Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oesophageal peristalsis is considered in relation to a central regulatory mechanism and circular smooth muscle contraction after cessation of a neural input. The roles of tonic pressure and transient inappropriate relaxation of the oesophageal sphincter in gastro- oesophageal reflux, and the return of refluxed material to the stomach by secondary peristalsis, are examined. Ingested food is accommodated through vagally mediated relaxation of the proximal stomach in response to swallowing. Gastric peristalsis contributes to the disintegration of solids and the regulation of their emptying from the stomach. In humans, vagotomy initially causes marked delay in gastric emptying, but gradual adaptation occurs and peristalsis improves. The movement of fluid across the pylorus is discussed. Duodenogastric reflux is evidently a normal event.
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PMID:Role of motility in the upper digestive tract. 638 79

Twenty-seven patients with gastroesophageal reflux were prospectively investigated to define the role of duodenogastric reflux in the development of reflux esophagitis. Duodenogastric reflux was detected and quantified by pH monitoring of the gastric environment 5 cm distal to the distal esophageal sphincter. Alkaline duodenogastric reflux was identified by the occurrence of spontaneous, intense gastric alkalinization during fasting periods. Patients with reflux with esophagitis were distinguished from those without esophagitis by having fewer of these episodes and, consequently, more acid stomachs than had patients without esophagitis. As previously shown, refluxers with esophagitis also had more frequent acid gastroesophageal reflux and prolonged gastric emptying. These findings suggest that refluxers with esophagitis have a functional gastropyloric disturbance resulting in delayed gastric emptying, decreased frequency of alkaline duodenogastric reflux episodes, and more frequent acid gastroesophageal reflux than do refluxers without esophagitis.
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PMID:Duodenogastric reflux and reflux esophagitis. 646 73

Duodenogastric reflux (DGR) is a natural event, occurring occasionally and whose pathological significance is not well known. The accuracy of 24-hour gastric pH-metry for the DGR diagnosis has been tested in adults but not in children. For this purpose we measured the area under curve (AUC) at pH 4, 6 and 7 and the percentage of total time above pH 4 (%pH4), 6 (%pH6) and 7 (%pH7), excluding the 2-hours post-prandial period in 88 children suspected of having gastroesophageal reflux (GER). Forty were considered normal whereas 40 had acid GER and 8 with GER. In the control group %pH4 was 9.68 +/- 14.1, %pH6 3.4 +/- 8.7 and %pH7 1.0 +/- 2.4. The values for AUC were 101 +/- 112.8, 16.5 +/- 22.3 and 3.3 +/- 6.1 pH unit/min, respectively. Comparable results were found in the acid GER group. On the other hand alkaline refluxes had higher figures for all parameters: %pH4 22.1 +/- 13.9, %pH6 12 +/- 13 y %pH7 7 +/- 12, AUC at pH 4,406.5 +/- 410, 136.1 +/- 194 at pH6 and 48.2 +/- 85.1 at pH7 (p < 0.05). Because of the large dispersion of values in the control group we selected the 95 percentile, as the upper limit of normal values instead of the mean +/- SD. Therefore the upper limit were 27 for %pH4, 9 for %pH6 and 3.8 for %pH7. The AUC, 316, 64 and 16 pH/min, respectively. These results prove that DGR in children is a very common event and confirm that DGR definitely contributes to alkaline GER.
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PMID:[Duodenogastric reflux: values in normal children and in children with gastroesophageal reflux]. 821 5

Duodenogastric reflux has long been considered to be important in the pathogenesis of many gastric disorders that exhibit regional variation within the stomach. Ambulatory gastric bilirubin monitoring is a new technique and, although extensively validated, reproducibility and gastric regional variation have not been specifically addressed. Fourteen patients with symptoms of gastroesophageal reflux and 12 healthy subjects underwent 24-h ambulatory gastric bilirubin monitoring with the bilirubin sensor in the upper stomach. Gastric bilirubin monitoring with two simultaneous bilirubin probes, one in the upper stomach and the other in the antrum, was performed on a separate occasion. Gastric bilirubin exposure in the initial and repeat studies showed a good correlation (R = 0.60, P < 0.01). Gastric bilirubin exposure in the upper stomach and the antrum showed a high degree of correlation (R = 0.90, P < 0.01). In conclusion, reproducible results are obtained with ambulatory gastric bilirubin monitoring and duodenogastric reflux does not exhibit significant regional variation within the stomach.
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PMID:Reproducibility and intragastric variation of duodenogastric reflux using ambulatory gastric bilirubin monitoring. 1127 Jul 98

Duodenogastric reflux (DGR) was assessed with 24-hour gastric bilirubin monitoring in 345 patients (219 men; 49 +/- 13 years) with foregut symptoms and 41 healthy subjects (24 men, 28 +/- 5 years). Bilirubin exposure was measured as percent time above absorbance level 0.25 and excessive DGR was defined above the 95th percentile of normal values (>24.8%). DGR was highest following Billroth II gastric resection (60 +/- 24%, N = 15). Patients after cholecystectomy (28 +/- 25%, N = 25), patients with gastroesophageal reflux disease (24 +/- 24%, N = 199), and patients with nonulcer dyspepsia (23 +/- 21%, N = 61) had a significantly higher exposure to DGR than healthy subjects (7 +/- 8%, P < 0.0001). In conclusion, gastric bilirubin monitoring is useful for the assessment of DGR specifically in symptomatic patients following gastric resection. Increased amounts of DGR may further be of clinical importance in patients with reflux disease or nonulcer dyspepsia and following cholecystectomy.
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PMID:Gastric bilirubin monitoring to assess duodenogastric reflux. 1249

Duodenogastric reflux is the retrograde flow of duodenal contents into the stomach that then mix with acid and pepsin. These agents can reflux into the esophagus (ie, duodenogastroesophageal reflux ) and cause gastroesophageal reflux disease (GERD) and its complications, including stricture, Barrett's esophagus, and adenocarcinoma of the esophagus. Medical and surgical treatments of DGER can be difficult. Best medical treatment is proton-pump inhibitors, which decrease DGER by inhibiting both gastric acidity and volume, making less gastric contents available to reflux into the esophagus. The addition of the gamma-aminobutyric (GABA(B)) receptor agonist baclofen may further reduce DGER in patients not responding to proton-pump inhibitors. Bile acid-binding agents (aluminum-containing antacids, cholestyramine, sucralfate, urosodeoxycholic acid) have physiologic rationale, but their efficacy is unproven. Prokinetic agents can reduce DGER and its upper gastrointestinal symptoms by promoting increased gastric emptying. In patients with medically refractory symptoms, a Roux-en-Y diversion or duodenal switch operation may be helpful.
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PMID:Duodenogastric Reflux-induced (Alkaline) Esophagitis. 1472 38

This study reviews current data regarding duodenogastric and gastroesophageal bile reflux-pathophysiology, clinical presentation, methods of diagnosis (namely, 24-hour intraluminal bile monitoring) and therapeutic management. Duodenogastric reflux (DGR) consists of retrograde passage of alkaline duodenal contents into the stomach; it may occur due to antroduodenal motility disorder (primary DGR) or may arise following surgical alteration of gastoduodenal anatomy or because of biliary pathology (secondary DGR). Pathologic DGR may generate symptoms of epigastric pain, nausea, and bilious vomiting. In patients with concomitant gastroesophageal reflux, the backwash of duodenal content into the lower esophagus can cause mixed (alkaline and acid) reflux esophagitis, and lead, in turn, to esophageal mucosal damage such as Barrett's metaplasia and adenocarcinoma. The treatment of DGR is difficult, non-specific, and relatively ineffective in controlling symptoms. Proton pump inhibitors decrease the upstream effects of DGR on the esophagus by decreasing the volume of secretions; promotility agents diminish gastric exposure to duodenal secretions by improving gastric emptying. In patients with severe reflux resistant to medical therapy, a duodenal diversion operation such as the duodenal switch procedure may be indicated.
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PMID:[Duodenogastric and gastroesophageal bile reflux]. 1728 81

The long-term use of proton pump inhibitors (PPIs) exacerbates corpus atrophic gastritis in patients with Helicobacter pylori (H. pylori) infection. To identify a potential mechanism for this change, we discuss interactions between pH, bile acids, and H. pylori. Duodenogastric reflux, which includes bile, occurs in healthy individuals, and bile reflux is increased in patients with gastroesophageal reflux disease (GERD). Diluted human plasma and bile acids have been found to be significant chemoattractants and chemorepellents, respectively, for the bacillus H. pylori. Although only taurine conjugates, with a pKa of 1.8-1.9, are soluble in an acidic environment, glycine conjugates, with a pKa of 4.3-5.2, as well as taurine-conjugated bile acids are soluble in the presence of PPI therapy. Thus, the soluble bile acid concentrations in the gastric contents of patients with GERD after continuous PPI therapy are considerably higher than that in those with intact acid production. In the distal stomach, the high concentration of soluble bile acids is likely to act as a bactericide or chemorepellent for H. pylori. In contrast, the mucous layer in the proximal stomach has an optimal bile concentration that forms chemotactic gradients with plasma components required to direct H. pylori to the epithelial surface. H. pylori may then colonize in the stomach body rather than in the pyloric antrum, which may explain the occurrence of corpus-predominant gastritis after PPI therapy in H. pylori-positive patients with GERD.
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PMID:Potential mechanism of corpus-predominant gastritis after PPI therapy in Helicobacter pylori-positive patients with GERD. 2523 31