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A mechanism by which Helicobacter pylori infection of the antrum contributes to the development of duodenal ulcer.
Gastroenterology. 1996 May; 110(5):1386-94.G

Abstract

BACKGROUND & AIMS

Helicobacter pylori infection and duodenal ulcer disease are firmly correlated. However, the bacteria do mainly colonize the antrum, indicating an indirect pathogenic mechanism. The aim of this study was to test a concept claiming that H. pylori infection of the antrum selectively blocks normal inhibitory reflex pathways to gastrin and parietal cells.

METHODS

The effect of antral distention was studied on gastric acid secretion stimulated by pentagastrin and on gastrin release stimulated by gastrin-releasing peptide in H. pylori-infected and noninfected patients with and without duodenal ulcer disease, as well as after eradication of the bacteria.

RESULTS

The inhibitory effect on gastric acid secretion induced by antral distention was absent in H. pylori-infected patients irrespective of whether or not they had duodenal ulcer disease. The inhibitory mechanism was restituted in 8 of 10 patients within 9 months after successful eradication of H. pylori infection. Similar results were obtained in studies on gastrin release.

CONCLUSIONS

H. pylori infection blocks normal, physiological inhibitory mechanisms from the antrum to both the gastrin cells and to the parietal cell region, resulting in increased gastrin release and impaired inhibition of gastric acid secretion, which will probably lead to an increased duodenal acid load as a general prerequisite for the development of duodenal ulcer disease.

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Publisher Full Text

Authors+Show Affiliations

Olbe L
Department of Surgery, Sahlgrenska Hospital, Göteborg, Sweden.
Hamlet A
No affiliation info available
Dalenbäck J
No affiliation info available
Fändriks L
No affiliation info available

MeSH

AdultAgedDuodenal UlcerFemaleGastric AcidGastric DilatationGastrin-Releasing PeptideGastrinsHelicobacter InfectionsHelicobacter pyloriHumansMaleMiddle AgedParietal Cells, GastricPentagastrinPeptidesPyloric AntrumStomach Diseases

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8613042

Citation

Olbe, L, et al. "A Mechanism By Which Helicobacter Pylori Infection of the Antrum Contributes to the Development of Duodenal Ulcer." Gastroenterology, vol. 110, no. 5, 1996, pp. 1386-94.
Olbe L, Hamlet A, Dalenbäck J, et al. A mechanism by which Helicobacter pylori infection of the antrum contributes to the development of duodenal ulcer. Gastroenterology. 1996;110(5):1386-94.
Olbe, L., Hamlet, A., Dalenbäck, J., & Fändriks, L. (1996). A mechanism by which Helicobacter pylori infection of the antrum contributes to the development of duodenal ulcer. Gastroenterology, 110(5), 1386-94.
Olbe L, et al. A Mechanism By Which Helicobacter Pylori Infection of the Antrum Contributes to the Development of Duodenal Ulcer. Gastroenterology. 1996;110(5):1386-94. PubMed PMID: 8613042.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A mechanism by which Helicobacter pylori infection of the antrum contributes to the development of duodenal ulcer. AU - Olbe,L, AU - Hamlet,A, AU - Dalenbäck,J, AU - Fändriks,L, PY - 1996/5/1/pubmed PY - 1996/5/1/medline PY - 1996/5/1/entrez SP - 1386 EP - 94 JF - Gastroenterology JO - Gastroenterology VL - 110 IS - 5 N2 - BACKGROUND & AIMS: Helicobacter pylori infection and duodenal ulcer disease are firmly correlated. However, the bacteria do mainly colonize the antrum, indicating an indirect pathogenic mechanism. The aim of this study was to test a concept claiming that H. pylori infection of the antrum selectively blocks normal inhibitory reflex pathways to gastrin and parietal cells. METHODS: The effect of antral distention was studied on gastric acid secretion stimulated by pentagastrin and on gastrin release stimulated by gastrin-releasing peptide in H. pylori-infected and noninfected patients with and without duodenal ulcer disease, as well as after eradication of the bacteria. RESULTS: The inhibitory effect on gastric acid secretion induced by antral distention was absent in H. pylori-infected patients irrespective of whether or not they had duodenal ulcer disease. The inhibitory mechanism was restituted in 8 of 10 patients within 9 months after successful eradication of H. pylori infection. Similar results were obtained in studies on gastrin release. CONCLUSIONS: H. pylori infection blocks normal, physiological inhibitory mechanisms from the antrum to both the gastrin cells and to the parietal cell region, resulting in increased gastrin release and impaired inhibition of gastric acid secretion, which will probably lead to an increased duodenal acid load as a general prerequisite for the development of duodenal ulcer disease. SN - 0016-5085 UR - https://www.unboundmedicine.com/medline/citation/8613042/A_mechanism_by_which_Helicobacter_pylori_infection_of_the_antrum_contributes_to_the_development_of_duodenal_ulcer_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0016508596002089 DB - PRIME DP - Unbound Medicine ER -