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

In a randomized, multicenter trial, nizatidine 150 mg or 300 mg, or placebo, was administered twice daily for six weeks to 515 patients with gastroesophageal reflux disease (GERD). Gelusil antacid tablets were taken as needed for pain. Significantly superior rates of endoscopically proven complete healing (normal-appearing mucosa) versus placebo occurred after three weeks with nizatidine 150 mg, and after six weeks with nizatidine 300 mg. Six-week healing rates were 38.5% for nizatidine 300 mg, 41.1% for nizatidine 150 mg, and 25.8% for placebo. The nizatidine 150 mg treatment group had significantly greater improvement in daytime and nighttime heartburn severity after one day of therapy versus placebo. Twice-daily administration of nizatidine 150 mg or 300 mg provides prompt relief from the major symptom of GERD, heartburn, and complete healing of esophagitis is seen in many patients.
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PMID:Nizatidine versus placebo in gastroesophageal reflux disease. A six-week, multicenter, randomized, double-blind comparison. Nizatidine Gastroesophageal Reflux Disease Study Group. 158 91

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

Gastroesophageal reflux disease (GERD) remains a ubiquitous problem, although therapeutic options continue to evolve. Effective therapy calls for understanding the pathogenesis. Key factors associated with GERD include incompetence of the lower esophageal sphincter, esophageal clearance, gastric contents, tissue resistance, and potency of the refluxate. Phase-type directed therapy remains the best treatment approach and histamine (H2)-receptor antagonists are now the cornerstone of therapy for patients not responsive to conservative measures. In a subset of patients with severe esophagitis who do not respond to conventional H2-receptor antagonist therapy, efficacy has been demonstrated with high-dose therapy. The acid suppressant omeprazole, highly effective in erosive esophagitis, is the drug of choice for esophagitis resistant to H2-receptor antagonists. Despite effective forms of therapy, relapse rates are high in patients with severe GERD, and maintenance therapy typically is required. With near uniformity, efficacy end points for these agents have been directed toward relief of heartburn, regurgitation, and dyspepsia. Few data exist correlating relief of GERD and improvement of chest pain. Although therapeutic strategies for treating GERD have improved, empiric treatment of suspected GERD in the patient with noncardiac chest pain does not appear to be the optimal approach and should be reserved for cases where diagnostic testing is limited or unavailable.
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PMID:Medical therapy for gastroesophageal reflux disease. 159 72

While the number of patients at risk for vomiting and aspiration has been reported to be high, the incidence of clinically important pulmonary aspiration is low. We sought to define the incidence of gastroesophageal reflux (GER) and to correlate this with the clinical variables of obesity, history of oesophagitis, bucking and changes in body position. Continuous oesophageal pH measurement was used to determine the frequency of gastroesophageal reflux in 44 patients having general anaesthesia for elective surgical procedures. Acid reflux to a pH value of less than four occurred in seven patients (15.9%) during anaesthesia. This was associated temporally with straining on the endotracheal tube in six subjects (13.6%). We conclude that traditional risk factors are not always predictive of those patients at risk of regurgitation and aspiration.
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PMID:Gastroesophageal reflux during anaesthesia. 159 71

Oesophageal mucosal specimens (n = 250) were taken from 25 normal subjects (14 females, 11 males; median age 52 years; range 19-63 years) and incubated in physiological saline, pepsin and bile acid solutions to determine whether conjugated bile acids modify the epithelial cytotoxic action of pepsin. Short (5 min) and long (22 min) incubations were carried out and the results were assessed by transmission electron microscopy. Six different parameters of epithelial damage were scored (0-4) by a single 'blinded' pathologist for each of four epithelial layers. The scores after incubation in saline (pH 7 and titrated to pH 2 with HCl) were not different from those of the controls (P = 0.35). Both pepsin and bile acids (pH 2) caused more damage than saline at pH 2 (P less than 0.001) which was similar for the two substances (P = 0.136). Conjugated bile acids in combination with pepsin (pH 2) did not alter the overall extent or pattern of damage caused by pepsin alone (pH 2); P = 0.142). Conjugated bile acids, in concentrations commonly encountered during gastro-oesophageal reflux, did not appear to modify the cytopathic effects of pepsin on oesophageal mucosal cells in vitro. Conjugated bile acids may not be important in the pathogenesis of oesophagitis in patients with acid/peptic gastro-oesophageal reflux.
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PMID:Bile acids do not modify the effects of pepsin on the fine structure of human oesophageal epithelium. 161 Mar 26

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

Twelve patients presenting with symptomatic esophagitis associated with hiatal hernia and gastroesophageal reflux underwent operative management under laparoscopic guidance. The antireflux procedure employed was the Nissen fundoplication. The authors completed the operation laparoscopically in nine patients. Postoperatively, patients were evaluated with repeat fiberoptic endoscopy, esophageal manometry, and barium contrast studies. Postoperative results were considered excellent on the basis of these studies and complete control of symptoms. The mortality rate was 0%. The only major operative complication was a pneumonia that occurred in one patient. At 1 month follow-up, six patients were totally asymptomatic. The authors conclude that laparoscopic treatment of gastroesophageal reflux associated with a hiatal hernia is feasible by a procedure that has already proven its value during open surgery.
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PMID:Laparoscopic Nissen fundoplication: preliminary report. 166 93

While an alkaline component to esophageal reflux disease is known to be present, little is known about its etiology and harmful effects. Simultaneous gastric and esophageal 24-hour pH monitoring was performed in 81 patients with foregut symptoms. The presence of a mechanically defective lower esophageal sphincter was determined by manometry and duodenogastric reflux by computer-assisted discriminant analysis of the gastric pH record. Heartburn, dysphagia, and regurgitation occurred more frequently in those with a mechanically defective sphincter (p < 0.05) and epigastric pain in those with duodenogastric reflux (p < 0.05). Esophagitis was more common and severe in those with a mechanically defective sphincter (p < 0.05). In these patients, the percentage of time over 24 hours that the esophageal pH was less than 4 was 40.5% in patients without duodenogastric reflux but only 10.2% in those with duodenogastric reflux (p < 0.005), suggesting acid damage in the former and alkaline damage in the latter. To establish the origin of the esophageal alkaline exposure, episodes of elevated fasting gastric pH greater than 4 lasting longer than 1 minute were searched for and identified in 45 patients. Esophageal pH tracings were compared for 30 minutes before and after these events. The esophageal pH was higher following these episodes in duodenogastric reflux patients (p < 0.05), suggesting a gastroduodenal origin of the esophageal alkalinization. This study shows that esophageal damage may be due to acid or alkaline reflux. The alkaline component of gastroesophageal reflux is important and should be considered in the evaluation of patients with foregut symptoms so that appropriate medical or surgical therapy can be instituted.
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PMID:Etiology and importance of alkaline esophageal reflux. 167 Feb 23

Prolonged esophageal pH monitoring is considered to be the most sensitive and specific test for the diagnosis of gastroesophageal reflux disease (GERD). However, the role of pH monitoring in predicting the clinical and endoscopic response of reflux esophagitis is not well defined. In this study, 106 patients with moderate to severe symptoms of GERD and esophagitis (grades 0-IV) by endoscopy were initially studied by ambulatory esophageal pH monitoring, and their clinical response to standard H2 antagonist therapy was monitored at 8 wk. Refractory patients were defined as those who failed to heal and/or had intractable reflux symptoms after 8 wk of H2 antagonist therapy, and who required continuous therapy with higher doses of H2 antagonists, addition of prokinetic agents, or omeprazole. There was a positive correlation (r = 0.89) between endoscopic severity of esophagitis upon entry into the study and refractoriness to standard medical therapy. However, there were no differences in the various pH parameters analyzed between the 58 patients who responded and the 48 patients who were refractory to medical therapy, regardless of the endoscopic grading of their esophagitis. We conclude that 24-h ambulatory esophageal pH monitoring does not predict refractoriness of reflux esophagitis to standard therapy. The decision for more aggressive methods of treatment probably requires assessment of symptomatic and endoscopic response after 8 week standard H2 antagonist therapy.
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PMID:Failure of initial 24-hour esophageal pH monitoring to predict refractoriness and intractability in reflux esophagitis. 167 86


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