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, Jens Hillingsø, Hanne Frøkiær, Klaus Bukhave, Jørgen Rask-Madsen

    Research output: Contribution to journalJournal articleResearchpeer-review

    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) E(2) 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 PGE(2) were performed in 16 healthy volunteers (5 Helicobacter pylori-positive) and 8 inactive DU patients (all H. pylori-positivr). Results: In healthy volunteers the rates of gastroduodenal bicarbonate secretion and the release of PGE(2), were not influenced by H. pylori status. In inactive DU patients the rates of basal (704 +/- 84 versus 356 +/- 40 mu mol/h: mean +/- SEM) and vagally stimulated (modified sham feeding) (1724 +/- 376 versus 592 +/- 52 mu mol/h) gastric bicarbonate secretion were higher (p < 0.05) than in the health, whereas the corresponding rates (339 +/- 42 versus 591 +/- 51 mu mol/h and 543 +/- 99 versus 778 +/- 69 mu mol/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 PGE(2), but only the basal release of PGE(2) into the duodenum was significantly increased (20 +/- 3 versus 5 +/- 1 ng/h; p < 0.05). Conclusion: Increased mucosal production of PGE(2) may be responsible for the abnormally high gastric secretion of bicarbonate in inactive DU patients. Th; 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.
    Original languageEnglish
    JournalScandinavian Journal of Gastroenterology
    Volume31
    Issue number1
    Pages (from-to)38-41
    ISSN0036-5521
    DOIs
    Publication statusPublished - 1996

    Cite this

    A, Mertz-Nielsen ; Hillingsø, Jens ; Frøkiær, Hanne ; Bukhave, Klaus ; Rask-Madsen, Jørgen. / Gastric bicarbonate secretion and release of prostaglandin E2 are increased in duodenal ulcer patients, but not in Helicobacter pylori positive healthy subjects. In: Scandinavian Journal of Gastroenterology. 1996 ; Vol. 31, No. 1. pp. 38-41.
    @article{2d7cdeff9b2c4865bb18f3a87ce6c08e,
    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) E(2) 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 PGE(2) were performed in 16 healthy volunteers (5 Helicobacter pylori-positive) and 8 inactive DU patients (all H. pylori-positivr). Results: In healthy volunteers the rates of gastroduodenal bicarbonate secretion and the release of PGE(2), were not influenced by H. pylori status. In inactive DU patients the rates of basal (704 +/- 84 versus 356 +/- 40 mu mol/h: mean +/- SEM) and vagally stimulated (modified sham feeding) (1724 +/- 376 versus 592 +/- 52 mu mol/h) gastric bicarbonate secretion were higher (p < 0.05) than in the health, whereas the corresponding rates (339 +/- 42 versus 591 +/- 51 mu mol/h and 543 +/- 99 versus 778 +/- 69 mu mol/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 PGE(2), but only the basal release of PGE(2) into the duodenum was significantly increased (20 +/- 3 versus 5 +/- 1 ng/h; p < 0.05). Conclusion: Increased mucosal production of PGE(2) may be responsible for the abnormally high gastric secretion of bicarbonate in inactive DU patients. Th; 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.",
    author = "Mertz-Nielsen A and Jens Hillings{\o} and Hanne Fr{\o}ki{\ae}r and Klaus Bukhave and J{\o}rgen Rask-Madsen",
    year = "1996",
    doi = "10.3109/00365529609031624",
    language = "English",
    volume = "31",
    pages = "38--41",
    journal = "Scandinavian Journal of Gastroenterology",
    issn = "0036-5521",
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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. / A, Mertz-Nielsen; Hillingsø, Jens; Frøkiær, Hanne; Bukhave, Klaus; Rask-Madsen, Jørgen.

    In: Scandinavian Journal of Gastroenterology, Vol. 31, No. 1, 1996, p. 38-41.

    Research output: Contribution to journalJournal articleResearchpeer-review

    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 - A, Mertz-Nielsen

    AU - Hillingsø, Jens

    AU - Frøkiær, Hanne

    AU - Bukhave, Klaus

    AU - Rask-Madsen, Jørgen

    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) E(2) 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 PGE(2) were performed in 16 healthy volunteers (5 Helicobacter pylori-positive) and 8 inactive DU patients (all H. pylori-positivr). Results: In healthy volunteers the rates of gastroduodenal bicarbonate secretion and the release of PGE(2), were not influenced by H. pylori status. In inactive DU patients the rates of basal (704 +/- 84 versus 356 +/- 40 mu mol/h: mean +/- SEM) and vagally stimulated (modified sham feeding) (1724 +/- 376 versus 592 +/- 52 mu mol/h) gastric bicarbonate secretion were higher (p < 0.05) than in the health, whereas the corresponding rates (339 +/- 42 versus 591 +/- 51 mu mol/h and 543 +/- 99 versus 778 +/- 69 mu mol/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 PGE(2), but only the basal release of PGE(2) into the duodenum was significantly increased (20 +/- 3 versus 5 +/- 1 ng/h; p < 0.05). Conclusion: Increased mucosal production of PGE(2) may be responsible for the abnormally high gastric secretion of bicarbonate in inactive DU patients. Th; 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) E(2) 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 PGE(2) were performed in 16 healthy volunteers (5 Helicobacter pylori-positive) and 8 inactive DU patients (all H. pylori-positivr). Results: In healthy volunteers the rates of gastroduodenal bicarbonate secretion and the release of PGE(2), were not influenced by H. pylori status. In inactive DU patients the rates of basal (704 +/- 84 versus 356 +/- 40 mu mol/h: mean +/- SEM) and vagally stimulated (modified sham feeding) (1724 +/- 376 versus 592 +/- 52 mu mol/h) gastric bicarbonate secretion were higher (p < 0.05) than in the health, whereas the corresponding rates (339 +/- 42 versus 591 +/- 51 mu mol/h and 543 +/- 99 versus 778 +/- 69 mu mol/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 PGE(2), but only the basal release of PGE(2) into the duodenum was significantly increased (20 +/- 3 versus 5 +/- 1 ng/h; p < 0.05). Conclusion: Increased mucosal production of PGE(2) may be responsible for the abnormally high gastric secretion of bicarbonate in inactive DU patients. Th; 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.

    U2 - 10.3109/00365529609031624

    DO - 10.3109/00365529609031624

    M3 - Journal article

    VL - 31

    SP - 38

    EP - 41

    JO - Scandinavian Journal of Gastroenterology

    JF - Scandinavian Journal of Gastroenterology

    SN - 0036-5521

    IS - 1

    ER -