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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Duodenogastric reflux is a pathophysiological phenomen occurring after motility disturbances on the antroduodenal junction and after operative procedures destroying, removing or bypassing the pylorus. The reflux of bile can lead to a symptomatic chronicatrophic gastritis and is an important factor in the pathogenesis of gastric ulcer type I. The pyloric regurgitation test, marking of the bile with Bromsulphalein or 14C-chenodesoxycholic acid are reliable methods to prove reflux. For treatment of bile reflux and postoperative alkaline reflux gastritis substances augmenting antral peristalsis and binding bile acids can be used. More effective are surgical procedures diverting the bile flow from the stomach or the gastric remnant.
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PMID:[Duodenogastric reflux]. 87 Oct 59

The functional results of pylorus-preserving resection of a stomach (PRS) in 68 patients with gastric ulcer disease were studied. According to the data of gastroscintigraphy and hepatoscintigraphy, it was established that number of patients with decreased motor-evacuatory function (MEF) of the stomach reduced from 31% before the operation to 11% at the long-term period after PRS. Duodenogastric reflux was noted in 10% of the patients as compared with 47% before the operation. MEF of the stomach normalized within 3-6 mos after the operation. Acid-producing function of the stomach after PRS steadily decreased until the development of a hypoacidic state. Basal pH of gastric, body at the long-term period was 3.39 +/- 0.59. An excellent and good result according to Visick scale was noted in 67 (98.5%) patients, a satisfactory one--in 1 (1.5%).
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PMID:[The results of pylorus-preserving resection of the stomach]. 179 54

Experimentally, the gastric and the duodenal mucosa can both be damaged by acute exposure to small intestinal juice. Though chronic exposure to bile causes mucosal erythema and hyperplasia, the gastric mucosal barrier is not damaged. Duodenogastric reflux is relevant in the pathogenesis of postoperative bilious vomiting and probably of "alkaline" reflux esophagitis. The exact mechanism of mucosal damage has not been established. Duodenogastric reflux is likely to be irrelevant in the pathogenesis of (microscopic) gastritis, of gastric ulcer, and of reflux esophagitis without previous gastric surgery.
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PMID:[Is a duodenogastric reflux of pathogenic significance?]. 305 2

The most important causes of peptic ulcers are increased gastric acid secretion, impaired mucosal circulation and damages to the mucosa. In contrast, motility plays only a minor role. The following motility disturbances are discussed in peptic ulcers: 1. Impaired gastric emptying may favor the development of gastric ulceration, if it is grossly delayed, and that of duodenal ulceration, if it is inappropriately accelerated. 2. Disturbances of duodenal motility in the fasted state may disturb bicarbonate secretion and, thus, become theoretically ulcerogenic. 3. Duodenogastric reflux has been discussed as a cause of gastric ulceration for a long time; yet, the proof is still missing. 4. According to own studies gastric ulcer is frequently accompanied by morphological and functional changes in the antrum; the cause-effect relationship, however, has yet to be elucidated.
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PMID:[Motility and peptic ulcer--possible pathogenetic relations]. 366 Sep 1

We studied reflux of duodenal contents into the stomach in patients with gastric ulcers, patients with duodenal ulcers, and normal subjects. Duodenogastric reflux was assessed in the fasting state and after cholecystokinin octapeptide administration (0.02 micrograms/kg intravenously). Slight reflux was observed in the fasting state in all three groups. However, after cholecystokinin octapeptide administration, reflux was significantly greater in gastric ulcer patients than in control patients for pancreatic phospholipase A2 (p less than 0.01) and lysophosphatidylcholine (p less than 0.001). Also in gastric ulcer patients, the gastric contents were significantly more alkaline (pH 5.26 +/- 0.58, p less than 0.001) during duodenogastric reflux than in normal subjects (pH 3.65 +/- 0.50) or duodenal ulcer patients (pH 2.67 +/- 0.63). Our results suggest that reflux of both pancreatic and biliary secretions might contribute to the gastric mucosal injury in gastric ulcer patients and we postulate that pancreatic phospholipase A2 might have a greater role in this process than has been previously acknowledged.
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PMID:Duodenogastric reflux in patients with gastric ulcer disease. 669 Jun 37

Duodenogastric reflux (DGR) was investigated with a sodium ion selective electrode in 10 normal controls, 10 patients with persistent pain after gastric surgery, and five patients with gastric ulcer. During an average study time of two and a half hours, normal controls had reflux for 12% of the study, whereas patients after gastric surgery had reflux for 91% of the study time (p < 0.0002). Patients with a gastric ulcer had reflux on average for 67% of the study (p < 0.001). The patients who had had gastric surgery had several symptoms, but there was no association between the number or nature of symptoms and the severity of DGR as determined by the sodium electrode. Patients with positive bile provocation tests did not show any significant difference in the duration of reflux compared with those with a negative provocation test (79% and 87%). There was also no relation between the results of the provocation test and the number and nature of symptoms. Continuous monitoring of intragastric sodium ions with a selective electrode is a practical means of assessing DGR. Results suggest that symptoms due to DGR may be related to the sensitivity of the gastric lining as well as the amounts of duodenal contents flowing back into the stomach.
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PMID:Duodenogastric reflux after gastric surgery and in gastric ulcer disease: continuous measurement with a sodium ion selective electrode. 817 51