scholarly journals Relation between gastric acid output, Helicobacter pylori, and gastric metaplasia in the duodenal bulb.

Gut ◽  
1996 ◽  
Vol 39 (4) ◽  
pp. 513-520 ◽  
Author(s):  
A W Harris ◽  
P A Gummett ◽  
M M Walker ◽  
J J Misiewicz ◽  
J H Baron
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Acid ◽  
Acid Output ◽  
Duodenal Bulb ◽  
Gastric Acid Output ◽  
Gastric Metaplasia

Gastric acid output, bacterial load and gastritis in Helicobacter pylori positive patients with duodenal ulcer

1995 ◽  
Vol 108 (4) ◽  
pp. A147
Author(s):  
PH Le Roux ◽  
AW Harris ◽  
MM Walker ◽  
JJ Misiewicz ◽  
JH Baron
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Gastric Acid ◽  
Acid Output ◽  
Bacterial Load ◽  
Gastric Acid Output

scholarly journals PAC1 Deficiency in a Murine Model Induces Gastric Mucosa Hypertrophy and Higher Basal Gastric Acid Output

2010 ◽  
Vol 43 (1) ◽  
pp. 76-84 ◽  
Author(s):  
Yuxin Lu ◽  
Patrizia Germano ◽  
Gordon V. Ohning ◽  
John P. Vu ◽  
Joseph R. Pisegna
Keyword(s):  
Gastric Mucosa ◽  
Gastric Acid ◽  
Murine Model ◽  
Acid Output ◽  
Gastric Acid Output

Effect of vagotomy on the acid response to gastric distension

1970 ◽  
Vol 48 (10) ◽  
pp. 670-674 ◽  
Author(s):  
R. M. Preshaw
Keyword(s):  
Motor Activity ◽  
Gastric Acid ◽  
Motor Response ◽  
Acid Output ◽  
The Body ◽  
Conscious Dogs ◽  
Truncal Vagotomy ◽  
Gastric Distension ◽  
Gastric Acid Output

Distension of the body of the stomach, in conscious dogs with vagally innervated antral pouches, caused an increase in gastric acid output, and an increase in antral motor activity. Truncal vagotomy inhibited the acid response to distension, but had no effect on the antral motor response. Denervation of the antral pouch by separating it from the main stomach caused little further diminution in the response.

scholarly journals Incidence of Gastric Metaplasia and Helicobacter pylori Infection in Duodenal Bulb – With Specific Reference to Patients With Duodenal Ulcers

1999 ◽  
Vol 6 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Minoru Kawaguchi ◽  
Toshihiko Saito
Keyword(s):  
Helicobacter Pylori ◽  
Duodenal Bulb ◽  
Mucosal Injury ◽  
Transitional Zone ◽  
Specific Reference ◽  
Rapid Urease Test ◽  
Duodenal Ulcers ◽  
Gastric Metaplasia ◽  
Urease Test ◽  
H Pylori

We determined the incidence of gastric metaplasia in the duodenal bulb of duodenal ulcer patients and the Helicobacter pylori (H. pylori) infection rate at sites with gastric metaplasia. Biopsy of the duodenal bulb showed the presence of gastric metaplasia in 61 of 86 patients (71%) overall and in 18 of 47 patients (38.3%) who had gastrectomy at an early gastric cancer. The histological diagnosis of H. pylori infection showed good agreement (83.3%) with the result of the rapid urease test, indicating that H. pylori occurs in regions with gastric metaplasia. This finding suggests that H. pylori infects gastric metaplasia in the duodenal bulb, causing mucosal injury, which is then transformed into duodenal ulcers. The exact mechanism by which gastric metaplasia is caused is unknown, but it is believed to occur in the transitional zone in the duodenal mucosa.

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