Cases reported "Barrett Esophagus"

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1/68. Importance of duodeno-gastro-esophageal reflux in the medical outpatient practice.

    BACKGROUND/AIMS: The role of acid and duodeno-gastro-esophageal reflux (DGER), also termed bile reflux, in esophageal mucosal injury is controversial. Several recent developments, especially availability of the recent bilirubin monitoring device (Bilitec), have resulted in clarifications in this area. In order to better understand the role of acid and DGER in esophageal mucosal injury, we summarized the recent publications in this area. METHODOLOGY: review of published medical literature (medline) on the clinical consequence of esophageal exposure to gastric acid or DGER. RESULTS: Recent data suggest that esophageal ph monitoring and pH > 7 is a poor marker for reflux of duodenal contents into the esophagus. DGER in non-acidic environments (i.e., partial gastrectomy patients) may cause symptoms but does not cause esophageal mucosal injury. Acid and duodenal contents usually reflux into the esophagus simultaneously, and may be contributing to the development of Barrett's metaplasia and possibly adenocarcinoma. proton pump inhibitors decrease acid and DGER by reducing intragastric volume available for reflux and raising intragastric pH. The promotility agent cisapride decreases DGER by increasing LES pressure and improving gastric emptying. CONCLUSIONS: 1) The term "alkaline reflux" is a misnormer and should no longer be used in referring to reflux of duodenal contents. 2) Bilitec is the method of choice in detecting DGER and should always be used simultaneously with esophageal pH-monitoring for acid reflux. 3) DGER alone is not injurious to esophageal mucosa, but can result in significant esophageal mucosal injury when combined with acid reflux. 4) Therefore, controlling esophageal exposure to acid reflux by using proton pump inhibitors also eliminates the potentially damaging effect of DGER.
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2/68. Clonal analysis of a case of multifocal oesophageal (Barrett's) adenocarcinoma by comparative genomic hybridization.

    Oesophageal adenocarcinomas arising in Barrett's epithelium occasionally present as multiple lesions. This could be due to either a multifocal presentation of the same tumour, or different neoplasms arising simultaneously in a dysplastic Barrett's oesophagus ('field cancerization'). This is a report of the genetic analysis of multiple neoplastic sites in a Barrett's oesophagus with an extensive area of dysplasia. In addition, the dysplastic Barrett's epithelium was evaluated. For the genetic screening, comparative genomic hybridization (CGH) allowed evaluation of the whole genome of each specimen. Five cancerous regions were selected and subsequently dissected from paraffin-embedded tissue blocks. The use of archival materials enabled a targeted collection of representative tumour locations. Multiple genetic aberrations were detected by CGH in all cancer sites. Losses on 3p, 4, 7q, 18q, and Y, as well as gains on 8q, 9q, 12p, 13q, 17q, 20p and X, were found in each specimen. In four out of the five lesions, simultaneous losses on 9p, 15q, and 16q, with concomitant gains on 5p, 7q, and 10p, were disclosed by CGH. Adjacent high-grade dysplastic Barrett's mucosa shared the losses on 3p, 4, 7q, 9p, 18, and Y, as well as the gains on 5p, 7q, 13q, 17q, and X, thereby confirming its precursor status. Within this single and rare case of multifocal Barrett's adenocarcinoma, a monoclonal genotype was present. This must have been caused by an extensive outgrowth of a single tumour.
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3/68. Recent advances in Barrett's esophagus: short-segment Barrett's esophagus and cardia intestinal metaplasia.

    The recent rapid increase in the incidence of adenocarcinoma of the distal esophagus and the gastric cardia has generated significant interest in the premalignant lesion, Barrett's esophagus. The traditional definition of Barrett's esophagus included the presence of 3 cm or greater of columnar mucosa in the distal esophagus. Studies have clarified that intestinal metaplasia was not only the most common and distinctive type of epithelium detected within the columnar mucosa, but also the one with greatest malignant potential; therefore, Barrett's esophagus has come to be defined by the histological presence of intestinal metaplasia. Previous studies evaluating the association of esophageal adenocarcinoma with Barrett's esophagus have only included patients with traditional or long-segment Barrett's esophagus. However, recent studies have suggested that dysplasia and adenocarcinoma can also be associated with short-segment Barrett's esophagus (SSBE), ie, less than 3 cm of columnar mucosa. Data are also emerging regarding the significance of intestinal metaplasia detected in biopsy specimens obtained immediately below the gastroesophageal junction, ie, from the gastric cardia. However, the premalignant potential of cardia intestinal metaplasia (CIM) is unknown at this time. Although the exact incidence of adenocarcinoma in SSBE is not known, endoscopic surveillance of such patients, although controversial, appears to be prudent at this time. With the currently available information, routine biopsy of a normal-appearing squamocolumnar junction is not advocated. This review critically evaluates and summarizes recent data on SSBE and CIM.
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4/68. Local treatment of early cancer in short Barrett's esophagus by means of argon plasma coagulation: initial experience.

    In recent years endoscopically controlled local therapeutic methods, such as photodynamic therapy, mucosectomy, or laser therapy, have been used with a curative aim for the destruction of early esophageal or gastric cancers. We report on our experience of treating histologically proven mucosal cancer in Barrett's esophagus with argon plasma coagulation (APC), in three patients. All the mucosal esophageal cancers, with a mean diameter of 4 mm, were successfully destroyed after one or two treatment sessions. Additionally, in two of the three patients the specialized columnar epithelium was replaced by normal squamous cell epithelium when APC treatment was combined with omeprazole. In the third patient with Barrett's esophagus, a partial squamous cell re-epithelialization was induced. No method-related mortality and morbidity were observed. During the mean follow-up of 24.3 /- 1.1 months (range 23-25 months) one tumor recurrence developed which was successfully treated with photodynamic therapy. In patients with small early Barrett's carcinoma APC might offer an effective, minimally invasive alternative to mucosectomy or photodynamic therapy, as the treatment procedure is less cumbersome and the equipment less expensive.
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5/68. Clinicopathological and immunohistochemical study of cancer arising from Barrett's esophagus.

    In japan, Barrett's esophageal cancer is a very rare disease. We examined clinicopathologically and immunohistologically 4 patients with Barrett's esophageal cancer who underwent surgical resection in our department. Barrett's esophageal mucosa was classified into 3 types for detailed observation. Specialized columnar epithelium (SCE) remained on the orifice side of carcinoma, and progression to adenocarcinoma was observed in some dysplastic glands. positive findings were detected on p53 immunohistochemical staining, and the ki-67 labeling index was higher than other types. SCE-type Barrett's esophagus may be a precancerous lesion arising prior to the development of adenocarcinoma.
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6/68. Intramucosal adenocarcinoma arising under squamous re-epithelialisation of Barrett's oesophagus.

    BACKGROUND: Eradication of Barrett's mucosa by thermal or photoablation combined with high doses of proton pump inhibitors is a potentially attractive strategy in the management of this preneoplastic condition. However, major concerns of this method are the persistence of residual metaplastic glands beneath the new squamous epithelium and the absence of any knowledge of its impact on long term outcome. CASE REPORT: The case of an intramucosal adenocarcinoma diagnosed 18 months after apparently complete squamous re-epithelialisation achieved using argon plasma coagulation and high dose omeprazole (40 mg/daily) is reported in a 68 year old patient presenting initially with a Barrett's oesophagus without dysplasia. Intramucosal adenocarcinoma was located under the new squamous layer and presented as a bulging area covered by the squamous epithelium. It probably originates from residual metaplastic glands after therapy although a pre-existing tumour cannot be definitely excluded. CONCLUSION: This observation might question future application of this experimental endotherapy in non-dysplastic Barrett's oesophagus. It suggests that the residual glands might still be premalignant and that the early diagnosis of neoplastic changes might be compromised by the squamous re-epithelialisation.
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7/68. Autofluorescence endoscopy: feasibility of detection of GI neoplasms unapparent to white light endoscopy with an evolving technology.

    BACKGROUND: Case studies are presented of fluorescence endoscopy in the upper and lower GI tract to illustrate the ability to detect early-stage lesions that were not observable with white light endoscopy or those in which the assessment of the stage or extension of the lesion were equivocal. methods: A new fluorescence imaging system was used in which blue light excites the naturally-occurring fluorescence of tissues (autofluorescence). The system produces real-time, false-color images that combine green and red fluorescence intensities. In general, abnormal lesions are seen to have an increase in the red-to-green fluorescence intensity compared with surrounding tissue. This system was evaluated in patients at 4 participating institutions, concurrently with standard white light endoscopy, with or without dye staining. RESULTS: Selected cases are presented in which fluorescence imaging identified specific lesions including focal high-grade dysplasia in Barrett's mucosa, signet ring carcinoma of the stomach, and flat adenoma in the colon. CONCLUSIONS: The capability of autofluorescence endoscopy to detect the presence and extent of occult malignant and premalignant GI lesions has been demonstrated. The future development and evaluation of this technology are discussed.
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8/68. adenocarcinoma complicating Barrett's esophagus: an analysis of cell proliferation.

    In japan, cases of Barrett's esophagus with concurrent adenocarcinoma are relatively rare. We report herein a case of long-segment Barrett's esophagus-associated adenocarcinoma in a 72-year-old Japanese man. The surgical specimen showed that an ulcerating tumor, measuring 5.5 x 3.9 cm, was present in the lower esophagus adjacent to the esophagogastric junction, the background lower esophagus having an erythematous appearance. Histologically, the ulcerating tumor was a well-to-moderately differentiated tubular adenocarcinoma, with a small area of signet ring cell carcinoma invading the adventitia. In addition, the esophageal epithelium was replaced by columnar epithelium (9.5 cm in length) with multifocal dysplastic changes. Immunohistochemically, the number of Ki-67-positive cells gradually increased, moving from the normal gastric mucosa (mean Ki-67 labeling index [mKLI], 2.6%) through Barrett's epithelium (mKLI, 12.9%), low-grade dysplasia (mKLI, 16.9%), and high-grade dysplasia (mKLI. 23.7%) to invasive carcinoma, in that order, with labeling higher in the invasive tubular adenocarcinoma elements (mKLI, 40.5%) than in areas of signet ring cell carcinoma (mKLI, 20.4%). Findings in our patient suggest that increased cellular proliferation plays an integral part, in the progression of Barrett's metaplasia to adenocarcinoma. The collection of further cases for analysis will be necessary to confirm this hypothesis.
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9/68. Barrett's adenocarcinoma of the esophagus with lymphoid stroma.

    We report a case of Barrett's adenocarcinoma of the esophagus with lymphoid stroma. We believe this is the first reported case of this entity, although six previous cases of esophageal lymphoepithelioma-like carcinoma have been reported. The esophageal tumor from a 58-year-old man was examined histologically. In situ hybridization to detect Epstein-Barr virus (EBV) was also performed. The tumor consisted of a poorly differentiated adenocarcinoma with dense lymphoid cell infiltration in the invasive portions and a well-differentiated adenocarcinoma without lymphoid stroma in the mucosa. Barrett's epithelium was observed adjacent to the carcinoma. No positive signals for EBV were detected in the tumor cells. Six previously reported patients with esophageal lymphoepithelioma-like carcinomas, and the current patient, all survived for longer than 24 months, a better outcome than that of patients with esophageal squamous cell carcinomas of usual type. The data suggest that this tumor arose as a mucosal, well-differentiated adenocarcinoma without lymphoid stroma and that EBV had no relation to either its pathogenesis or progression.
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10/68. p53 immunoreactivity in Barrett's metaplasia, dysplasia, and adenocarcinoma--a case report.

    Barrett's esophagus is a condition in which the stratified squamous epithelium of the esophagus is replaced by a columnar epithelium with malignant potential. Mutations of the tumor-suppressor gene p53 have been implicated in the evolution of esophageal carcinomas. The aim of this study was to determine whether p53 immunoreactivity in Barrett's esophagus is a marker of neoplasia and, if so, when it occurs in the metaplasia-dysplasia-carcinoma sequence. We treated a patient with esophageal carcinoma arising from the Barrett's esophagus. Consecutive evidence existed for a metaplasia-dysplasia-carcinoma in the same specimen. Immunohistochemical staining with the monoclonal antibody was used to detect the intranuclear protein product of mutated p53. No p53 immunoreactivity was seen in specimen of Barrett's mucosa. p53 immunoreactivity was found only in specimen of dysplasia and carcinoma. Immunoreactivity occurs late in the metaplasia-dysplasia-carcinoma sequence, during the transition to high-grade dysplasia.
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