Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study has investigated the relationship between duodenogastric reflux, gastritis and certain symptoms 6-12 months after three operations for uncomplicated duodenal ulcer. The operations studied were proximal gastric vagotomy (PGV, 20 cases), truncal vagotomy and pyloroplasty (TV+P, 22 cases) and truncal vagotomy and antrectomy (TV+A, 21 cases). Duodenogastric reflux was assessed both by a radiological technique and by measuring the concentration of bilirubin in the gastric aspirate before and after operation. Incidence and severity of postoperative gastritis were determined by endoscopic biopsy. Symptoms were assessed by symptomatic score and Visick grading. There was a significant correlation between duodenal reflux and histological evidence of both severe superficial gastritis and glandular atrophy (P less than 0-01). There was also a close association between the degree of reflux and the presence of severe heartburn, epigastric pain and bile vomiting after operation. The amount of reflux did not differ before operation. There was significantly less reflux following PGV than after either TV+P (P less than 0-025) or TV+A (P less than 0-001). The results indicate that an operation which preserves an innervated and intact antrum and pylorus will protect against postoperative duodenogastric reflux, gastritis and symptoms.
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PMID:The importance of an innervated and intact antrum and pylorus in preventing postoperative duodenogastric reflux and gastritis. 0 Jan 23

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

Duodenogastric reflux (DGR) has been found to give rise to a hypochlorhydria secondary to alkaline reflux. We investigated whether there is a link between DGR and the gastrin, somatostatin, and serotonin cell numbers and the granular content of gastrin, somatostatin, and serotonin in endocrine cells in human antral mucosa. We investigated 38 selected Helicobacter pylori-negative patients with visual primary excessive DGR in upper endoscopy and symptoms of epigastric pain and bile vomiting. Ten control patients were included in this study. None of the patients had peptic ulcer or had received any medication. Antrum (10 biopsies from five different zones: the lesser and major curvature, the anterior and posterior wall, and the pylorus) and corpus (two biopsies from major curvature about 10 cm below the cardia) biopsy specimens were collected for routine histology, as well as for light and electron immunohistochemistry. In patients without atrophy or intestinal metaplasia and in patients with mild atrophy or mild intestinal metaplasia, the number of gastrin and somatostatin cells was not different from that in controls. In moderate atrophy or moderate intestinal metaplasia, however, the number of gastrin and somatostatin cells decreased. Serotonin cell number was significantly higher in all patients with DGR as compared with controls. The mean somatostatin granular content was increased (3.6+/-0.2 vs. 3.2+/-0.1). In addition, lysosomes with engulfed somatostatin granules were found. The mean serotonin granular content was decreased (2.3+/-0.3 vs. 2.9+/-0.3), while the mean gastrin granular content remained unchanged (2.5+/-0.3 vs. 2.4+/-0.2). Ultrastructurally, the granules in serotonin-positive cells corresponded to the gastric variant or to the intestinal variant of serotonin cells. The endocrine cells were found to have few granules positive for serotonin. It is concluded that DGR inhibits somatostatin granular release, but stimulates both serotonin granular release and serotonin cell growth.
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PMID:Effects of duodenogastric reflux on gastrin cells, somatostatin cells and serotonin cells in human antral gastric mucosa. 1531 Jan 46

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