HIelicobacter pylori related hypergastrinaemia is the result of a selective increase in gastrin 17

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 ofH 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 inHpylon infection is the result of an increase in one of the main biologically active forms of the hormone. (Gut 1993; 34: 757-761) University Department of Medicine and Therapeutics, Western Infirmary, Glasgow GIl 6NT R S Chittajallu GM Fullarton K E L McColl Department of Medicine, Queen's University, Belfast G Mulholland