Disease relevance of Duodenogastric Reflux

• Although high bile acid concentration was found in the duodenogastric reflux in most patients with CF, the less toxic profile of the bile acids might possibly contribute to the low frequency of Barrett's esophagus in CF [1].
• Gastric symptoms and duodenogastric reflux in patients referred for gastroesophageal reflux symptoms and endoscopic esophagitis [2].
• In conclusion, cisapride stimulates antral motility and decreases biliary reflux in patients with dyspepsia and increased duodenogastric reflux [3].
• We studied a prospective series of 107 randomly chosen dyspepsia patients without gastric ulcer for the association of spiral Campylobacter-like organisms (CLO) with features of antral and fundal gastritis and duodenogastric reflux [4].
• In the rat model, esophageal adenocarcinoma reproducibly develops following surgically induced duodenal reflux into the esophagus and administration of nitrosamine [5].

High impact information on Duodenogastric Reflux

• Possible role of duodenogastric reflux on the development of remnant gastric carcinoma induced by N-methyl-N'-nitro-N-nitrosoguanidine in rats [6].
• In this study, we investigated the effects of bile acids and duodenal reflux on COX-2 expression in cultured esophageal cells and tissue, respectively [7].
• A gastrojejunostomy, pyloromyotomy, and duodenal closure distal to the papilla were added in the other three groups, creating duodenogastric reflux; two were stimulated with histamine and one had a truncal vagotomy and no histamine [8].
• Non-invasive estimation of duodenogastric reflux using technetium-99m p-butyl-iminodiacetic acid [9].
• CONCLUSIONS: The GABA(B) receptor agonist baclofen improves duodenal reflux and associated reflux symptoms that persist during PPI therapy [10].

Chemical compound and disease context of Duodenogastric Reflux

• However, little is known about the effect of omeprazole on duodenogastric reflux (DGR) and duodenogastro-oesophageal reflux (DGOR) [11].
• The discrepancy, which is significant (p less than 0.01), is caused by a marked increase in duodenogastric reflux after cimetidine [12].
• The hypersecretion of gastric acid in response to pentagastrin, caused by duodenal reflux, was tested in dogs [13].
• Atropine (40 micrograms/kg) decreased the supine gastric emptying rate to 1.1 +/- 0.2 (p less than 0.05) and increased the supine duodenogastric reflux rate to 2.74 (0.04-9.80) X 10(-2)/min (p less than 0.05) [14].
• H pylori positive patients who were found to have duodenogastric reflux were treated with amoxycillin (1 g/d) and metronidazole (1.5 g/d) for seven days and four tablets of bismuth subcitrate daily for four weeks [15].

Biological context of Duodenogastric Reflux

• We have studied the effects of aspirin and a synthetic derivative of prostaglandin E2 on duodenogastric reflux during fasting in six normal subjects, while concomitantly monitoring gastrointestinal motility by means of a perfused catheter system [16].

Anatomical context of Duodenogastric Reflux

• Duodenal reflux induces cyclooxygenase-2 in the esophageal mucosa of rats: evidence for involvement of bile acids [7].
• The prostaglandin E2 derivative protects gastric mucosa by mechanisms other than reducing duodenogastric reflux and ameliorating the motility disturbances caused by aspirin [16].
• Rather than an index of immune activation, gastric juice neopterin concentration represents a marker of duodenogastric reflux [17].
• Disorders of gallbladder function related to duodenogastric reflux in technetium-99m DISIDA hepatobiliary scintigraphy [18].
• Statistically, no increase in the duodeno-gastric reflux can be verified under secretin/pancreozymin stimulation of the pancreas [19].

Gene context of Duodenogastric Reflux

• Complete duodenogastric reflux has similar effects on the pancreas but the gut peptide involved is gastrin [20].
• Effects of duodenogastric reflux on gastrin cells, somatostatin cells and serotonin cells in human antral gastric mucosa [21].
• Duodenogastric reflux suppressed somatostatin concentrations in both systemic and portal venous blood, but this did not occur when bile alone was diverted into the stomach [22].
• Duodenogastric reflux caused a significant increase in pancreatic weight, DNA, and plasma CCK and gastrin concentrations at both two and six weeks [23].
• Gastric carcinogenesis in the rat induced by duodenogastric reflux without carcinogens: morphology, mucin histochemistry, polyamine metabolism, and labelling index [24].

Analytical, diagnostic and therapeutic context of Duodenogastric Reflux

• Intravenous infusion of trimebutine inhibited both the increased duodenogastric reflux and the frequency of pyloric relaxation in the cholecystectomized dog [25].
• AIM: To investigate the role of antroduodenal motor function in increased duodenogastric reflux following cholecystectomy and the effect of trimebutine maleate (trimebutine) on the duodenogastric reflux in conscious dogs [25].
• Gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine: role of gastrectomy and duodenal reflux [26].
• In five dogs with Heidenhain pouches, proximal gastric vagotomy and suprapyloric antrectomy did not alter the rate of gastric emptying of 300 mL of 1% dextrose or of 40 plastic spheres, or disrupt the barricade preventing duodenogastric reflux [27].
• Children with confirmed duodenogastric reflux by scintigraphy were given a prokinetic drug (cisapride) [28].

References