Gastric bicarbonate secretion and release of prostaglandin E2 are increased in duodenal ulcer patients but not in Helicobacter pylori-positive healthy subjects

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Standard

Gastric bicarbonate secretion and release of prostaglandin E2 are increased in duodenal ulcer patients but not in Helicobacter pylori-positive healthy subjects. / Mertz-Nielsen, A.; Hillingsø, J.; Frøkiær, H.; Bukhave, K.; Rask-Madsen, J.

I: Scandinavian Journal of Gastroenterology, Bind 31, Nr. 1, 1996, s. 38-43.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Mertz-Nielsen, A, Hillingsø, J, Frøkiær, 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, bind 31, nr. 1, s. 38-43. https://doi.org/10.3109/00365529609031624

APA

Mertz-Nielsen, A., Hillingsø, J., Frøkiær, 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. https://doi.org/10.3109/00365529609031624

Vancouver

Mertz-Nielsen A, Hillingsø J, Frøkiær H, Bukhave K, Rask-Madsen J. 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. 1996;31(1):38-43. https://doi.org/10.3109/00365529609031624

Author

Mertz-Nielsen, A. ; Hillingsø, J. ; Frøkiær, H. ; Bukhave, K. ; Rask-Madsen, J. / Gastric bicarbonate secretion and release of prostaglandin E2 are increased in duodenal ulcer patients but not in Helicobacter pylori-positive healthy subjects. I: Scandinavian Journal of Gastroenterology. 1996 ; Bind 31, Nr. 1. s. 38-43.

Bibtex

@article{7c393d94432d4eeebe761304f4c9f349,
title = "Gastric bicarbonate secretion and release of prostaglandin E2 are increased in duodenal ulcer patients but not in Helicobacter pylori-positive healthy subjects",
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 μmol/h; mean ± SEM) and vagally stimulated (modified sham feeding) (1724 ± 376 versus 592 ± 52 μmol/h) gastric bicarbonate secretion were higher (p < 0.05) than in the health, whereas the corresponding rates (339 ± 42 versus 591 ± 51 μmol/h and 543 ± 99 versus 778 ± 69 μmol/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.",
keywords = "Bicarbonate secretion, Duodenal ulcer, Duodenum, Helicobacter pylori, Prostaglandins, Stomach",
author = "A. Mertz-Nielsen and J. Hillings{\o} and H. Fr{\o}ki{\ae}r and K. Bukhave and J. Rask-Madsen",
note = "Funding Information: ACKNOWLEDGEMENTS The study was supported by grants from Director J. Madsen{\textquoteright}s Foundation, P. Carl Petersen{\textquoteright}s Foundation, and the Danish Medical Research Council (project 12-0219). The skilful technical assistance of H. Fuglsang, T. Gartner, and I-L. Uffval is gratefully acknowledged. We thank Dr. P. Andersen for measuring antibody titres against Helicobacter pylori.",
year = "1996",
doi = "10.3109/00365529609031624",
language = "English",
volume = "31",
pages = "38--43",
journal = "Scandinavian Journal of Gastroenterology. Supplement",
issn = "0085-5928",
publisher = "Taylor & Francis",
number = "1",

}

RIS

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 - Frøkiær, H.

AU - Bukhave, K.

AU - Rask-Madsen, J.

N1 - Funding Information: ACKNOWLEDGEMENTS The study was supported by grants from Director J. Madsen’s Foundation, P. Carl Petersen’s Foundation, and the Danish Medical Research Council (project 12-0219). The skilful technical assistance of H. Fuglsang, T. Gartner, and I-L. Uffval is gratefully acknowledged. We thank Dr. P. Andersen for measuring antibody titres against Helicobacter pylori.

PY - 1996

Y1 - 1996

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 μmol/h; mean ± SEM) and vagally stimulated (modified sham feeding) (1724 ± 376 versus 592 ± 52 μmol/h) gastric bicarbonate secretion were higher (p < 0.05) than in the health, whereas the corresponding rates (339 ± 42 versus 591 ± 51 μmol/h and 543 ± 99 versus 778 ± 69 μmol/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.

AB - 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 μmol/h; mean ± SEM) and vagally stimulated (modified sham feeding) (1724 ± 376 versus 592 ± 52 μmol/h) gastric bicarbonate secretion were higher (p < 0.05) than in the health, whereas the corresponding rates (339 ± 42 versus 591 ± 51 μmol/h and 543 ± 99 versus 778 ± 69 μmol/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.

KW - Bicarbonate secretion

KW - Duodenal ulcer

KW - Duodenum

KW - Helicobacter pylori

KW - Prostaglandins

KW - Stomach

UR - http://www.scopus.com/inward/record.url?scp=0030060722&partnerID=8YFLogxK

U2 - 10.3109/00365529609031624

DO - 10.3109/00365529609031624

M3 - Journal article

C2 - 8927938

AN - SCOPUS:0030060722

VL - 31

SP - 38

EP - 43

JO - Scandinavian Journal of Gastroenterology. Supplement

JF - Scandinavian Journal of Gastroenterology. Supplement

SN - 0085-5928

IS - 1

ER -

ID: 331794612