjects with Helicobacter pylon infection is caused by the action of the ammonia produced by the organism's urease activity on the antral G cells. To investigate this hypothesis we examined the effect on plasma gastrin of increasing the bacterium's ammonia production by infusing urea intragastrically to eight H pylori positive duodenal ulcer patients. After a 60 minute control intragastric infusion of dextrose solution at 2 ml/ minute, a similar infusion containing urea (50 mmol/l) was continued for four hours. During the urea infusion, the median gastric juice urea concentration rose from 1.1 mmoVI (range 0.3-1.6) to and this resulted in an increase in the ammonium concentration from 2-3 mmol/l (range 1.3-5.9) to 6*1 mmoil/ (range 4.2-11.9) (p<001). This appreciable rise in ammonia production did not result in any change in the plasma gastrin concentration. The experiment was repeated one month after eradication of H pylori, at which time the median basal gastrin was 20 ng/l (range 15-25), significantly less than the value before eradication (30 ng/l range 15-60) (p<005). On this occasion, the gastric juice ammonium concentration was considerably reduced at 0 4 mmolIl (range 0.1-0.9) and the urea infusion did not raise the ammonium concentration or change the plasma gastrin concentration. In conclusion, augmenting H pylori ammonia production does not cause any early change in plasma gastrin.
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