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Gastric bicarbonate secretion and release of prostaglandin E2 are increased in duodenal ulcer patients but not in Helicobacter pylori-positive healthy subjects.
Scand J Gastroenterol. 1996 Jan; 31(1):38-43.SJ

Abstract

BACKGROUND

Duodenal ulcer (DU) patients have impaired proximal duodenal mucosal bicarbonate secretion at rest and in response to luminal acid with higher acid-stimulated mucosal release of prostaglandin (PG) E2 than healthy subjects. Our purpose was to determine whether this abnormality was present also in the stomach of DU patients.

METHODS

Simultaneous determinations of gastric and duodenal bicarbonate secretion and luminal release of PGE2 were performed in 16 healthy volunteers (5 Helicobacter pylori-positive) and 8 inactive DU patients (all H. pylori-positive).

RESULTS

In healthy volunteers the rates of gastroduodenal bicarbonate secretion and the release of PGE2 were not influenced by H. pylori status. In inactive DU patients the rates of basal (704 +/- 84 versus 356 +/- 40 mumol/h; mean +/- SEM) and vagally stimulated (modified sham feeding) (1724 +/- 376 versus 592 +/- 52 mumol/h) gastric bicarbonate secretion were higher (p < 0.05) than in the health, whereas the corresponding rates (339 +/- 42 versus 591 +/- 51 mumol/h and 543 +/- 99 versus 778 +/- 69 mumol/h) in duodenal bicarbonate secretion were lower (p < 0.05). In addition, inactive DU patients had higher basal (148 +/- 32 versus 53 +/- 5 ng/h) and stimulated (291 +/- 84 versus 131 +/- 25 ng/h) gastric release of PGE2, but only the basal release of PGE2 into the duodenum was significantly increased (20 +/- 3 versus 5 +/- 1 ng/h; p < 0.05).

CONCLUSION

Increased mucosal production of PGE2 may be responsible for the abnormally high gastric secretion of bicarbonate in inactive DU patients. The defective duodenal secretion of bicarbonate observed in these patients may be a consequence of previous ulceration rather than the mere presence of H. pylori infection.

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Publisher Full Text

Authors+Show Affiliations

Mertz-Nielsen A
Dept. of Medical Gastroenterology, Hvidovre Hospital, Denmark.
Hillingsø J
No affiliation info available
Frøkiaer H
No affiliation info available
Bukhave K
No affiliation info available
Rask-Madsen J
No affiliation info available

MeSH

AdultBicarbonatesCase-Control StudiesDinoprostoneDuodenal UlcerFemaleGastric JuiceHelicobacter InfectionsHelicobacter pyloriHumansMaleMiddle AgedStomach Diseases

Pub Type(s)

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

Language

eng

PubMed ID

8927938

Citation

Mertz-Nielsen, A, et al. "Gastric Bicarbonate Secretion and Release of Prostaglandin E2 Are Increased in Duodenal Ulcer Patients but Not in Helicobacter Pylori-positive Healthy Subjects." Scandinavian Journal of Gastroenterology, vol. 31, no. 1, 1996, pp. 38-43.
Mertz-Nielsen A, Hillingsø J, Frøkiaer H, et al. Gastric bicarbonate secretion and release of prostaglandin E2 are increased in duodenal ulcer patients but not in Helicobacter pylori-positive healthy subjects. Scand J Gastroenterol. 1996;31(1):38-43.
Mertz-Nielsen, A., Hillingsø, J., Frøkiaer, H., Bukhave, K., & Rask-Madsen, J. (1996). Gastric bicarbonate secretion and release of prostaglandin E2 are increased in duodenal ulcer patients but not in Helicobacter pylori-positive healthy subjects. Scandinavian Journal of Gastroenterology, 31(1), 38-43.
Mertz-Nielsen A, et al. Gastric Bicarbonate Secretion and Release of Prostaglandin E2 Are Increased in Duodenal Ulcer Patients but Not in Helicobacter Pylori-positive Healthy Subjects. Scand J Gastroenterol. 1996;31(1):38-43. PubMed PMID: 8927938.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Gastric bicarbonate secretion and release of prostaglandin E2 are increased in duodenal ulcer patients but not in Helicobacter pylori-positive healthy subjects. AU - Mertz-Nielsen,A, AU - Hillingsø,J, AU - Frøkiaer,H, AU - Bukhave,K, AU - Rask-Madsen,J, PY - 1996/1/1/pubmed PY - 1996/1/1/medline PY - 1996/1/1/entrez SP - 38 EP - 43 JF - Scandinavian journal of gastroenterology JO - Scand J Gastroenterol VL - 31 IS - 1 N2 - BACKGROUND: Duodenal ulcer (DU) patients have impaired proximal duodenal mucosal bicarbonate secretion at rest and in response to luminal acid with higher acid-stimulated mucosal release of prostaglandin (PG) E2 than healthy subjects. Our purpose was to determine whether this abnormality was present also in the stomach of DU patients. METHODS: Simultaneous determinations of gastric and duodenal bicarbonate secretion and luminal release of PGE2 were performed in 16 healthy volunteers (5 Helicobacter pylori-positive) and 8 inactive DU patients (all H. pylori-positive). RESULTS: In healthy volunteers the rates of gastroduodenal bicarbonate secretion and the release of PGE2 were not influenced by H. pylori status. In inactive DU patients the rates of basal (704 +/- 84 versus 356 +/- 40 mumol/h; mean +/- SEM) and vagally stimulated (modified sham feeding) (1724 +/- 376 versus 592 +/- 52 mumol/h) gastric bicarbonate secretion were higher (p < 0.05) than in the health, whereas the corresponding rates (339 +/- 42 versus 591 +/- 51 mumol/h and 543 +/- 99 versus 778 +/- 69 mumol/h) in duodenal bicarbonate secretion were lower (p < 0.05). In addition, inactive DU patients had higher basal (148 +/- 32 versus 53 +/- 5 ng/h) and stimulated (291 +/- 84 versus 131 +/- 25 ng/h) gastric release of PGE2, but only the basal release of PGE2 into the duodenum was significantly increased (20 +/- 3 versus 5 +/- 1 ng/h; p < 0.05). CONCLUSION: Increased mucosal production of PGE2 may be responsible for the abnormally high gastric secretion of bicarbonate in inactive DU patients. The defective duodenal secretion of bicarbonate observed in these patients may be a consequence of previous ulceration rather than the mere presence of H. pylori infection. SN - 0036-5521 UR - https://www.unboundmedicine.com/medline/citation/8927938/Gastric_bicarbonate_secretion_and_release_of_prostaglandin_E2_are_increased_in_duodenal_ulcer_patients_but_not_in_Helicobacter_pylori_positive_healthy_subjects_ L2 - https://www.tandfonline.com/doi/full/10.3109/00365529609031624 DB - PRIME DP - Unbound Medicine ER -