Immunostaining of antral gastrin cells is quantitatively increased in <i>Helicobacter pylori</i> gastritis

Sankey, E A; Helliwell, Peter; Dhillon, A.P.

doi:10.1111/j.1365-2559.1990.tb01083.x

Cited by 19 publications

(3 citation statements)

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“…6 21-25 Studies of antral biopsies from H pylori infected individuals have shown that gastrin synthesis is increased. 26 ''Overall, our data are consistent with the notion that the major defect leading to enhanced gastrin concentrations is related to disruption of the inhibitory effect of somatostatin on the G cell''…”

Section: Discussionsupporting

confidence: 88%

Gastrin (G) cells and somatostatin (D) cells in patients with dyspeptic symptoms: Helicobacter pylori associated and non-associated gastritis

Liu

Vosmaer²,

Tytgat³

et al. 2005

Journal of Clinical Pathology

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Background: Gastrin G cells and somatostatin D cells are important regulators of gastric acid secretion and alterations in their relative numbers may play a key role in gastroduodenal disease. Aim: To investigate the effect of Helicobacter pylori infection on the density of immunoreactive G and D cells in gastric antral and corpus biopsies from patients with dyspeptic complaints. Methods: One hundred and twenty two patients with dyspeptic complaints had two antrum and two corpus biopsies taken during upper endoscopy. The severity of inflammation and the density of H pylori were evaluated semiquantitatively. In addition, the density and distribution of neuroendocrine cells, especially G and D cells, were examined using immunohistochemistry. Patients were divided into three groups, those with H pylori positive gastritis, H pylori negative gastritis, and histologically normal gastric mucosa. Results: The number of immunoreactive G cells was significantly higher and the number of immunoreactive D cells lower in patients with H pylori positive gastritis compared with H pylori negative gastritis or histological normal gastric mucosa. The percentage of G cells as a percentage of mucosal endocrine cells was also raised and that of D cells was decreased. Conclusions: Helicobacter pylori infection produces alterations in the number of endocrine cells responsible for regulating acid secretion in relation to intragastric pH and feeding. The alterations correlate best with the severity of inflammation and not with H pylori density.

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Section: Discussionsupporting

confidence: 88%

Gastrin (G) cells and somatostatin (D) cells in patients with dyspeptic symptoms: Helicobacter pylori associated and non-associated gastritis

Liu

Vosmaer²,

Tytgat³

et al. 2005

Journal of Clinical Pathology

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“…Sankey et al. (28) demonstrated significantly elevated G cell density in the mucosa of infected patients. He also found the G cells of infected patients to have increased immunoreactivity compared with those of healthy controls, suggesting that cell hyperactivity may be a factor.…”

Section: Discussionmentioning

confidence: 99%

Serum gastrin concentration and changes in G and D cell densities in gastric antrum in children with chronic gastritis

Czaja

Szarszewski

Kamińska

et al. 2007

International Journal of Clinical Practice

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The mean G/D cell ratios in groups I and III were almost identical. The mean fasting serum gastrin concentration was higher in children with both chronic gastritis and H. pylori infection compared with patients without infection or without antral inflammation. No difference in the G cell density or D cell density in children was found, regardless of the presence or absence of gastritis or H. pylori infection.

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“…Data regarding G cells and Hp gastritis in adults indicate that, although gastrin cell function may be augmented by Hp infection, G cell counts are not increased (34,35). However, in children with Hp gastritis, G cells have recently been reported to be increased (15).…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Infection in Children with Antral Gastrin Cell Hyperfunction

Rindi,

Annibale,

Bonamico

et al. 1994

J. pediatr. gastroenterol. nutr.

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SummaryAntral gastrin cell hyperfunction (AGCH) is a rare syndrome characterized by persistent hypergastrinemia and important peptic symptoms in the absence of a gastrin‐producing tumor. The pathogenesis of AGCH is still unknown and debated. Helicobacter pylori (Hp) infection has been reported as a possible cause of sustained hypergastrinemia. To assess the relevance of Hp infection in pediatric AGCH patients, Hp status, G cell function, acid secretion, and antral G and D cell populations were investigated in six children presenting with gastrointestinal bleeding of unknown origin, sideropenic anemia, and variable abdominal symptoms. All patients had moderate high basal gastrinemia with abnormally increased peak values after meals and elevated values of basal acid output (BAO), maximal acid output (MAO), and pentagastrin‐stimulated acid output (PAO). Circulating pepsinogen I was also significantly increased. Three children had Hp infection, as assessed by enzyme‐linked immunosorbent assay, urease test, and histology. Endoscopy showed duodenal erosions in three children, with ulcer in two Hp‐positive cases. At histology, moderate gastritis was observed only in the three Hp‐positive cases. In all patients, quantitative assessment of antral gastrin and somatostatin cells gave significantly elevated G cell counts; D cells were at the lower reference limit and the G/D cell ratio was significantly elevated. These data indicated a diagnosis of AGCH, possibly due to the elevated G/D cell ratio, and suggest HP infection as an overlapping factor complicating the clinical picture in some cases.

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Immunostaining of antral gastrin cells is quantitatively increased in Helicobacter pylori gastritis

Cited by 19 publications

References 13 publications

Gastrin (G) cells and somatostatin (D) cells in patients with dyspeptic symptoms: Helicobacter pylori associated and non-associated gastritis

Gastrin (G) cells and somatostatin (D) cells in patients with dyspeptic symptoms: Helicobacter pylori associated and non-associated gastritis

Serum gastrin concentration and changes in G and D cell densities in gastric antrum in children with chronic gastritis

Helicobacter pylori Infection in Children with Antral Gastrin Cell Hyperfunction

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