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

Two children have been found to have partially obstructing lesions beyond the esophagus in association with mid-esophageal stricture. Both were found to have columnar epithelium-lined (Barrett) esophagus, and gastro-esophageal reflux. The more distal obstruction, in the pylorus and descending duodenum respectively, may have contributed to the development of the Barrett esophagus. It is recommended that any barium study of the esophagus which reveals an unexplained stricture should include visualization through the duodenojejunal junction as an aid to diagnosis, management, and understanding.
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PMID:Postesophageal narrowing associated with Barrett esophagus. 17 15

Two patients had both scleroderma and a columnar epithelium-lined lower esophagus (Barrett esophagus). Features of Barrett's esophagus included high esophageal strictures in both patients and ulcer craters in the columnar area of one. Biopsy confirmed columnar epithelium in the lower esophagus of each patient. In these patients, the Barrett esophagus probably was a complication of scleroderma and resulted from long-standing gastroesophageal reflux.
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PMID:Barrett's esophagus occurring as a complication of scleroderma. 68 90

Barrett's esophagus was diagnosed in 26 men in a five-year period by demonstrating esophageal specialized columnar epithelium in target biopsies obtained at endoscopy or in peroral suction biopsies of the esophageal mucosa. The clinical, radiologic and manometric features of these patients were reviewed retrospectively. Esophageal lesions associated with this epithelium included distal and midesophageal strictures and ulcers, alone or in combination, or simply esophagitis. One patient had an associated adenocarcinoma. Twenty of 26 (77%) had heartburn or regurgitation, 16 (62%) had easily elicited reflux of barium while supine and 16 of 17 tested had lower esophageal sphincter pressure in the incompetent range. Ninety-six percent had one or more of these parameters positive. This series demonstrates a wide spectrum of esophageal lesions in Barrett's esophagus, and supports the concept that this lesion occurs as a consequence of gastroesophageal reflux and erosive esophagitis. The case of adenocarcinoma in this series adds to the concern that the columnar lined lower esophagus may be a premalignant lesion.
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PMID:Barrett's esophagus. Clinical review of 26 cases. 68 53

Alcohol drinking induces acute and chronic lesions of the GI tract; some other GI disorders do occur more frequently in drinkers than in other persons. Alcoholics suffer from gastroesophageal reflux, Barrett's syndrome, exophageal cancer and Mallory-Weiss syndrome as well as from hemorrhagic erosive gastritis more often than normal. It is still unsettled if chronic gastritis can be due to alcohol drinking. Alcohol inhibits to some degree the absorption of water, electrolytes, disaccharides and vitamin B12 in the small intestine; it may as well impair intestinal motility and cause diarrhea. Many aspects of the effects of alcohol on the GI tract still remain to be elucidated. The main stay of therapy is abstenence.
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PMID:[Alcohol and gastrointestinal tract (author's transl)]. 70 68

The surgically created squamocolumnar junction in patients who have undergone an esophagogastrostomy after partial esophagogastrectomy provides a unique opportunity to study mucosal regeneration in the setting of gastroesophageal reflux. The pathological and clinical findings in 17 such patients are presented. In each patient the anastomosis had been performed between histologically documented squamous-lined esophagus and gastric fundus. Cardiac type mucosa had regenerated in the region of the anastomosis in 9 patients and was detected as early as 2 months after operation. In addition, 3 patients, 2 of whom had cardiac type mucosa, had acquired Barrett or Barrett-like mucosa on the distal esophagus by 76 to 119 months. Gastroesophageal reflux was prominent in all 3 of these patients. The findings strongly support the hypothesis that the distinctive mucosa of Barrett's esophagus develops after reflux-induced ulceration and subsequent mucosal regeneration by immature cells that are derived from cardiac and/or fundic mucosa, and which undergo specialized differentiation in the presence of reflux.
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PMID:Regnerative of cardiac type mucosa and acquisition of Barrett mucosa after esophagogastrostomy. 83 21

A review of 26 cases of columnar-lined (Barrett's) esophagus suggests that this lesion is more common than generally appreciated, usually arising consequent to reflux esophagitis. The radiologically detectable lesions frequently do not support the idea that Barrett's esophagus presents only with high esophageal ulcer and/or stricture. Hiatal hernia, gastroesophageal reflux, stricture, ulcers, and even minor mucosal abnormalities may be present alone or in combination, and may be variably located.
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PMID:The columnar-lined esophagus--analysis of 26 cases. 84 30

A case of adenocarcinoma developing at the squamocolumnar epithelial junction of a Barrett oesophagus is reported. This rare tumour was remarkable because of the youth of the patient and because of the signet-cell cytological pattern of the neoplasm. It is postulated that both the columnar epithelial lining of the lower part of the oesophagus and the malignant change are a consequence of long-standing oesophageal reflux.
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PMID:Adenocarcinoma in a Barrett oesophagus. 115 92

The epidemiology and natural history of reflux induced peptic esophageal diseases remain incompletely understood. That is why it is easy to explain that the traditional therapeutic efforts were mostly restricted to the use of acid-reducing or neutralizing drogs. The author tries to survey--mainly on theoretical bases--a new approach of the maintenance treatment of peptic esophagitis and consequential columnar metaplasia. The mechanism of the esophageal antireflux barrier is composed by the (a) lower esophageal sphincter tone, (b) upper esophageal sphincter tone, (c) esophageal acid clearance and (d) esophageal epithelial resistance. The data of a 100-patient-group of gastroesophageal reflux disease cases were retrospectively evaluated principally considering the efficacy of antisecretory treatment relating to the accompanying diseases, recurrence of symptoms and prevention the development of Barrett's columnar lined esophagus and Barrett's ulceration. The decrease of exposure by damaging factors is an essential criterion of antisecretory therapy, having several disadvantages. Based only to logically well established arguments the author believes that gastroesophageal reflux disease and consecutive conditions might be an ideal model for studying and introducing esophageal cyto (-mucosal, -tissue) protection, considering that in the esophagus--in contradiction to the stomach--the cell and tissue injury, induced by several pathogenic agents, does not develop rapidly, and when the organ damage develops gradually, interventions may be possible to protect esophageal cell and the mucosa directly.
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PMID:Esophageal mucosal protection--why do we need a special approach? 134 81

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

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


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