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Query: UMLS:C0154059 (Esophagus)
 2,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The esophagus is regularly exposed to hypertonic luminal environments, some of which have the capacity to increase epithelial permeability. The present experiments were designed to determine what impact such environments have on epithelial resistance to injury by acid. Rabbit esophageal epithelium mounted in Ussing chambers was exposed to luminal acid while monitoring electrical resistance (R), a marker of epithelial permeability, and morphology was assessed in tissues luminally pretreated with either urea (1 M), mannitol (1 M), or normal Ringer. Hypertonic mannitol, which had little effect on R, was associated with a minor increase in susceptibility to acid injury, pH 1.6. In contrast, hypertonic urea lowered R and was associated with marked injury upon exposure to acid. This susceptibility to acid injury occurred within 15 minutes of exposure and converted a non-damaging concentration of acid (pH 2.0) to a damaging one. Moreover, urea's effects were abolished if it was removed from the bath allowing R to return to baseline before acidification. We conclude that hypertonic luminal environments that impair epithelial barrier function predispose the esophagus to acid injury. Such findings may provide insight into additional mechanisms contributing to the development of heartburn following meals.
Dis Esophagus 1998 Apr
PMID:Luminal hypertonicity and the susceptibility of rabbit esophagus to acid injury. 977 64

The aim of this study was to assess prevalence of GERD before and after Helicobacter pylori (HP) eradication utilizing 24-h esophageal pH/manometry studies. Helicobacter pylori status was confirmed by the Campylobacter like organism test. Those testing positive underwent 24-h pH/manometry followed by HP eradication therapy and urea breath test. Patients were followed up at 6 months and then at 1 year when they underwent a repeat 24-h pH/manometry. Twenty patients, 10 with non-ulcer dyspepsia (NUD) and 10 with duodenal ulcer (DU) were enrolled, though only 10 patients attended for a repeat 24-h pH/manometry study. The patients were well matched, though patients with NUD had a significantly higher symptom score at entry compared with the DU group (8.5 vs 5.7, P < 0.05). The pH and esophageal manometry data were similar in the two groups. Overall nine patients (45%; DU = 5, NUD = 4) had evidence of GERD prior to HP eradication and it persisted one year after cure of the infection. The reflux disease occurred in the presence of normal LES pressure (mean 15.6 +/- 3.3 mmHg). New onset GERD was uncommon after cure of HP infection, occurring in only one patient with NUD. Overall HP eradication had no impact on percentage of time pH < 4 (4.69 +/- 3 vs 4.79 +/- 3), episodes > 5 min (9.8 +/- 16 vs 15.5 +/- 25.3) and Johnson DeMeester Score (16.8 +/- 7.5 vs 26.8 +/- 18). In addition successful cure of HP produced no significant changes in LES pressure (17.9 +/- 3.8 mmHg vs 19.3 +/- 4.6 mmHg), and other esophageal manometry data. Half of HP-positive patients with NUD and DU have evidence of GERD before HP eradication. This persists after successful cure of the infection. New onset GERD occurs very uncommonly one year after HP eradication.
Dis Esophagus 2003
PMID:Gastroesophageal reflux before and after Helicobacter pylori eradication. A prospective study using ambulatory 24-h esophageal pH monitoring. 1464 Dec 88

To evaluate the endoscopic and histological changes in upper gastrointestinal tract of patients with chronic renal failure 50 patients and 50 controls were studied. Upper gastrointestinal endoscopy was done and 2 biopsies each were taken from oesophagus, corpus and antrum of the stomach and duodenum. Sections were stained with haematoxylin & eosin, Alcian blue--Periodic acid Schiff's (pH 2.5), and Loeffler's methylene blue stains. Oesophagus was endoscopically normal in most of the patients. Predominant histological finding was chronic oesophagitis which was significantly higher in patients than controls (47.1% Vs 26%; p<0.05). Significantly higher (p<0.001) number of patients had gastritis, oedema and pale mucosa on endoscopic examination of stomach. Predominant histological changes were mucosal oedema (82.35%), gastritis (23.5%) and increase in number of bi- and multinucleated parietal cells with vacuolation and fragmentation of the cytoplasm (29%). Prevalence of H. pylori was less in patients as controls (35.2% Vs 54%; p< 0.01). Endoscopic examination of duodenum mainly showed duodenitis, pale mucosa, oedema and nodularity. Brunner's gland hyperplasia (82.4%), duodenitis (70.6%) and gastric metaplasia (29.4%) were the main histological features. H. pylori was seen in 5.9% cases of gastric metaplasia in duodenum. Patients with CRF have significant upper gastrointestinal tract abnormalities which mainly occur due to metabolic changes in response to high urea concentration in gastric juice and are not related to H. pylori infection.
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PMID:Endoscopic and histological changes in upper gastrointestinal tract of patients with chronic renal failure. 1629 60

It is commonly considered that acidity in a gastric tube used as an esophageal substitute after esophagectomy decreases due to truncal vagotomy. However, there have been few, if any, studies on the factors influencing the acidity in the gastric tube. It is well known that Helicobacter pylori (H. pylori) plays an important role in acid secretion of the stomach. The aim of this study was to investigate whether or not H. pylori infection also influenced the acidity in the gastric tube as an esophageal substitute. We investigated the changes in the levels of gastric acidity and the status of H. pylori infection from the preoperative period to 1 year after surgery. In 65 Japanese patients who underwent resection of esophageal cancer followed by reconstruction using a gastric tube, 24-h gastric pH monitoring and examination of H. pylori infection using the 13C-urea breath test and biopsy specimen obtained from the gastric mucosa under upper gastrointestinal endoscopy were performed pre- and postoperatively. Twenty-seven among the 65 patients underwent the same examinations at 1 year after surgery. The levels of postoperative gastric acidity and at 1 year after surgery were significantly lower than that of preoperative gastric acidity (P = 0.031, P = 0.001, respectively). There was no difference in the levels of gastric acidity between 1.5 months and 1 year after surgery (P = 0.282). The levels of gastric acidity in the stomach and in the gastric tube were significantly influenced by H. pylori infection, while age, gender, and past history of peptic ulcer showed no influence. The level of gastric acidity in patients who had H. pylori infection pre- and postoperatively were significantly lower than that in patients who had no H. pylori infection pre- and postoperatively (P < 0.0001). H. pylori infection was indicated to be an important factor influencing the levels of gastric acidity in the reconstructed esophagus as well as in the stomach before surgery.
Dis Esophagus 2007
PMID:Helicobacter pylori infection influences the acidity in the gastric tube as an esophageal substitute after esophagectomy. 1761 83

The frequency of oesophageal adenocarcinoma is increasing in Western countries for unknown reasons, and correlates with a corresponding increase in the pre-malignant condition, Barrett's Oesophagus, which raises the risk of adenocarcinoma by some 40- to 125-fold. We have examined how disease progression correlates with changes in expression of the p14ARF (ARF) tumour suppressor, a key regulator of the p53 tumour suppressor pathway that is silenced in some 30% of cancers overall, but for which a role in oesophageal cancer is unclear. We have used quantitative PCR, RT-PCR, methylation-specific PCR and chromatin-immunoprecipitation to examine the regulation and function of ARF in oesophageal adenocarcinoma tissue specimens and cell lines. We find highly significant reductions (P< 0.001) in ARF expression during disease progression from normal oesophageal epithelium to Barrett's Oesophagus to adenocarcinoma, with 57/76 (75%) adenocarcinomas displaying undetectable levels of ARF expression. Retention of ARF expression in adenocarcinoma is a highly significant indicator of increased survival (P< 0.001) and outperforms all clinical variables in a multivariate model. CpG methylation as well as histone H3 methylation of lysines 9 and 27 contribute independently to ARF gene silencing in adenocarcinoma cell lines and can be reversed by 5-aza-2'-deoxycytidine. The results suggest that silencing of ARF is involved in the pathogenesis of oesophageal adenocarcinoma and show that either DNA or histone methylation can provide the primary mechanism for ARF gene silencing. Silencing of ARF could provide a useful marker for increased risk of progression and poor prognosis.
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PMID:Progressive silencing of p14ARF in oesophageal adenocarcinoma. 1841 May 30

The aim of this study was to determine the factors influencing acidity in the gastric conduit after esophagectomy for cancer. Acidity and bile reflux in the stomach and in the gastric conduit were examined by 24-h pH monitoring and bilimetry in 40 patients who underwent transthoracic subtotal esophagectomy followed by esophageal reconstruction using a gastric conduit, which was pulled up to the neck through a posterior mediastinal route in 17 patients, through a retrosternal route in 10 patients, and through a subcutaneous route in 13 patients. They were examined at 1 week before surgery, at 1 month after surgery, and at 1 year after surgery. Helicobacter pylori infection was examined pathologically and using the (13) C-urea breath test. The factors influencing acidity of the gastric conduit were analyzed using the stepwise regression model. Gastric acidity assessed by percentage (%) time of pH < 4 was reduced after surgery and was significantly less in patients with H. pylori infection compared with those without H. pylori infection throughout the period from 1 week before surgery to 1 year after surgery. Duodenogastric reflux (DGR) assessed by % time absorbance > 0.14 into the lower portion of the gastric conduit was significantly increased after surgery throughout the period from 1 month after surgery to 1 year after surgery. Multivariate analysis showed that the acidity in the gastric conduit was influenced by H. pylori infection and DGR at 1 month after surgery, and by H. pylori infection and the route for esophageal reconstruction at 1 year after surgery. Acidity in the gastric conduit was significantly decreased after surgery. Acidity in the gastric conduit for esophageal substitutes is influenced by H. pylori infection and surgery. DGR influences the gastric acidity in the short-term after surgery, but not in the long-term after surgery.
Dis Esophagus 2011 Nov
PMID:What influences the acidity in the gastric conduit in patients who underwent cervical esophagogastrostomy for cancer? 2148 42