Helicobacter pylori infection is associated with low antral somatostatin content in young adults. Implications for the pathogenesis of hypergastrinemia.
BACKGROUND
Recent studies on the role of Helicobacter pylori in the pathogenesis of duodenal ulcers have focused on the mechanism by which H. pylori infections cause exaggerated gastrin release.


METHODS
We determined meal-stimulated serum gastrin concentrations and antral somatostatin content in 24 asymptomatic volunteers (6 H. pylori-infected, 18 H. pylori-uninfected). Somatostatin content was determined by radioimmunoassay in biopsy specimens obtained from the antrum.


RESULTS
Fasting and integrated 2-h gastrin concentrations were significantly higher in H. pylori-positive volunteers than in H. pylori-negative volunteers (fasting, 111 +/- 16.3 pmol/l versus 53.4 +/- 3.5 pmol/l; p < 0.05; integrated 2-h, 267 +/- 41.2 pmol/l versus 70.1 +/- 2.1 pmol/l; p < 0.01). Antral somatostatin content was 0.764 +/- 0.173 ng/mg and 2.931 +/- 0.414 ng/mg in H. pylori-positive and -negative volunteers, respectively (p < 0.01).


CONCLUSIONS
Low antral somatostatin content may cause hypergastrinemia in asymptomatic healthy volunteers, and H. pylori may contribute to the pathogenesis of duodenal ulcer, through this mechanism.
Haruma
K
K
First Dept. of Internal Medicine, Hiroshima University School of Medicine, Japan.
Sumii
K
K
Okamoto
S
S
Yoshihara
M
M
Sumii
M
M
Kajiyama
G
G
Wagner
S
S
D000328:Adult; D001706:Biopsy; D004381:Duodenal Ulcer / Q000378:metabolism / Q000382:microbiology; D005755:Gastrins / Q000096:biosynthesis* / Q000097:blood; D005773:Gastroscopy; D016481:Helicobacter Infections / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D008297:Male; D011706:Pyloric Antrum / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D011863:Radioimmunoassay; D013004:Somatostatin / Q000032:analysis / Q000096:biosynthesis*
D005755:Gastrins; D013004:Somatostatin