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

We prospectively evaluated gastric acid output (mEq/h), gastric volume output (ml/h), ambulatory 24-h esophageal pH monitoring, and the endoscopic appearance of the esophagus in 23 patients undergoing treatment of chronic long-standing pyrosis. Twelve of these 23 individuals (52%) remained symptomatic after 3 mo of standard antisecretory treatment with ranitidine, 150 mg twice daily. When compared with initial responders, those patients who did not experience complete symptomatic relief on therapy had significantly higher basal acid output (p less than 0.001), basal volume output (p less than 0.02), and basal upright (but not supine) reflux time (p less than 0.05). Nine of the 12 patients who did not respond to initial treatment had gastric acid hypersecretion (basal acid output greater than 10 mEq/h), and 10 of the 12 had Barrett's epithelium compared with only 1 patient in the initial-responder group (p less than 0.001). All 12 nonresponders were treated for an additional 3 mo with increased doses of ranitidine (mean, 1280 mg/day; range, 600-1800 mg/day), and complete disappearance of pyrosis occurred in 10 of the 12, although no significant endoscopic regression was observed in the extent of the underlying columnar mucosa in those with Barrett's esophagus over the 6-mo duration of the study. A significant correlation was shown between the daily ranitidine dose required to eliminate symptoms and the pretreatment basal acid output (r = 0.81, p less than 0.001); gastric acid output had to be almost totally suppressed (i.e., less than 1 mEq/h) for pyrosis to disappear completely. No side effects occurred with any of these high doses of ranitidine. We conclude that a subgroup of patients with long-standing symptomatic gastroesophageal reflux disease who do not respond to standard ulcer-healing doses of histamine2-receptor antagonists are hypersecretors of basal gastric acid and require increased acid-suppressive therapy. Many of these individuals also have underlying Barrett's epithelium.
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PMID:Gastric acid hypersecretion in refractory gastroesophageal reflux disease. 221 Feb 69

Regression of Barrett's epithelium after antireflux operations remains a controversial topic. We evaluated the effect of antireflux procedures in patients with Barrett's esophagus on the regression of columnar epithelium and dysplasia and its potential protective effect on the subsequent development of carcinoma. Of the 241 patients with Barrett's esophagus treated at the Lahey Clinic from 1973 to 1989, 37 patients underwent an antireflux operation. Regression was defined as histological evidence of regenerating squamous mucosa that completely or partially replaced the columnar epithelium. Improvement in lower esophageal sphincter pressure to 12 mm Hg or greater occurred in 19 of 26 patients (73%) who had perioperative manometry. Symptomatic relief of esophagitis occurred in 34 of 37 patients (92%). Four patients had partial regression with regenerating squamous mucosa juxtaposed with areas of columnar epithelium. Carcinoma developed in 3 of 37 patients (8.1%). One patient had recurrence of severe symptoms of reflux esophagitis before development of carcinoma. Patients with Barrett's esophagus who have undergone a successful antireflux operation with symptomatic relief and evidence of improvement in lower esophageal sphincter pressures rarely show regression of Barrett's mucosa and may still be at risk for development of carcinoma. Therefore, the indications for antireflux operation in Barrett's esophagus should remain the same as for other patients with gastroesophageal reflux, but yearly endoscopic and histological surveillance should be continued postoperatively.
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PMID:Effect of antireflux operation on Barrett's mucosa. 232 44

The role of duodenogastric reflux in the pathogenesis of gastroesophageal reflux disease is not clear. Using hepatobiliary scanning techniques, we found evidence of duodenogastric reflux in six of 13 patients with Barrett's esophagus. This compares with only two positive studies in 19 control subjects. This difference is statistically significant (P = 0.038, two-tailed Fisher's exact test). Three of nine patients who had gastroesophageal reflux without Barrett's esophagus had evidence of duodenogastric reflux, a frequency not significantly different from either of the other groups. Gastroesophageal reflux of bile and pancreatic enzymes, in addition to gastric acid may contribute to the greater esophageal damage often seen in Barrett's esophagus. The presence of duodenogastric reflux in these patients may have important pathophysiologic and therapeutic implications.
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PMID:Duodenogastric reflux in patients with Barrett's esophagus. 234 9

In the present paper we analyze the importance of gastro-oesophageal reflux in 20 patients with Barrett's oesophagus and in 20 patients with esophagitis without Barrett's mucosa; ten of this last group had mild esophagitis and ten severe inflammatory changes. In all the cases the oesophageal pH was measured during 24 hours; the results showed that although the reflux was more important in the group of patients with Barrett's esophagus than in the whole group of patients with esophagitis without Barrett's esophagus, figures were similar in the group with severe oesophagitis and the group with Barrett's oesophagus. We conclude that the pathogenesis of Barrett's esophagus includes factors other than gastroesophageal reflux.
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PMID:[Quantification of gastro-esophageal reflux in Barrett's esophagus]. 237 53

This chapter reviews the pathologic aspects of gastroesophageal reflux and reflux esophagitis. High-grade and low-grade changes due to reflux are discussed in the context of peptic complications such as hemorrhage, ulcer, stricture, and acquisition of Barrett mucosa. The limitations of histopathologic criteria in squamous epithelium for the diagnosis of reflux esophagitis, such as elongated vascular papillae and widened basal zone, are described. The pathogenesis of and criteria for diagnosis of Barrett esophagus are addressed. The neoplastic complication of adenocarcinoma arising in Barrett esophagus is discussed. Finally, the implications of columnar epithelial dysplasia and potential markers in Barrett mucosa for surveillance of Barrett patients are reviewed.
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PMID:Reflux esophagitis and Barrett esophagus. 240 72

To evaluate the consequences of dysplasia in Barrett's esophagus, six patients with esophageal mucosal biopsies showing dysplastic Barrett's mucosa in the absence of clinically evident esophageal carcinoma were identified and their clinicopathologic features reviewed. The patients, four men and two women, averaged 60 years and had long histories of gastroesophageal reflux. Four patients had high-grade dysplasia; two had low-grade. Dysplastic Barrett's mucosa appeared to arise most commonly from specialized-type Barrett's mucosa. After a mean follow-up of 29 months, four patients, all with high-grade dysplasia, had esophageal resections. Three of the four were found to have invasive adenocarcinoma, which extended through the esophageal wall in two patients. The fourth patient had a noninvasive adenomatous polyp ("Barrett's adenoma"), an infrequently described form of dysplasia in Barrett's esophagus. The two patients with low-grade dysplasia had developed no clinical indications of carcinoma. The results confirm that dysplastic Barrett's mucosa, particularly the high grade, is a morphologic marker for adenocarcinoma. Biopsy surveillance of patients with Barrett's esophagus is histologically feasible, but prospective studies are required to prove its effectiveness.
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PMID:Dysplasia in Barrett's esophagus. A clinicopathologic study of six patients. 241 26

Fifty-eight patients had surgery for carcinoma of the esophagus at Scripps Clinic, La Jolla, Calif, from 1976 to 1986. Esophagectomy with reconstruction by colon interposition was done in 24 patients with adenocarcinoma arising in columnar-lined epithelium (Barrett's). In 5 patients, obstructive symptoms had not yet developed and the diagnosis was made by endoscopy performed for evaluation of gastroesophageal reflux. Dysphagia had just started in 12 additional patients and no weight loss had been noted. The operation was palliative in 14 patients and potentially curative in the other 10. Only 3 patients had negative lymph nodes. Ten patients were alive after 2 to 11 years. Encouraging results were indicated for surgical treatment of adenocarcinoma of the esophagus developing in Barrett's epithelium. A good outcome can be obtained with resection even in patients with lymph node metastases.
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PMID:Early diagnosis of adenocarcinoma developing in Barrett's esophagus. 247 86

This study was designed to evaluate the utility of 99mTc pertechnetate esophageal scintigraphy for identifying Barrett's esophagus. Seventeen patients with Barrett's esophagus and seven patients with reflux esophagitis were studied. Eight of 17 patients with Barrett's esophagus had a positive image (sensitivity 47%). In contrast, none of the seven patients with esophagitis had a positive image (specificity 100%). Pentagastrin did not have a significant effect on the sensitivity. There was no correlation between the type of Barrett's epithelium and the sensitivity of the imaging results. However, the test is more frequently positive in those patients with more extensive disease. Our study indicates that technetium pertechnetate imaging should not be used as a screening test for the detection of Barrett's esophagus in patients with symptoms of gastroesophageal reflux, as the negative predictive value of the test is limited.
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PMID:Technetium pertechnetate esophageal imaging for detection of Barrett's esophagus. 254 24

Efficient esophageal clearance has an important defence role in the pathogenesis of the gastroesophageal reflux disease (GERD). Many GERD patients have esophageal disturbances associated with or secondary to reflux, producing delayed clearance. This delay exposes the esophageal mucosa to the reflux acid content. To determine esophageal transit we scanned the esophageal transit of a 15 ml bolus containing colloidal 300/cCi 99m Tc. The esophageal transit was calculated in seconds according to formula E.T. = T 1/2 x 5. The study included 74 GERD patients. The following investigations were carried out in all the cases: esophageal X-ray, GER scintigram, endoscopy, esophageal biopsy, Bernstein test and esophageal transit scintigram. Endoscopy revealed lesions of the esophagus (of 1st, 2nd and 3rd degree) in 39 patients, Barrett syndrome in 8 cases and normal in 27. Esophageal transit scanning was normal in 18 cases (24%), and prolonged in 56 cases (76%). Only 7 (39%) of the 18 patients with a normal transit presented lesions of the mucosa, the latter being more frequent in patients with a prolonged transit, i.e. 40 of 56 patients (71.5%). The mean value of the transit in different degrees of esophagitis (I, II, III) and Barrett syndrome were: 12.73 +/- 5.36; 13.30 +/- 7.90; 10.35 +/- 5.78; 17.25 +/- 11.17. In conclusion esophageal transit scanning is a useful test in GERD patients as it has a prognostic value. A prolonged esophageal transit is frequently associated with lesions, the more severe the slower is the transit. Moreover the test may indicate certain drugs acting upon the esophageal motor disturbances.
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PMID:[Is an esophageal transit scintigram necessary in patients with gastroesophageal reflux?]. 257 47

An alcoholic man with known reflux esophagitis and Barrett's esophagus developed fever, epigastric pain, subcutaneous crepitus, and leukocytosis from an esophageal perforation at a Barrett's ulcer. Possible risk factors for perforation in this patient included alcoholism, severe gastroesophageal reflux, corticosteroid therapy, noncompliance with antacid and H2 blocker therapy, and the presence of acid-secreting parietal cells in the Barrett's epithelium. Five cases of this complication have previously been reported in a review of the literature, which included 536 cases of Barrett's esophagus or esophageal perforation. This entity may present with a clinical triad of a patient (a) in acute distress with fever and epigastric or noncardiac chest pain and without signs of peritonitis, (b) with symptoms of or known gastroesophageal reflux, and (c) with chest examination revealing subcutaneous crepitus, or chest roentgenogram revealing subcutaneous emphysema, pneumomediastinum, or hydropneumothorax.
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PMID:Esophageal perforation at a Barrett's ulcer. 258 67


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