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

Abstract

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)

Effects of Helicobacter pylori Infection on the Link between Regenerating Gene Expression and Serum Gastrin Levels in Mongolian Gerbils

“…Mild hypergastrinemia is generally observed in patients with chronic H. pylori-induced gastritis (Levi et al, 1989;Mulholland et al, 1993) and, although H. pylori-induced gastritis has been reported to cause hypergastrinemia either directly or indirectly via the production of various cytokines (Beales et al, 1997;Calam, 1996;Lehmann et al, 1996), our present data favor the idea that reduced gastric acidity is responsible for such hypergastrinemia.…”

Helicobacter pylori Infection and the Risk of Colorectal Adenoma and Adenocarcinoma: an Updated Meta-analysis of Different Testing Methods

“…CagA binds and activates human phosphatase (SHP2), which then acts as an oncoprotein promoting cell growth (Lochhead et al, 2007). In addition, hypergastrinemia, which is associated with H. pylori colonization, has been hypothesized as a possible mechanism for tumorigenesis because of its trophic effect on the intestinal mucosa (Mulholland et al, 1993;Sobhani et al, 1993;A. Hartwich et al, 2001).…”

Helicobacter pylori Can Induce Heparin-Binding Epidermal Growth Factor Expression via Gastrin and Its Receptor

“…Consequently, the effect of additional exogenous gastrin on H. pylori-induced effects was also examined. G17 was added simultaneously with the bacteria to better model the serum hypergastrinemia that can occur as a result of H. pylori infection (39).…”