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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the pathogenic role of gastroesophageal reflux in Barrett's esophagus (BE) is now widely accepted, the pattern of pH profile in the esophagus of patients with BE is not well documented. The aim of this study was to assess the severity and "extent" of acid exposure in patients with BE using an automated single or two-channel 24-hour pH monitoring system. Eighteen patients with histologically proven BE were compared with 3 other groups: a) 100 patients with clinical symptoms and pHmetrically proven acid reflux divided in 2 sub-groups: 38 patients without esophagitis at endoscopy, and 62 patients with esophagitis (Savary-Miller classification; grade I: n = 24, grade II: n = 27, grade III: n = 8, grade IV: n = 3) and b) 9 healthy volunteers. In 17 patients with BE, and in 14 patients with reflux and healthy volunteers, 2 electrodes were placed 5 (electrode E1) and 10 cm (electrode E2) above the lower esophageal sphincter. In the other patients, pH was monitored using a single pH electrode (E1) only. The mucosal acid exposure at E1 (percentage of time below pH 4 on total period, day and night), the number of reflux episodes longer than 5 min were significantly higher in the BE group when compared with the other groups. The number of patients with abnormal acid exposure at E2 was significantly higher (P less than 0.01) in the BE group (15/17 cases) than in the reflux group (5/14 cases). The mean duration of acid reflux was significantly longer in BE than in other groups at both recording sites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Barret's esophagus and acid gastroesophageal reflux. Two-channel pH-metric measurements and manometric study]. 152 94

We recorded esophageal alkaline exposure time (AET) in 52 patients with gastroesophageal reflux and in 20 control subjects to determine whether esophageal pH monitoring can measure reflux of bile acids and trypsin from the duodenum. Patients underwent a further 16-h study (divided into 2-h periods) in which AET was correlated with bile acid and trypsin concentrations in esophageal aspirates. Patients had greater nocturnal AET than controls (22.7 versus 0.9%, p = 0.005). Patients with a stricture had a greater AET than patients with erosive esophagitis (25.2 versus 13%, p less than 0.05). There was no relationship between esophageal bile acid concentrations and AET, and total bile acid concentrations were similar regardless of whether a 2-h period contained alkaline episodes. Esophageal bile acid concentrations were no different, in patients with a normal esophagus, esophagitis, stricture, or Barrett's esophagus. Trypsin was found in only 5% of aspirates, and could not be predicted by AET. We conclude that measurement of AET is not useful in the clinical evaluation of duodeno-esophageal bile reflux, and bile acids and trypsin are not important in the pathogenesis of reflux esophagitis.
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PMID:Bile acids and trypsin are unimportant in alkaline esophageal reflux. 155 3

Gastro-esophageal reflux disease encompasses a spectrum of disorders in which gastric reflux leads to symptoms and/or damage to the esophageal mucosa. Although a common problem in clinical practice, our understanding of the pathophysiology of the condition has not been matched by our knowledge of its epidemiology and natural history. This review examines some of the difficulties inherent in epidemiological studies with particular emphasis on the nature and variety of reflux symptoms and their relationship to esophagitis, the natural history and complications of reflux disease, Barrett's esophagus, and the possible role of gastroesophageal reflux in lung disease, especially asthma.
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PMID:Epidemiology of gastro-esophageal reflux disease. 156 13

Adenocarcinoma arising in Barrett's esophagus has recently been described in two children aged 11 and 14 years. The long-term follow-up of Barrett's esophagus in children is not well described. We evaluated 16 cases of Barrett's esophagus in children treated at this institution during the last 16 years. Ages ranged from 1.2 to 16 years (mean, 10.3 years). There were 11 boys and 5 girls. Barrett's esophagus was documented by endoscopy in 14 instances and at autopsy in 2 patients with secretory diarrhea and tetralogy of Fallot who died of sepsis. Two children had cancer (neuroblastoma, leukemia) and died of their malignant disease. Five patients had cerebral palsy, 1 esophageal atresia, 1 Fanconi's anemia, and 5 were otherwise normal children. Six were treated medically. Eight patients underwent Nissen fundoplication for complications of gastroesophageal reflux (GER). Five patients were available for follow-up endoscopy (mean, 2 years; range, 1.1 to 5.4 years). Endoscopy was performed on a yearly basis, obtaining biopsy specimens from multiple levels of the esophagus. Four children had satisfactory clinical response to an antireflux procedure including the resolution of a stricture in one case. However, in all 5 cases persistent metaplastic epithelium was documented and showed no evidence of regression. Although there has been speculation that Barrett's esophagus in children may be more likely to revert to normal squamous epithelium than in the adult, there has been only one case of regression in 180 cases of Barrett's esophagus occurring in children described in 37 reports in the literature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Persistence of Barrett's esophagus in children after antireflux surgery: influence on follow-up care. 156 27

Secretion of gastric acid and volume, serum gastrin concentration, and ambulatory 24-hr esophageal pH monitoring were evaluated prospectively in 12 patients with idiopathic gastric acid hypersecretion (basal acid output greater than 10.0 meq/hr) undergoing treatment for refractory chronic long-standing pyrosis. Treatment lasted six months and consisted of three months of ranitidine (mean 2150 mg/day, range 1200-3000 mg/day), followed by three months of omeprazole (mean 33 mg/day, range 20-60 mg/day). Both ranitidine and omeprazole significantly reduced gastric acid output (P less than 0.001) and gastric volume output (P less than 0.001) compared to a basal evaluation and resulted in complete disappearance of pyrosis. Total reflux time (percent 24 hr intraesophageal pH less than 4) was significantly reduced by ranitidine (P less than 0.02) and omeprazole (P less than 0.001) compared to basal evaluation; however, the effects of omeprazole were significantly greater than ranitidine (P less than 0.05). Omeprazole caused a significant increase in serum gastrin concentration compared to both basal and ranitidine (P less than 0.05). Endoscopically documented erosive esophagitis was present in nine of the 12 patients, and seven of the 12 patients had Barrett's epithelium. All 12 patients had complete resolution of pyrosis and healed esophagitis by six months, but no significant endoscopic regression was observed in the extent of Barrett's epithelium. No side effects occurred with these high doses of ranitidine or omeprazole. These results indicate that high-dose ranitidine and omeprazole are effective therapy for refractory gastroesophageal reflux disease. However, with omeprazole, total reflux times are reduced more than with ranitidine, often into the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of omeprazole and ranitidine in treatment of refractory gastroesophageal reflux disease in patients with gastric acid hypersecretion. 158 94

The factors contributing to the development of esophageal mucosal injury in gastroesophageal reflux disease (GERD) are unclear. The lower esophageal sphincter, esophageal acid and acid/alkaline exposure, and the presence of excessive duodenogastric reflux (DGR) was evaluated in 205 consecutive patients with GERD and various degrees of mucosal injury (no mucosal injury, n = 92; esophagitis, n = 66; stricture, n = 19; Barrett's esophagus, n = 28). Manometry and 24-hour esophageal pH monitoring showed that the prevalence and severity of esophageal mucosal injury was higher in patients with a mechanically defective lower esophageal sphincter (p less than 0.01) or increased esophageal acid/alkaline exposure (p less than 0.01) as compared with those with a normal sphincter or only increased esophageal acid exposure. Complications of GERD were particularly frequent and severe in patients who had a combination of a defective sphincter and increased esophageal acid/alkaline exposure (p less than 0.01). Combined esophageal and gastric pH monitoring showed that esophageal alkaline exposure was increased only in GERD patients with DGR (p less than 0.05) and that DGR was more frequent in GERD patients with a stricture or Barrett's esophagus. A mechanically defective lower esophageal sphincter and reflux of acid gastric juice contaminated with duodenal contents therefore appear to be the most important determinants for the development of mucosal injury in GERD. This explains why some patients fail medical therapy and supports the surgical reconstruction of the defective sphincter as the most effective therapy.
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PMID:Complications of gastroesophageal reflux disease. Role of the lower esophageal sphincter, esophageal acid and acid/alkaline exposure, and duodenogastric reflux. 163

The exact relation between gastro-oesophageal reflux and asthma remains poorly understood. To determine whether gastro-oesophageal reflux in asthmatics results in oesophagitis, endoscopy and oesophageal biopsy were performed on 186 consecutive adult asthmatics. The presence or absence of reflux symptoms was not used as a selection criterion for asthmatics. Endoscopy was performed by two endoscopists using predefined criteria. All asthmatics had discrete wheezing and either a previous diagnosis of asthma or documented reversible airways obstruction of at least 20%. The oesophageal mucosa was graded as normal if no erosions or ulcerations were present in the tubular oesophagus; as oesophagitis if a mucosal break with exudate (erosions and/or ulcerations) was present; and as Barrett's if specialised (intestinal) columnar epithelium was present. A hiatal hernia was diagnosed if greater than or equal to 2 cm of gastric mucosa appeared above the diaphragm during endoscopy. Thirty nine per cent of the patients with asthma had oesophagitis or Barrett's oesophagus, or both. There was no difference in the oesophageal mucosal status between asthmatics who required and those who did not require bronchodilators. Fifty eight per cent of asthmatics had a hiatal hernia. It is concluded that oesophagitis is common and independent of the use of bronchodilator therapy in asthmatics.
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PMID:Prevalence of oesophagitis in asthmatics. 164 24

Bioptates obtained from 163 mature persons have been studied, using spiral sections. When the conditions of functioning are altered (at the gastro-esophageal reflux) the organ's integument can destroy, but the defects formed in the lining are covered with a simple cylinder epithelium of the cardial glands. A connection between Barrett's syndrome in the esophagus with its cardial gland is demonstrated. The most widely distributed histological forms of Barrett's esophagus are described.
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PMID:[Specificity of histological interrelations of cardial glands of the esophagus with its multi-layer lining]. 169 12

We have studied for periods averaging 111 months 16 survivors out of a series of 20 children treated for oesophageal atresia (EA) by neonatal end-to-end anastomosis. Twelve of them had gastroesophageal reflux (GER) manifested by either digestive (vomiting, dysphagia, pyrosis, haemorrhage or foreign body impaction) or respiratory symptoms (repeated neumoniae or frequent u.r.i.). pH-studies decealed very increased acid exposure in these patients. Manometric studies showed disorganized peristalsis with near-absence of propulsive waves and predominance of mass-contractions. Interestingly both lower esophageal sphincter pressure and length were normal. Five children had histological esophagitis and 2 had Barrett's esophagus. Seven patients have had an anti-reflux procedure and two more should be operated in the near future. Our experience reveals that GER incidence in EA is very high, that esophageal function is severely impaired in this condition, that mucosal lesions can be serious and that funduplication is effective. Since it has been demonstrated that esophageal dysfunction in EA patients is due to structural anomalies, spontaneous improvement should not be expected in them and surgical treatment should be largely indicated. EA patients require long-term gastro-enterologic follow-up.
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PMID:[Motor function of the esophagus following surgery for atresia]. 174 78

Barrett's esophagus is a condition in which the normal stratified squamous epithelium is replaced by a specialized metaplastic columnar epithelium. It develops as a consequence of chronic gastroesophageal reflux and predisposes to the development of esophageal adenocarcinoma. Adenocarcinoma develops in Barrett's esophagus by a multistep process in which specialized metaplasia progresses to dysplasia, then to early adenocarcinoma, and eventually to deeply invasive and metastatic disease. This neoplastic progression is associated with a process of genomic instability that generates abnormal clones of cells, some of which have aneuploid or increased G2/tetraploid DNA content. A systematic protocol of endoscopic biopsy can detect Barrett's adenocarcinomas at an early stage, when they may be curable.
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PMID:Barrett's esophagus and esophageal adenocarcinoma. 178 15


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