HELICOBACTER-PYLORI RELATED HYPERGASTRINEMIA IS THE RESULT OF A SELECTIVE INCREASE IN GASTRIN-17

Helicobacter pylori infection increases the serum concentration of gas trin, and this may be one of the mechanisms by which it predisposes to duodenal ulceration. Different forms of circulating gastrin were stud ied both basally and postprandially in 13 duodenal ulcer patients befo re and one month after eradication of H pylori. Three antisera that ar e specific for particular regions of the gastrin molecules were used. Gel chromatography indicated that >90% of the circulating gastrin cons isted of gastrin (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 pmol/l (8-39) (p<0.05), entir ely because of a fall in G17 from 6 pmol/I (<2.4-25) to <2.4 pmol/I (< 2.4-23) (p<0.001). The median (range) basal G34 values were similar be fore (15 pmol (2-36)) and after (10 pmol (2-30)) eradication. The medi an total immunoreactive gastrin concentration determined 20 minutes po stprandially fell from 59 pmol/l (38-114) to 33 pmol/l (19-88) (p<0.00 5), and again this was entirely the result of a fall in G17 from 43 pm ol/l (9-95) to 17 pmol/l (<2.4-52) (p<0.001). The median postprandial G34 values were similar before (13 pmol/l, range 6-42) and after (15 p mol/l, range 6-30) eradication. Eating stimulated a noticeable rise in G17 but little change in G34, both in the presence and absence of H p ylori. The finding that H pylori infection selectively increases G17 e xplains why the infection causes mainly postprandial hypergastrinaemia . G17 is increased selectively because H pylori predominantly affects the antral mucosa which is the main source of G17 whereas G34 is mainl y duodenal in origin. This study also indicates that the increased con centration of gastrin in H pylori infection is the result of an increa se in one of the main biologically active forms of the hormone.