Campylobacter Pylori and Duodenal Ulcers: The Gastrin Link

Levi, S; Haddad, Ghesan; Ghosh, P.; Beardshall, K; Playford, Raymond J.; Calam, J.

doi:10.1016/s0140-6736(89)92752-9

Cited by 308 publications

(108 citation statements)

References 13 publications

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“…While the link between hypergastrinemia and acid hypersecretion in H. pylori infection had been established early in H. pylori research activities [11,15], the implication of neural pathways became recognized later in time. H. pylori infection leads to disruption of the normal antral-fundic connections which contribute to control acid secretion.…”

Section: Acid Secretion In Peptic Ulcer Diseasementioning

confidence: 99%

The Intriguing Relationship of <i>Helicobacter pylori</i> Infection and Acid Secretion in Peptic Ulcer Disease and Gastric Cancer

Malfertheiner

2011

Dig Dis

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Helicobacter pylori infection induces chronic inflammation of the gastric mucosa and thus profoundly affects gastric physiology. In the acute phase of infection, gastric acid secretion is transiently impaired. The morphological damage of the gastric mucosa, changes in gastric hormone release, and disruption of neural pathways all contribute to influence gastric acid secretion in a distinct manner. Changes in gastric acid secretion, whether impaired or increased, are intimately related with the topographic phenotypes of gastritis and the presence of atrophy or absence of corpus atrophy. The interplay of gastritis phenotype and acid secretion are key determinants in disease outcomes. Corpus-predominant gastritis and corpus atrophy are accompanied by hypochlorhydria and carry the highest risk for gastric cancer, whereas antrum-predominant gastritis with little involvement of the corpus-fundic mucosa is associated with hyperchlorhydria and predisposes to duodenal ulcer disease.

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Section: Acid Secretion In Peptic Ulcer Diseasementioning

confidence: 99%

The Intriguing Relationship of <i>Helicobacter pylori</i> Infection and Acid Secretion in Peptic Ulcer Disease and Gastric Cancer

Malfertheiner

2011

Dig Dis

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“…pylori infection raises plasma gastrin remains unclear. Levi et al (26) postulated that it was due to the elevation of antral surface p H by the organism's ammonia production, but subsequent studies have indicated that this is not the case (5-7). The present study indicates that the hypergastrinaemia in duodenal ulcer patients with H .…”

Section: Acid Output ( M M O L L H )mentioning

confidence: 99%

Effect of Helicobacter pylori on Parietal Cell Sensitivity to Pentagastrin in Duodenal Ulcer Subjects

Chittajallu

Howie

McColl

1992

Scandinavian Journal of Gastroenterology

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We have investigated the possibility that hypergastrinaemia in chronic Helicobacter pylori infection is a compensatory response to reduced parietal cell sensitivity to gastrin. The acid response to 45-min infusions of pentagastrin at sequential doses (micrograms/kg/h) of 0, 0.031, 0.062, 0.124, and 0.6 was compared before and 1 month after eradication of H. pylori in eight duodenal ulcer patients. The median acid outputs (mmol/h) with the respective infusions were 5.0, 7.5, 26.5, 30.8, and 37.0 when H. pylori-positive and similar at 4.5, 7.1, 22.7, 28, and 31.5 when H. pylori-negative. The median estimated dose of pentagastrin required to produce 50% maximal response (D50) was similar before (0.060 micrograms/kg/h) and after (0.057 micrograms/kg/h) eradication of H. pylori. The median estimated maximal response to pentagastrin (mmol/h) was also similar before (39.2) and after (32.3) treatment. The median basal gastrin concentration was 48 ng/l (range, 22-77) before treatment and fell to 33 ng/l (range, 8-37) after eradication of H. pylori (p = 0.03). These findings show that the parietal cell sensitivity to pentagastrin is unaffected by chronic H. pylori infection in duodenal ulcer subjects and that the hypergastrinaemia cannot be attributed to the bacterium inhibiting parietal cell function.

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“…Recently, the changes in gastric acid caused by H. pylori infection have drawn more attention, for inhibition of gastric acid secretion promoted duodenal ulcer healing even in the presence of H. pylori and inflammation of gastric antrum [27] . The possible hypotheses in explaining the relationship between H. pylori infection and duodenal ulcer have been described as "gastrin link" [2,28,29] or "somatostatin link" [10,30] , as duodenal ulcer patients with H. pylori infection often have hypergastrinemia, which may increase parietal cell mass and reduce somatostatin secretion known to promote the gastric secretion [4][5][6][27][28][29][30] . On the contrary, there was no consistent relationship between chronic H. pylori infection and acid secretion observed [11,12,30,31] .…”

Section: Discussionmentioning

confidence: 99%

Reduced secretion of epidermal growth factor in duodenal ulcer patients with Helicobacter pylori infection

Chen¹,

Zhang²,

Jiang³

et al. 2011

WJG

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AIM:To investigate the concentration changes of epidermal growth factor (EGF) in duodenal ulcer patients with Helicobacter pylori (H. pylori ) infection. METHODS:Immunoreactive concentration of somatostatin, gastrin and epidermal growth factor of gastric and saliva juice in healthy volunteers, and chronic gastritis and duodenal ulcer patients with H. pylori infection were measured by radioimmunoassay. RESULTS:Gastrin concentration of gastric juice in H. pylori -positive chronic gastritis (P > 0.05) and duodenal ulcer patients (P < 0.01) was higher than that of healthy volunteers (P < 0.05), whereas som atostatin concentration of gastric juice in chronic gastritis (P < 0.05) and duodenal ulcer patients (P < 0.01) was lower than that in healthy volunteers. Furthermore, EGF levels of gastric and saliva juice in duodenal ulcer patients with H. pylori infection (n = 10, 272.0 ng/L ± 96.3 ng/L and 8.3 ng/L ± 2.4 ng/L, respectively) were significantly lower than that in healthy volunteers (n = 12, 405.6 ng/ L ± 35.6 ng/mL and 22.0 ng/L ± 17.0 ng/L, respectively) and in H. pylori -positive chronic gastritis patients (n = 25, 423.0 ng/L ± 104.0 ng/L and 22.0 ng/L ± 11.1 ng/L, respectively (P < 0.05). CONCLUSION:A lower secretion of EGF may be a causative factor in the pathogenesis of H. pylori -positive duodenal ulcer.

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Campylobacter Pylori and Duodenal Ulcers: The Gastrin Link

Cited by 308 publications

References 13 publications

The Intriguing Relationship of <i>Helicobacter pylori</i> Infection and Acid Secretion in Peptic Ulcer Disease and Gastric Cancer

The Intriguing Relationship of <i>Helicobacter pylori</i> Infection and Acid Secretion in Peptic Ulcer Disease and Gastric Cancer

Effect of Helicobacter pylori on Parietal Cell Sensitivity to Pentagastrin in Duodenal Ulcer Subjects

Reduced secretion of epidermal growth factor in duodenal ulcer patients with Helicobacter pylori infection

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