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)

Review of 34 cases of pathologically proved Barrett-type adenocarcinoma of the esophagus seen at the University of Michigan during 1962-1983 revealed that it constituted 5% of all carcinomas of the esophagus and 20% of all adenocarcinomas involving the esophagus during that period. Despite many similarities to conventional squamous cell carcinoma and gastric cardiac carcinoma, certain distinguishing features were identified. Radiologically, diagnosis of Barrett carcinoma should be suggested when a patient with a longstanding history of gastroesophageal reflux, chronic esophagitis, and hiatus hernia with or without features of Barrett esophagus demonstrates a long vertical segment of esophageal involvement by an infiltrating or varicoid-appearing lesion. This review analyzes the clinical and radiologic distinguishing features of Barrett carcinoma and compares those of gastric cardiac carcinoma and conventional squamous cell carcinoma of the esophagus.
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PMID:Barrett carcinoma of the esophagus: clinical and radiographic analysis of 34 cases. 387 54

Three cases of patients with esophageal involvement by scleroderma, chronic reflux esophagitis, and adenocarcinoma of the distal esophagus are presented. An underlying columnar metaplasia (Barrett esophagus) was identified in two patients and postulated in the third. It is believed that scleroderma patients with symptomatic chronic gastroesophageal reflux should be investigated for Barrett epithelium. If it is present, these patients should be followed and considered as having an increased risk for development of adenocarcinoma of the esophagus.
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PMID:Adenocarcinoma of the esophagus in patients with scleroderma. 660 35

An attempt is made to correlate clinical respectively endoscopic and histomorphological findings in patients with gastroesophageal reflux disease. The histological stage Ia cannot be identified endoscopically. However, certain correlations can be found between endoscopic stage I (the "red spot") on the one hand and the histological stage Ib (hyperemic capillaries) on the other, just as well as between subsequent endoscopical and histological stages. The histomorphological stage IV corresponds to the clinical stage IV and represents the ultimate complication of the reflux disease, esophageal stenosis caused by ulceration plus endobrachyesophagus. In this stage no restitutio ad integrum is possible anymore. The initial changes of the gastroesophageal reflux disease occur within the epithelium and the papillae and can be recognized microscopically in biopsies taken during endoscopy. Changes in the submucosal layer are of no importance during the early reversible stages. The lining of the endobrachyoesophagus with cylindrical epithelium ("Barrett mucosa") is probably the consequence of reflux. This type of lining presents an irregular picture from the morphological as well as from the clinical point of view and is to be considered as a pre-stage of adenocarcinoma of the esophagus.
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PMID:[Reflux disease of the esophagus]. 668 Jul 60

The authors take a conservative stand on the relationship of Barrett esophagus to adenocarcinoma of the esophagus. They indicate the need for a definitive, large, cooperative, prospective study of all patients who have symptoms and many volunteers who had mild symptoms of esophageal reflux to prove or disprove that relationship.
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PMID:Barrett Esophagus. 669 Nov 27

Barrett's esophagus denotes the presence of columnar epithelium in the esophagus instead of the usual stratified squamous epithelium. Barrett's esophagus had been thought to represent a mediastinal extension of the stomach in patients with a congenital short esophagus. Subsequent clinical and experimental data have established the abnormality as an acquired condition resulting from chronic gastroesophageal reflux. Although roentgenographic studies may show a mild-esophageal stricture or an esophageal ulcer, definitive diagnosis requires endoscopy with directed biopsy of erythematous mucosa in the esophagus, or manometrically guided biopsies for showing the presence of columnar epithelium above the lower esophageal sphincter. Although the origin of the cells causing this epithelium is still unclear, three distinct epithelial types have been found: atrophic gastric-fundic, junctional, and specialized columnar. Esophageal strictures and esophageal ulcers are complications associated with Barrett's esophagus, but its major significance is the association with the development of adenocarcinoma of the esophagus. Treatment of Barrett's esophagus is aimed at preventing gastroesophageal reflux with the additional need for close endoscopic surveillance for the development of dysplasia or early adenocarcinoma. Whether the diagnosis of Barrett's esophagus mandates anti-reflux surgery (fundoplication) remains controversial.
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PMID:Barrett's esophagus. 704 50

Intragastric pressure measurements and cineradiographic contrast studies were done in monkeys in order to determine the pressure at which esophageal reflux occurred. Antireflux operative procedures were performed above and below the diaphragm, and the results compared. The Nissen fundoplication proved to be the most effective type of mechanical antireflux valve and worked equally well placed above and below the diaphragm. Of 200 consecutive adult patients undergoing operative correction of esophageal reflux, 19 had severe esophageal strictures. Through a transthoracic approach, two patients had subdiaphragmatic Nissen fundoplications, one with adenocarcinoma of the esophagus had an esophageal resection, and 16 had supradiaphragmatic Nissen fundoplications; those 16 patients form the basis of this report. No patients died; superficial, temporary esophageal ulcerations developed in two. Follow-up times have ranged from six months to eight years; the results in all cases have been good. Experimental and clinical evidence supports the belief that this less radical approach is the treatment of choice in the management of severe esophageal strictures secondary to reflux esophagitis.
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PMID:Supradiaphragmatic correction of esophageal reflux strictures. 723 69

Barrett's esophagus is defined as a disorder in which the normal stratified squamous mucosa of the esophagus is replaced by columnar epithelium. Patients with Barrett's esophagus are at risk to develop an adenocarcinoma of the esophagus. Pathologic gastroesophageal reflux is correlated to the disease and therapeutical options must aim to stop this noxa in order to prevent columnar metaplasia, and subsequent dysplasia and/or neoplasia. The Authors report the case of a patient in whom the complete regression of the metaplasia was observed after medical therapy.
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PMID:[Complete regression of Barrett's esophagus after drug therapy]. 754 22

A new stimulus for research into the etiology and pathogenesis of Barrett's columnar-lined lower esophagus has been provided by the discovery that Barrett's esophagus has a very high prevalence in the general population and that adenocarcinoma of the esophagus and cardia is the fastest-growing cancer in the United States. Gastroesophageal reflux disease is the single most important factor in the pathogenesis of Barrett's esophagus, and duodenal juices may play a key role in the development of complications of stricture, ulceration, and possibly even malignant degeneration. Treatment is, therefore, aimed at abolishing all forms of reflux. Acid suppression, if used, needs to be given in massive doses to be effective in gastric hypersecretion and has no effect on other constituents of the refluxed material. Antireflux surgery has been shown to be superior to all forms of medical treatment. Regression is rare after any therapy, but continued surveillance is essential, with increased vigilance in patients with dysplasia or DNA abnormalities on flow cytometry. The role of cigarettes and alcohol in malignant degeneration is refuted.
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PMID:Barrett's esophagus. 758 62

Primary adenocarcinoma of the esophagus, previously considered a rare neoplasm, has shown a dramatic increase in its incidence rate among White men in the United States since 1970. The reason for this increase is unknown. Since the presence of Barrett's esophagus is essential for the development of most esophageal adenocarcinomas, the increasing incidence of esophageal adenocarcinoma may be related to an increasing prevalence of Barrett's esophagus, and its precursor, gastroesophageal reflux. An association between this increasing incidence and an increasing use of pharmaceutical agents that relax the lower esophageal sphincter is proposed. The data on the dollar amount and approximate quantity in milligrams purchased per capita through retail pharmacies and hospitals in the United States from 1957 to 1986 are presented for four categories of such agents. An upward trend is observed for all four categories.
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PMID:Rising incidence rate of esophageal adenocarcinoma and use of pharmaceutical agents that relax the lower esophageal sphincter (United States). 782 45

In Barrett's esophagus the normal stratified squamous epithelium lining the esophagus becomes replaced by metaplastic columnar epithelium containing goblet cells; it develops as a complication of chronic gastroesophageal reflux disease and predisposes the patient to adenocarcinoma. The frequency with which it leads to adenocarcinoma is not established with certainty, but the reported prevalence averages approximately 10% when the diagnosis of Barrett's esophagus is first made. The estimated incidence of adenocarcinoma varies from one in 152 to one in 441 cases per patient year, or a 30- to 125-fold excess risk. Esophageal adenocarcinoma arises only in patients with metaplastic columnar epithelium. Dysplasia precedes adenocarcinoma in Barrett's esophagus and arises from the metaplastic epithelium; it has been proposed as a marker for detecting patients at high risk for developing carcinoma. Problems with the use of dysplasia as a marker for cancer risk include difficulty in differentiating it from reactive change, variability in diagnosis and grading between observers and when the same observer interprets the sections on different occasions, and lack of understanding of its natural history. Methods other than dysplasia for detecting patients at highest risk for developing carcinoma have been sought, but flow cytometric analysis of DNA content is the only one proven to be valuable to date. Flow cytometric abnormalities correlate well with histological progression in Barrett's esophagus. The prevalence of elevated S phase and G2/tetraploid fractions and of aneuploid cell populations increases with histological progression from metaplasia to indefinite/low grade dysplasia to high grade dysplasia and cancer. Flow cytometric abnormalities in endoscopic biopsy specimens identify those patients with a higher risk of progression to high grade dysplasia or adenocarcinoma.
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PMID:Barrett's esophagus, dysplasia, and adenocarcinoma. 792 21


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