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

• Published in: Gut Vol. 34; no. 6; pp. 757 - 761
• Main Authors: Mulholland, G, Ardill, J E, Fillmore, D, Chittajallu, R S, Fullarton, G M, McColl, K E
• Format: Journal Article
• Language: English
• Published: London BMJ Publishing Group Ltd and British Society of Gastroenterology 01.06.1993; BMJ; BMJ Publishing Group LTD
• Subjects: Adult; Bacterial diseases; Bacterial diseases of the digestive system and abdomen; Biological and medical sciences; Duodenal Ulcer - blood; Eating - physiology; Female; Gastrins - blood; Helicobacter Infections - blood; Helicobacter pylori; Human bacterial diseases; Humans; Infectious diseases; Male; Medical sciences; Middle Aged; Protein Precursors - blood; Human; Assay; Gastrointestinal hormone; Spirillales; Helicobacter pylori; Postprandial; Gastrin; Spirillaceae; Bacteria; Chromatography; Comparative study; Hypergastrinemia
• ISSN: 0017-5749; 1468-3288; 1458-3288
• DOI: 10.1136/gut.34.6.757

Helicobacter pylori 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 pylori. Three antisera that are specific for particular regions of the gastrin molecules were used. Gel chromatography indicated that > 90% of the circulating gastrin consisted 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), entirely because of a fall in G17 from 6 pmol/l (< 2.4-25) to < 2.4 pmol/l (< 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 pmol/l (38-114) to 33 pmol/l (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 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 pmol/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 pylori. The finding that H pylori infection selectively increases G17 explains 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 mainly duodenal in origin. This study also indicates that the increased concentration of gastrin in H pylori infection is the result of an increase in one of the main biologically active forms of the hormone.