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Effect of Helicobacter pylori infection on antral gastrin and somatostatin cells and on serum gastrin concentrations.

Park SM, Lee HR, Kim JG, Park JW, Jung G, Han SH, Cho JH, Kim MK - Korean J. Intern. Med. (1999)

Bottom Line: The number of D-cells was significantly lower in patients with H. pylori infection than in uninfected patients in both duodenal and gastric ulcer patients (1.3 +/- 0.4 vs 2.5 +/- 1.6, respectively, p < 0.001).The ratio of G-cells to D-cells was also significantly higher in infected patients compared with uninfected patients for both gastric and duodenal ulcers (5.7 +/- 2.7 vs 3.5 +/- 1.9, respectively, p < 0.001).These results strongly suggest that Helicobacter pylori infection induces reduction of the number of antral D-cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, College of Medicine, Chung-Ang University, Seoul, Korea.

ABSTRACT

Objectives: Helicobacter pylori infection induces selective reduction of the number of antral D-cells and results in abnormal regulation of serum gastrin secretion. The purpose of this study was to investigate the relationship between H. pylori infection and the numbers of G-cells and D-cells.

Methods: The numbers of antral G-cells and D-cells, the ratio of G-cells to D-cells and fasting serum gastrin concentrations were compared between 37 patients with (29 with duodenal ulcers and 8 with gastric ulcers) and 33 without H. pylori infection (22 with duodenal ulcers and 11 with gastric ulcers). Serum gastrin concentrations were measured using the radioimmunoassay technique. Antral mucosal biopsy specimens were examined using immunohistochemical staining with antibodies specific for gastrin and somatostatin and the numbers of G-cells and D-cells per gastric gland were counted.

Results: Fasting serum gastrin concentrations were significantly higher in patients with H. pylori infection compared to patients without infection (80.3 +/- 23.5 vs 47.6 +/- 14.1 pg/ml, p < 0.001). The number of G-cells per gastric gland was similar in infected and uninfected patients (7.1 +/- 3.1 vs 7.3 +/- 3.9, respectively, p > 0.5). The number of D-cells was significantly lower in patients with H. pylori infection than in uninfected patients in both duodenal and gastric ulcer patients (1.3 +/- 0.4 vs 2.5 +/- 1.6, respectively, p < 0.001). The ratio of G-cells to D-cells was also significantly higher in infected patients compared with uninfected patients for both gastric and duodenal ulcers (5.7 +/- 2.7 vs 3.5 +/- 1.9, respectively, p < 0.001).

Conclusions: These results strongly suggest that Helicobacter pylori infection induces reduction of the number of antral D-cells. The resulting relative hypofunction of the inhibitory action of D-cells against G-cells may be responsible for increased serum gastrin secretion.

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The Number of G cells per Gastric Gland in Patients with and without infection. (p<0.5)
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f2-kjim-14-1-15-3: The Number of G cells per Gastric Gland in Patients with and without infection. (p<0.5)

Mentions: The mean number of G-cells per gastric gland was similar in patients with and without H. pylori infection. (7.1±3.1 vs 7.3±3.9, respectively, p>0.5) (Fig. 2). There were no differences in the number of G-cells between GU and DU patients within both the infected group (8.6±4.3 vs 6.7±2.6, respectively, p>0.5) and the uninfected group (6.6±2.3 vs 7.7±4.5, p>0.5).


Effect of Helicobacter pylori infection on antral gastrin and somatostatin cells and on serum gastrin concentrations.

Park SM, Lee HR, Kim JG, Park JW, Jung G, Han SH, Cho JH, Kim MK - Korean J. Intern. Med. (1999)

The Number of G cells per Gastric Gland in Patients with and without infection. (p<0.5)
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4531904&req=5

f2-kjim-14-1-15-3: The Number of G cells per Gastric Gland in Patients with and without infection. (p<0.5)
Mentions: The mean number of G-cells per gastric gland was similar in patients with and without H. pylori infection. (7.1±3.1 vs 7.3±3.9, respectively, p>0.5) (Fig. 2). There were no differences in the number of G-cells between GU and DU patients within both the infected group (8.6±4.3 vs 6.7±2.6, respectively, p>0.5) and the uninfected group (6.6±2.3 vs 7.7±4.5, p>0.5).

Bottom Line: The number of D-cells was significantly lower in patients with H. pylori infection than in uninfected patients in both duodenal and gastric ulcer patients (1.3 +/- 0.4 vs 2.5 +/- 1.6, respectively, p < 0.001).The ratio of G-cells to D-cells was also significantly higher in infected patients compared with uninfected patients for both gastric and duodenal ulcers (5.7 +/- 2.7 vs 3.5 +/- 1.9, respectively, p < 0.001).These results strongly suggest that Helicobacter pylori infection induces reduction of the number of antral D-cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, College of Medicine, Chung-Ang University, Seoul, Korea.

ABSTRACT

Objectives: Helicobacter pylori infection induces selective reduction of the number of antral D-cells and results in abnormal regulation of serum gastrin secretion. The purpose of this study was to investigate the relationship between H. pylori infection and the numbers of G-cells and D-cells.

Methods: The numbers of antral G-cells and D-cells, the ratio of G-cells to D-cells and fasting serum gastrin concentrations were compared between 37 patients with (29 with duodenal ulcers and 8 with gastric ulcers) and 33 without H. pylori infection (22 with duodenal ulcers and 11 with gastric ulcers). Serum gastrin concentrations were measured using the radioimmunoassay technique. Antral mucosal biopsy specimens were examined using immunohistochemical staining with antibodies specific for gastrin and somatostatin and the numbers of G-cells and D-cells per gastric gland were counted.

Results: Fasting serum gastrin concentrations were significantly higher in patients with H. pylori infection compared to patients without infection (80.3 +/- 23.5 vs 47.6 +/- 14.1 pg/ml, p < 0.001). The number of G-cells per gastric gland was similar in infected and uninfected patients (7.1 +/- 3.1 vs 7.3 +/- 3.9, respectively, p > 0.5). The number of D-cells was significantly lower in patients with H. pylori infection than in uninfected patients in both duodenal and gastric ulcer patients (1.3 +/- 0.4 vs 2.5 +/- 1.6, respectively, p < 0.001). The ratio of G-cells to D-cells was also significantly higher in infected patients compared with uninfected patients for both gastric and duodenal ulcers (5.7 +/- 2.7 vs 3.5 +/- 1.9, respectively, p < 0.001).

Conclusions: These results strongly suggest that Helicobacter pylori infection induces reduction of the number of antral D-cells. The resulting relative hypofunction of the inhibitory action of D-cells against G-cells may be responsible for increased serum gastrin secretion.

Show MeSH
Related in: MedlinePlus