Adenocarcinoma in situ in Barrett's esophagus with stricture of 10-yr duration: a cytological diagnosis.
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Barrett's esophagus
Esophageal adenocarcinoma
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Barrett's esophagus is associated with adenocarcinoma of the cardia and esophagus, regardless of its extent. The aim of this study was to compare the prevalence and incidence of dysplasia and adenocarcinoma in short segment and traditional long segment Barrett's esophagus.Seventy-four patients with short segment Barrett's and 78 with traditional Barrett's entered the study.There were no significant differences in age or gender between the two groups of patients with Barrett's esophagus. A greater percentage of patients with short segment barrett's were black (p = 0.04). The prevalence of dysplasia at diagnosis in patients with short segment Barrett's was 8.1% versus 24.4% in patients with traditional Barrett's (p < 0.007). Adenocarcinoma was noted at diagnosis only in patients with traditional Barrett's (p < 0.0005). Twenty-six patients with short segment Barrett's and 29 with traditional Barrett's were followed prospectively for 12-40 months. Dysplasia developed during follow-up in two patients with short segment Barrett's and in six patients with traditional Barrett's (p < 0.05). Neither high grade dysplasia nor cancer developed in any patients with short segment Barrett's. High grade dysplasia did develop in two patients with traditional Barrett's esophagus, and mucosal adenocarcinoma developed in one. The frequency of dysplasia on the latest surveillance examination continued to be significantly higher for patients with traditional Barrett's (p = 0.03). Follow-up surveillance biopsy specimens of Barrett's mucosa frequently demonstrated an absence of goblet cells in patients with short segment Barrett's compared with patients with traditional Barrett's (p < 0.0001).The prevalence of dysplasia or adenocarcinoma and the incidence of dysplasia in patients with traditional Barrett's esophagus are significantly higher than in patients with short segment Barrett's esophagus. Further prospective surveillance is required to determine whether the incidence of adenocarcinoma in patients with short segment Barrett's esophagus is significantly lower.
Barrett's esophagus
Intestinal metaplasia
Esophageal disease
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Barrett's esophagus
Reflux esophagitis
Esophagitis
Esophageal disease
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Barrett's esophagus
Esophagectomy
Intestinal metaplasia
Endoscopic mucosal resection
Metaplasia
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Abstract Background: The incidence of esophageal adenocarcinoma has risen dramatically over the past half century, and the underlying reasons are incompletely understood. Broad shifts to the upper gastrointestinal microbiome may be partly responsible. The goal of this study was to describe alterations in the esophageal microbiome that occur with progression from Barrett's esophagus to esophageal adenocarcinoma. Methods: A case–control study was performed of patients with and without Barrett's esophagus who were scheduled to undergo upper endoscopy. Demographic, clinical, and dietary intake data were collected, and esophageal brushings were collected during the endoscopy. 16S rRNA gene sequencing was performed to characterize the microbiome. Results: A total of 45 patients were enrolled and included in the analyses [16 controls; 14 Barrett's esophagus without dysplasia (NDBE); 6 low-grade dysplasia (LGD); 5 high-grade dysplasia (HGD); and 4 esophageal adenocarcinoma]. There was no difference in alpha diversity between non–Barrett's esophagus and Barrett's esophagus, but there was evidence of decreased diversity in patients with esophageal adenocarcinoma as assessed by Simpson index. There was an apparent shift in composition at the transition from LGD to HGD, and patients with HGD and esophageal adenocarcinoma had decreased Firmicutes and increased Proteobacteria. In addition, patients with HGD or esophageal adenocarcinoma had increased Enterobacteriaceae and Akkermansia muciniphila and reduced Veillonella. In the study population, patients taking proton pump inhibitors had increased Streptococcus and decreased Gram-negative bacteria overall. Conclusions: Shifts in the Barrett's esophagus–associated microbiome were observed in patients with HGD and esophageal adenocarcinoma, with increases in certain potentially pathogenic bacteria. Impact: The microbiome may play a role in esophageal carcinogenesis.
Esophageal adenocarcinoma
Barrett's esophagus
Esophageal disease
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Barrett's esophagus
Esophageal adenocarcinoma
Esophageal disease
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OBJECTIVE: To investigate the expression of c-myb in reflux esophagitis, Barrett esophagus and esophageal adenocarcinoma. METHODS: The expression levels of c-myb in the esophageal mucosa tissue of patients with reflux esophagitis, Barrett esophagus and esophageal adenocarcinoma were detected by real-time fluorescent quantitative RT-PCR. RESULTS: The expression levels of c-myb mRNA in Barrett esophagus and esophageal adenocarcinoma tissues was significantly higher than that in normal and reflux esophagitis esophageal tissue (P<0.05 or 0.01), and increased progressively with the development of reflux esophagitis into Barrett esophagus and esophageal adenocarcinoma. CONCLUSIONS: The expression level of c-myb mRNA is closely related with the development of Barrett esophagus and esophageal adenocarcinoma, and may be used as a valuable index for monitoring the early onset and intervention of Barrett esophagus and esophageal adenocarcinoma.
Barrett's esophagus
Reflux esophagitis
Esophagitis
Esophageal adenocarcinoma
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The presence of gastric metaplasia in the distal esophagus is better known as Barrett's Esophagus (BE). It is an acquired condition caused by gastro-esophageal reflux disease and is associated with a high risk of adenocarcinoma development in the distal esophagus and cardia. The definition of BE has changed over the years as only the specialized metaplasia, with the characteristic "goblet cells", has been shown to carry a risk of cancer development. BE is currently defined as the presence of intestinal metaplasia in the distal esophagus. The prevalence of intestinal metaplasia of the distal esophagus in patients undergoing endoscopy with multiple biopsies for dyspeptic symptoms, varies from 9-21% at the level of the cardia and from 1.2-8% at 3 cm above the esophago-gastric junction, with a decreasing caudo-cranial frequency. Among the BE population (intestinal metaplasia 3 or more cm long) there is a prevalence of male sex and white race, with an average age between the 5(th) and 7(th) decade. The risk of BE mucosa advancing to esophageal adenocarcinoma is not well established: incidence rates from 1/52 years-patient to 1/441 years-patient and a calculated risk from 30 to 125 times higher than in the normal population were reported. These discrepancies are probably related to: 1) temporal differences of the studies, 2) retrospective versus prospective type of the studies, 3) length of follow-up, 4) number of individuals surveilled, 5) regional variations. A literature analysis confirmed that the differences are mostly related to the number of patients studied (the larger the population the lower the incidence), are generally inversely proportional to the follow-up length (the shorter the follow-up the higher the incidence) and depend on the type of the studies (the incidence is higher in the retrospective studies than in the prospective one's). Surveillance program: esophageal adenocarcinoma is a lethal tumor with a 20% 5-year survival rate. The guidelines of The American College of Gastroenterology advice a two-year surveillance rate for BE patients without dysplasia. The difficulty with BE surveillance programs-- even if worthwhile on a single patient basis-- is that they are very expensive and at the present none of the endoscopic surveillance prospective studies has shown a positive impact in the survival rate. From our knowledge it doesn't seem wise to abandon a precautionary surveillance strategy, but further studies are needed to better understand the risk population: at the moment our advice is to monitor male patients in good general conditions with a BE segment longer than 3 cm.
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A n a c h t e ( m a T o a p T 3 i c o p a 1 t o a p s arrett’s esophagus is defined by the replacement of squamous esophageal epithelium by intestinal metalasia in the distal esophagus. Barrett’s esophagus is a airly frequent complication of gastroesophageal reflux isease (GERD); 5% to 10% of patients with GERD suffer rom Barrett’s esophagus. GERD is essential for the develpment of Barrett’s esophagus.1 Intestinal metaplasia is a remalignant lesion that may develop further into dysplaia and lead to adenocarcinoma of the esophagus.2 The atter accounts for almost 50% of esophageal cancer cases n western countries; the largest increase in its incidence as recorded during the past two decades.3 Patients with arrett’s esophagus have a 2% to 25% risk of developing ild-to-severe dysplasia and a 2% to 5% risk of having denocarcinoma, namely 30 to 150 times higher than the isk of the general population. Forty percent to 50% of Patients ho have Barrett’s esophagus with high-grade dysplasia can evelop adenocarcinoma within 5 years.4,5 Esophageal adenocarcinoma is associated with a poor rognosis because of its delayed diagnosis. Endoscopy creening and surveillance programs therefore may recogize earlier adenocarcinoma that can be treated adeuately. It remains controversial, however, whether such creening and surveillance in the general population will ecrease the incidence of adenocarcinoma and improve he survival of these patients. Furthermore, whether creening and surveillance are cost-effective remains a atter of considerable debate.6-8 Medical therapies using high doses of proton pump inibitors (PPIs) or surgical therapies (eg, fundoplication) ave been proposed to reverse Barrett’s esophagus and brogate the trigger event in the cascade of the metaplasiaysplasia-cancer sequence, namely GERD. On the one and, retrospective surgical therapies have however failed o demonstrate a significant benefit in BE regression and n the development of adenocarcinoma.9-11 Similarly, igh doses of PPIs offer only a modest remission, with artial restoration of squamous islands within the intesti-
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Barrett's esophagus
Metaplasia
Esophagitis
Reflux esophagitis
Intestinal metaplasia
Esophageal disease
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