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

Barrett's esophagus is a premalignant condition that may often pass unrecognized in clinical practice. In adults, this condition is generally believed to be caused by chronic gastroesophageal reflux resulting in a metaplastic change in the epithelium of the esophagus. Diagnosis of Barrett's esophagus is established by careful biopsy of the involved esophageal mucosa. Periodic surveillance is recommended because of the risk of carcinoma. Antireflux surgery has not been shown to result consistently in the regression of the metaplastic epithelium, but potent acid suppression offers a new therapeutic approach that leads to healing of esophagitis and the potential regression of Barrett's epithelium.
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PMID:Barrett's esophagus: observations on diagnosis and management. 134 63

Gastroesophageal reflux disease (GERD) represents a spectra of symptoms and of reflux damage to the esophagus. This reflux damage is due to a prolonged acid exposure of the esophagus arising from an imbalance between protective motility factors and aggressive acid secretory factors. Initially, patients may be managed by modifying their food intake and by supportive anti-gravity measures. However, many individuals will require drug therapy. Symptomatic relief can be achieved with pro-kinetic agents, antacids, sucralfate suspension, H2-receptor antagonists and H(+)-K+ ATPase pump blockers. There are limitations in the study design of experiments which have compared one agent with another. Accepting these design limitations, it would appear that pump blockers lead to higher rates of endoscopic healing than the use of standard doses of H2-receptor antagonists. However, higher doses of H2-receptor antagonists will likely give higher rates of symptomatic relief and endoscopic healing of GERD. Recurrence of symptoms and esophagitis occur in a high proportion of patients with GERD, and some patients may need to be considered for maintenance therapy.
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PMID:Medical treatment of gastroesophageal reflux disease: options and priorities. 134 50

Peptic stricture and Barrett's oesophagus are not only the major, but also the most common, complications of gastro-oesophageal reflux disease. The clinical problems that these manifestations present are highly significant, and in patients with peptic stricture the resultant dysphagia can be a major disability that causes nutritional problems. Dilation of a stricture exposes the patient to a small, but significant, risk of oesophageal perforation. Barrett's oesophagus per se rarely causes morbidity, but carries a significant risk of developing oesophageal carcinoma, with its attendant morbidity and mortality. Successful anti-reflux surgery for peptic stricture and Barrett's oesophagus effectively abolishes pathological oesophageal acid exposure and provides the best indicator of the potential benefits that may be obtained from treatment with acid-inhibitory drugs. The reported experience clearly indicates that successful anti-reflux surgery results in resolution of peptic stricture following initial dilation, concomitant with persistent control of oesophageal acid exposure. In patients with Barrett's oesophagus, healing of oesophagitis is well documented after successful surgery, but it is unclear whether the Barrett's epithelium progresses or regresses significantly in all but a minority of patients. It is now established that acid pump inhibition can reduce pathological oesophageal acid exposure as effectively as successful anti-reflux surgery. In a minority of patients, however, omeprazole, 40 or 60 mg daily, divided into two doses, is necessary to achieve this effect. This is particularly true for patients with the more severe forms of disease, in whom peptic stricture and Barrett's oesophagus are most prevalent. Results indicate that peptic stricture can resolve during effective gastric acid inhibition with omeprazole, and results from controlled trials on the management of these patients with omeprazole are awaited. Similarly, there are reports of regression of Barrett's oesophagus during omeprazole therapy, but the completeness and predictability of any such effect have not yet been adequately evaluated. There is sufficient experience from long-term omeprazole treatment of gastro-oesophageal reflux disease to indicate that maintenance of a satisfactory response of peptic stricture or Barrett's oesophagus depends upon continued effective gastric acid inhibition.
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PMID:Acid suppression in the long-term treatment of peptic stricture and Barrett's oesophagus. 135 69

Hoarseness is not generally appreciated to be a manifestation of pediatric gastroesophageal reflux. We describe a case in which treatment of well-documented gastroesophageal reflux and esophagitis in a young girl with hoarseness and nocturnal cough led to resolution of these symptoms. Possible pathogenetic mechanisms and the difficulty in associating hoarseness with reflux by standard reflux testing are discussed.
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PMID:Hoarseness in a child with gastroesophageal reflux. 139 93

Gastroesophageal reflux is a common event characterized by orad movement into the esophagus of gastric and/or duodenal contents. Reflux may produce either no damage to the esophageal mucosa or erosions, exudates, ulcerations, strictures, and/or Barrett's (columnar-lined) esophagus. In addition to the esophagus, all the anatomic structures from the pharynx to the lung may be affected by reflux. Numerous factors promote abnormal esophageal mucosal contact time with acid and pepsin. These include incompetent lower esophageal sphincter, impaired esophageal clearance, increased frequency of reflux episodes, delayed gastric emptying, and the presence of a hiatal hernia. The relative contribution of each of these factors in the pathogenesis of esophageal mucosal disease has not been clearly defined. Epidemiologic and clinical data support an association between gastroesophageal reflux and pulmonary disease. Most asthmatic patients, independent of bronchodilator use, have evidence of gastroesophageal reflux, as demonstrated by ambulatory pH testing, endoscopy, and the presence of reflux symptoms. Studies with antireflux agents indicate that partial or complete symptom relief and healing of esophagitis are obtained in about half the patients using H2-receptor antagonists and almost all patients using omeprazole. Preliminary evidence suggests that surgical correction of reflux may lead to improved pulmonary status. Controlled clinical trials are needed, however, to further determine whether effective gastric acid suppression will improve reflux-associated pulmonary disease.
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PMID:Gastroesophageal reflux disease and its consequences. 139 7

Epidemiological studies of gastro-oesophageal reflux disease (GORD) are confounded by the lack of a standardized definition and a diagnostic 'gold-standard' for the disorder. In Western countries, 20-40% of the adult population experience heartburn, which is the cardinal symptom of GORD, but only some 2% of adults have objective evidence of reflux oesophagitis. The incidence of GORD increases with age, rising dramatically after 40 years of age. There is also wide geographical variation in prevalence. Complications, including oesophageal ulcer and stricture, and Barrett's oesophagus, are found in up to 20% of patients with verified reflux oesophagitis. The signs and symptoms of GORD often wax and wane in intensity, and spontaneous remissions have been reported. In most cases, however, GORD is a chronic condition that returns shortly after discontinuing therapy. Although GORD causes substantial morbidity, the annual mortality rate due to GORD is very low (approximately 1 death per 100,000 patients), and even severe GORD has no apparent effect on longevity, although the quality of life can be significantly impaired. There are data to suggest that the use of non-steroidal anti-inflammatory drugs (NSAIDs) contributes to oesophagitis and stricture formation in patients with GORD. Although these data are not conclusive, it seems prudent, if possible, to avoid the use of NSAIDs in patients with GORD, particularly those with oesophageal stricture.
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PMID:Epidemiology and natural history of gastro-oesophageal reflux disease. 139 43

Gastro-oesophageal reflux disease (GORD) results from an abnormally prolonged dwell time of acidic gastric contents in the oesophagus. Although GORD is primarily a motor disorder, the injurious effects of gastric acid are central to the pathogenic process of oesophagitis, and the severity of disease correlates with the degree and duration of oesophageal acid exposure. In the majority of patients with mild disease, oesophageal acid exposure occurs predominantly during post-prandial periods. Conventional doses of H2-receptor antagonists cannot overcome the integrated stimulus to acid secretion resulting from a meal, and are thus relatively ineffective in preventing daytime, post-prandial oesophageal acid exposure. In patients with more severe grades of oesophagitis, there are abnormally high levels of nocturnal acid exposure, with the intra-oesophageal pH being less than 4.0 for 36% of the time, compared with 5% of the time in patients with mild GORD. Control of nocturnal acid secretion thus becomes increasingly important. This may be made worse by relative gastric acid hypersecretion in some patients with severe GORD. The long duration of action and effective inhibition of meal-stimulated acid secretion probably explains the superiority of omeprazole in treating GORD. Preliminary meta-analysis shows that the healing rate of erosive oesophagitis at 8 weeks by antisecretory agents is directly related to the duration of suppression of gastric acid secretion achieved over a 24-hour period (r = 0.87; p less than 0.05).
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PMID:Appropriate acid suppression for the management of gastro-oesophageal reflux disease. 139 46

In an attempt to ascertain radiologic efficacy in patients with evidence of gastroesophageal reflux disease (GERD) at pH testing, radiographic findings were correlated with pH values obtained with an esophageal monitor worn for a 24-hour period in 112 patients. Fifteen (30%) of 50 patients with abnormal pH test results had esophagitis diagnosed radiographically, compared with six (10%) of 62 with normal pH test results (P < .05). The severity of abnormal pH monitoring results was classified but did not correlate significantly with the prevalence of esophagitis diagnosed radiographically. Hiatal hernia was also more common (80% vs 60%) in patients with abnormal pH test results (40 of 50 patients) than in those with normal results (37 of 62 patients) (P < .05). Pharyngeal, laryngeal, and pulmonary symptoms were common indications for evaluation, and 14 of 27 (52%) patients with hoarseness had an abnormal pH tracing. Only a minority of patients with evidence of GERD as defined by abnormal pH test results had reflux esophagitis diagnosed radiographically.
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PMID:Gastroesophageal reflux disease: correlation of esophageal pH testing and radiographic findings. 141 Mar 59

Twenty-five patients with systemic sclerosis and severe gastro-oesophageal reflux disease were treated with 20-80 mg omeprazole daily for up to 5 years. Efficacy of treatment was assessed by symptom score, by endoscopic and histopathological surveillance of the oesophageal and gastric mucosa, and by laboratory screening including serum gastrin concentration. Statistically significant relief of symptoms and healing of oesophagitis confirmed the efficacy of this treatment. However, complete healing of oesophagitis was not achieved in half of the patients due to residual gastro-oesophageal acid reflux. Repeated adjustments of the maintenance dose of omeprazole may be needed for this group of patients. From the safety point-of-view, nothing was observed to discourage the long-term use of omeprazole in this group of patients.
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PMID:Omeprazole in the long-term treatment of severe gastro-oesophageal reflux disease in patients with systemic sclerosis. 142 Jul 48

The combination of a histamine H2-receptor antagonist and a muscarinic receptor antagonist has been reported to result in greater suppression of intragastric acidity than either agent alone. The present randomized, double-blind, multicentre trial compared the effects of the oral combination of 150 mg ranitidine b.d. plus 50 mg pirenzepine b.d. with 150 mg ranitidine b.d. plus placebo pirenzepine b.d. in the treatment of patients with reflux oesophagitis. All 157 patients had symptoms of gastro-oesophageal reflux with endoscopically confirmed oesophageal erosions (Savary and Miller grades I-III). After four weeks of treatment, healing rates were 32/75 (43%) in the combined treatment group and 34/76 (45%) in the group receiving ranitidine alone. After eight weeks, the cumulative healing rates had increased to 48/72 (67%) and 51/75 (68%), respectively. More patients receiving ranitidine plus pirenzepine had complete relief of day- and night-time heartburn after four weeks compared with those receiving ranitidine alone (day: 59% vs. 38%, P = 0.02; night: 69% vs. 52%, P = 0.04). After eight weeks, symptom relief was comparable in both groups. Clinical adverse effects were reported by nine patients receiving ranitidine and by 19 patients receiving the combination. It is concluded that combining ranitidine with pirenzepine does not aid the healing of reflux oesophagitis but does improve symptom relief at four weeks.
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PMID:The effect of combined therapy with ranitidine and pirenzepine in the treatment of reflux oesophagitis. 142 Jul 52


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