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

Adenocarcinoma arising in Barrett's esophagus has recently been described in two children aged 11 and 14 years. The long-term follow-up of Barrett's esophagus in children is not well described. We evaluated 16 cases of Barrett's esophagus in children treated at this institution during the last 16 years. Ages ranged from 1.2 to 16 years (mean, 10.3 years). There were 11 boys and 5 girls. Barrett's esophagus was documented by endoscopy in 14 instances and at autopsy in 2 patients with secretory diarrhea and tetralogy of Fallot who died of sepsis. Two children had cancer (neuroblastoma, leukemia) and died of their malignant disease. Five patients had cerebral palsy, 1 esophageal atresia, 1 Fanconi's anemia, and 5 were otherwise normal children. Six were treated medically. Eight patients underwent Nissen fundoplication for complications of gastroesophageal reflux (GER). Five patients were available for follow-up endoscopy (mean, 2 years; range, 1.1 to 5.4 years). Endoscopy was performed on a yearly basis, obtaining biopsy specimens from multiple levels of the esophagus. Four children had satisfactory clinical response to an antireflux procedure including the resolution of a stricture in one case. However, in all 5 cases persistent metaplastic epithelium was documented and showed no evidence of regression. Although there has been speculation that Barrett's esophagus in children may be more likely to revert to normal squamous epithelium than in the adult, there has been only one case of regression in 180 cases of Barrett's esophagus occurring in children described in 37 reports in the literature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Persistence of Barrett's esophagus in children after antireflux surgery: influence on follow-up care. 156 27

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

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

Adenocarcinoma of the esophagus is a well-known complication of Barrett esophagus, especially in white men. We present three cases of squamous carcinoma of the esophagus in Barrett patients. All three patients were white men. None had a history of symptomatic gastroesophageal reflux or of Barrett esophagus, but all had substantial usage of alcoholic beverages and tobacco. All three tumors were located in squamous-lined mucosa above the Barrett mucosa. Columnar epithelial dysplasia was present in the Barrett mucosa of two of our patients, and the third patient had a squamous carcinoma of the pharynx. Squamous carcinoma represented 2% of Barrett-associated esophageal carcinomas at our institution in 1980 through 1986. Five additional cases were found in the literature, and all were also in white men. This demographic predominance stood in striking contrast to the 26% prevalence of white patients among those with squamous carcinoma of the esophagus at our institution (P less than 0.0002) and to the 50% prevalence of white men among our patients with Barrett esophagus (P less than 0.02). Two of the literature cases also had substantial alcohol and tobacco usage and had synchronous adenocarcinoma arising in Barrett mucosa. Our findings of a strikingly high prevalence of white men and of multifocal neoplastic changes in the upper aerodigestive tract suggest a pathogenetic relationship between squamous carcinoma of the esophagus and Barrett esophagus, possibly due to alcoholic beverage and tobacco usage. Endoscopic surveillance of Barrett patients for early detection of adenocarcinoma has been recommended; contemporaneous evaluation of the squamous-lined esophagus by biopsy and cytopathology may be advisable.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Squamous carcinoma of the esophagus in patients with Barrett esophagus. 292 88

Barrett esophagus has become a common lesion in the esophagus; it is presumably caused by reflux esophagitis. Double-contrast barium esophagraphy improves radiographic evaluation of Barrett esophagus. The presence of midesophageal stricture, mucosal reticular pattern, and deep esophageal ulceration suggests the presence of Barrett esophagus. Other findings, such as hiatal hernia, thickened mucosal folds, and gastroesophageal reflux, are also frequently seen in Barrett esophagus but are not specific. Adenocarcinoma may complicate Barrett mucosa, usually with severe dysplasia. Adenocarcinoma has morphologic forms similar to squamous cell carcinoma in the esophagus. Barium esophagram, CT scans, and endoscopic sonography are used to evaluate and stage adenocarcinoma in the esophagus.
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PMID:Barrett esophagus and adenocarcinoma. 797 6

Smoking and alcohol consumption predispose to oesophageal mucosal damage and exacerbates gastro-oesophageal reflux. The alcohol and smoking habits of patients with severe oesophagitis (n = 24), Barrett's columnar lined oesophagus (CLO) (n = 58), and adenocarcinoma arising in CLO (n = 23) were studied. There was no significant difference between the age (median 67, 64, and 65 years respectively) or duration of symptoms (median 10 years) in each group. Patients with benign CLO were significantly more likely to be non-smokers and non-drinkers, or both than patients with both severe oesophagitis and adenocarcinoma (p < 0.001). Of those who smoked or drank, patients with CLO had a smoking history of a median 15 pack years (range 2-60 pack years), which was less than both the severe oesophagitis (median 45.5, range 5-150 pack years) (p < 0.01), and adenocarcinoma groups (median 55.25, range 4-200 pack years) (p < 0.001). Patients with adenocarcinoma had smoked for more years in total (median 38.5, range 4-54 years) than patients with CLO (median 29.5, range 6-55 years) (p < 0.01). Patients with severe oesophagitis (median 38.5, range 27-55 years) and adenocarcinoma patients had a similar long history of smoking both of which were greater than CLO patients (p < 0.003). Half of the severe oesophagitis group drank more than 40 units/week and six more than 100 units/week (median 40, range 1-->100 units/week), whereas CLO patients who drank did so more moderately (median 10, 1-100 units/week) (p < 0.02). Adenocarcinoma patients also had a somewhat greater alcohol intake than CLO patients, median 15 (1-100 units/week) (p<0.02). Smoking and alcohol consumption do not predispose to the development od metaplastic columnar lined oesophagus in patients with severe gastro-oesophageal reflux but are strongly associated with the development of adenocarcinoma in patients with established Barrett's oesophagus.
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PMID:The role of smoking and alcohol in metaplasia and cancer risk in Barrett's columnar lined oesophagus. 831 2

Esophageal adenocarcinoma arises from Barrett's esophagus, which is induced by gastro-esophageal reflux. This refluxate often contains duodenal contents, whose backflow triggers gastric carcinoma, suggesting the hypothesis that refluxed duodenal contents cause esophageal carcinoma. This study examines the role of duodenal and gastric reflux in the absence of exogenous carcinogens in esophageal carcinogenesis. Wistar male rats, 120 in all, each weighing approximately 250 g, were used. Three experimental procedures were performed to produce gastro-duodeno-esophageal reflux, duodeno-esophageal reflux and gastro-esophageal reflux, for comparison with 2 control procedures, Roux-en-Y reconstruction and a sham operation. The animals were fed a standard diet and were examined 50 weeks after surgery. While no carcinoma was found among the 16 gastro-esophageal-reflux, 11 Roux-en-Y and 12 sham-operation animals, 10 of the 12 animals with gastro-duodeno-esophageal reflux (83%) and 10 of the 13 with duodeno-esophageal reflux (77%) developed esophageal carcinoma. The difference between groups was significant (p < 0.001). Two animals with gastro-duodeno-esophageal reflux had esophageal double and triple carcinomas respectively. Of the 23 carcinomas, 16 were adenocarcinoma, 4 adenosquamous carcinoma, and 3 squamous-cell carcinoma. Adenocarcinoma developed from the columnar-lined epithelium near the esophago-jejunostoma, while adenosquamous and squamous-cell carcinoma arose from the squamous esophagitis. These observations demonstrate that refluxed duodenal contents per so are responsible for esophageal carcinogenesis.
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PMID:Reflux of duodenal or gastro-duodenal contents induces esophageal carcinoma in rats. 876 May 98

Adenocarcinoma of the esophagus and gastric cardia are the most rapidly increasing cancers in developed countries. Adenocarcinoma of the esophagus is associated with chronic gastroesophageal reflux, and Barrett's esophagus is a precursor. This disease most frequently affects middle-aged white men. Endoscopic surveillance should be performed on patients with Barrett's esophagus, and esophagectomy is often performed on persons with high-grade dysplasia. Ablation of Barrett's esophagus has been proposed to prevent cancer but the outcomes are unproven. Squamous carcinoma of the esophagus most often affects black men and is associated with alcohol and tobacco use. The diagnosis of esophageal cancer is made by endoscopy with biopsy. Optimal staging is with endoscopic ultrasonography for depth of invasion and regional nodes and CT scanning for distant metastases. Neoadjuvant chemotherapy and radiation therapy followed by surgery is widely practiced, but survival benefits remain to be proven. Palliation of dysphagia may be achieved with surgery, radiation therapy, or endoscopic means, with the latter having fewer complications.
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PMID:Esophageal cancer prevention, cure, and palliation. 1095 Apr 58

Adenocarcinoma of the gastric cardia is increasing in incidence. The purpose of this study was to determine whether intestinal metaplasia of the esophagogastric and having a malignant potential junction can be considered as an ultra-short segment Barrett's esophagus. To study the epidemiologic and histological features of the intestinal metaplasia of esophagogastric junction two groups of patients were compared for the prevalence of this condition. Group 1 included 82 patients with gastroesophageal reflux symptoms et group 2 consisted of 82 healthy individuals. Both groups had two biopsy specimens taken from the esophagogastric junction. Histological evidence of intestinal metaplasia was defined as specialized columnar epithelium containing goblet cells staining with alcian blue at pH 2.5. Intestinal metaplasia of the esophagogastric junction was present in 12 patients in group 1 and 9 individuals in group 2. The global prevalence of this condition was 12.8% and there was not a statistically significant difference in the prevalence of this condition between the two groups. A significant difference could not be found when sex was considered. There was a significant association between this condition and older age (p = 0.01). Intestinal metaplasia of the esophagogastric junction and Barrett's esophagus do not have the same epidemiologic features. Therefore, we suggest that screening biopsy specimens of the esophagogastric junction be limited to study protocols at this time.
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PMID:[Intestinal metaplasia at the gastroesophageal junction - epidemiologic and histologic aspects. Report of 164 cases]. 1177 30


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