Acid secretion and sensitivity to gastrin in patients with duodenal ulcer: effect of eradication of Helicobacter pylori

• Published in: Gut Vol. 34; no. 7; pp. 888 - 892
• Main Authors: Moss, S F, Calam, J
• Format: Journal Article
• Language: English
• Published: London BMJ Publishing Group Ltd and British Society of Gastroenterology 01-07-1993; BMJ; BMJ Publishing Group LTD
• Subjects: Acute Disease; Adult; Aged; Bacterial diseases; Bacterial diseases of the digestive system and abdomen; Biological and medical sciences; Bismuth - therapeutic use; Drug Therapy, Combination; Duodenal Ulcer - drug therapy; Duodenal Ulcer - metabolism; Gastric Acid - metabolism; Gastrins - metabolism; Gastrins - pharmacology; Helicobacter Infections - drug therapy; Helicobacter pylori; Human bacterial diseases; Humans; Infectious diseases; Male; Medical sciences; Metronidazole - therapeutic use; Middle Aged; Organometallic Compounds - therapeutic use; Parietal Cells, Gastric - drug effects; Tetracycline - therapeutic use; Human; Duodenal disease; Spirillales; Duodenum; Secretion; Spirillaceae; Eradication; Result; Gastrointestinal hormone; Acids; Helicobacter pylori; Gastrin; Digestive diseases; Bacteria; Ulcer
• ISSN: 0017-5749; 1468-3288; 1458-3288
• DOI: 10.1136/gut.34.7.888

The effect of ulcer healing with eradication of Helicobacter pylori (H pylori) on gastric function was investigated in nine patients with duodenal ulcer disease. One month after eradication there were significant reductions in both basal plasma gastrin concentration, from a median (range) of 19 (1-22) to 6 (2-15) pmol/l (p < 0.05), and of basal acid secretion from 8.3 (2.4-24) to 2.6 (1.4-8.1) mM H+/h, (p < 0.01). The peak acid secretion rate was unchanged from 37 (16-59) to 37 (21-59) mM H+/h. After treatment there was no change in the parietal cell sensitivity to stepped infusions of gastrin heptadecapeptide: the median concentration of gastrin required for 50% of maximal acid secretion (EC50) was 41 (14.8-126) before and 33 (23-125) pmol/l after eradication of H pylori. The metabolic clearance rate of gastrin was also unaffected by the eradication of H pylori. Thus eradication of H pylori infection from patients with active duodenal ulcers is accompanied by falls in both basal gastrin release and basal acid secretion without a change in the parietal cell sensitivity to gastrin. Cyclical changes in H pylori infection may cause the variations in basal acid secretion that are seen in duodenal ulcer disease.