Gene/Protein Disease Symptom Drug Enzyme Compound
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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 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

Barrett's esophagus, a condition in which the distal esophagus is lined by columnar epithelium, is almost always caused by gastroesophageal reflux and often occurs in conjunction with a sliding hiatal hernia. Patients are typically white men in their 50s who smoke and drink, and they present with complaints of regurgitation, heartburn, and/or dysphagia. Endoscopic biopsies are required to confirm the diagnosis. Complications, such as stricture, ulcer, dysplasia, and malignant degeneration, occur in many cases. Adenocarcinoma is the most serious complication. Medical treatment, including life-style changes as well as pharmacologic therapy, usually relieves symptoms and heals esophagitis, but when it fails, antireflux surgery is indicated. Patients without evidence of dysplasia should undergo endoscopy yearly; those with mild dysplasia require more frequent surveillance. If biopsies disclose severe dysplasia, esophagogastrectomy should be performed.
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PMID:Barrett's esophagus. A continuing conundrum. 206 52

The authors review the literature about the assessment of risks of adenocarcinoma occurring over the natural history of Barrett's oesophagus with an incidence much higher than in the general population. The best marker is histological analysis of the cylindric epithelium for signs of dysplasia or early carcinoma. Although there is much controversy about the practical benefit of regular surveillance, the authors recommend a yearly endoscopy with multiple site biopsies. With the new potent drugs aimed at controlling gastro-oesophageal reflux, regression of metaplasia might occur, as the authors have observed in 3 patients treated by 60 mg omeprazole. However, prospective studies are needed to confirm this finding and its possible effect on reducing the risk of adenocarcinoma.
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PMID:[Barrett's esophagus. Characterization and monitoring policy]. 213 May 86

Adenocarcinoma arising in association with the columnar-lined esophagus is now recognized with increasing frequency. The incidence of malignant degeneration in Barrett's esophagus, its etiology, and pathogenesis are all issues of ongoing debate. The role of gastroesophageal reflux in driving the malignant change remains unproven. Surgical resection is the treatment of choice; however, prognosis is generally poor. Surveillance of patients with non-malignant Barrett's esophagus permits detection of early lesions where resection results in excellent long-term survival.
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PMID:Adenocarcinoma in Barrett's esophagus. 223 86

Although squamous cell carcinoma of the esophagus occurs with increased incidence in primary achalasia, esophageal adenocarcinoma has been considered rare in this condition. We report a patient with long-standing achalasia in whom adenocarcinoma of the esophagus occurred many years after Heller esophagomyotomy, presumably related to Barrett's esophagus complicating gastro-esophageal reflux disease.
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PMID:Esophageal adenocarcinoma in a patient with surgically treated achalasia. 225 39

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

Barrett's esophagus is a complication of gastroesophageal reflux. Radiological findings included gastroesophageal reflux and oesophagitis. It is an important precancerous disorder in the development of esophageal adenocarcinoma. The authors reported 4 cases confirmed by endoscopy and pathology.
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PMID:[Barrett's esophagus: a report of 4 cases]. 262 10

Barrett's esophagus is a disease that is common in patients with gastroesophageal reflux of acid but may also occur in association with bile reflux and rarely with other factors. It cannot be reliably distinguished from patients with reflux alone on the basis of demographic factors, clinical characteristics, or manometry. Radiology only serves to make Barrett's epithelium less likely in the presence of a completely normal study. The gold standard for diagnosing Barrett's esophagus is still multiple biopsies taken at the time of endoscopy. By performing multiple biopsies at various levels, the gastroenterologist will be effective not only in diagnosis but in selecting and screening that subset of patients with dysplasia that may predict coexisting or future adenocarcinoma. Treatment of high-grade dysplasia or carcinoma is resection, whereas medical treatment or fundoplication is still directed at the severity and complications of gastroesophageal reflux rather than at Barrett's characteristics alone. A decision tree given in Figure 5 summarizes these recommendations.
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PMID:Barrett's esophagus: detection and management. 266 73


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