11/189. Esophageal collision tumor (Large cell neuroendocrine carcinoma and papillary carcinoma) arising in a barrett esophagus. We report herein a unique case of an esophageal collision tumor composed of a papillary adenocarcinoma and a large cell neuroendocrine carcinoma arising in a barrett esophagus. hematoxylin-eosin and silver staining patterns, immunohistochemistry, and electron microscopy of the large cell neuroendocrine component are discussed. ( info) |
12/189. 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. ( info) |
13/189. Esophageal leiomyomatosis in a woman with a history of vulvar leiomyoma and Barrett's esophagus: a case report and review of the literature. BACKGROUND: The diagnosis and treatment of esophageal pathology remains a challenge despite advances in preoperative endoscopy, radiographic staging, and perioperative care. CASE REPORT: In this article, we present an interesting case of esophageal leiomyomatosis in a woman with a history of vulvar leiomyoma and Barrett's esophagus. This paper represents the first reported simultaneous occurrence of these three pathologic entities in the English literature. CONCLUSIONS: The clinical presentation and characteristic pathologic findings in patients with esophageal leiomyomatosis are reviewed. Diagnostic and therapeutic approaches to esophageal masses are discussed including the indications for esophageal resection. ( info) |
14/189. Perforation of Barrett's ulcer: a challenge in esophageal surgery. BACKGROUND: Barrett's ulcer, which develops within Barrett's esophagus, is frequently responsible for bleeding. Perforation is a rare complication constituting a great challenge for diagnosis and management. methods: Three personal cases and 31 published reports of perforated Barrett's ulcer were reviewed retrospectively. The site of perforation, clinical presentation, management, and outcome were assessed. RESULTS: The clinical presentation proved to be heterogeneous and was determined by the site of perforation: this was the pleural cavity (20% of cases), mediastinum (20%), left atrium (16.6%), tracheobronchial tract (13.3%), aorta (13.3%), pericardium (10%), or pulmonary vein (6.6%). Early esophagectomy and esophageal diversion-exclusion were the most frequent procedures, and overall mortality was 45%. CONCLUSIONS: The poor prognosis of perforated Barrett's ulcer should be improved by earlier diagnosis and adequate emergent operation. Although early esophagectomy constitutes the recommended procedure, esophageal diversion-exclusion, which allows control of both sepsis and bleeding, is also of interest. ( info) |
15/189. Barrett's esophagus in a child with de lange syndrome: report of one case. Barrett's esophagus, a premalignant condition, is recognized as stratified squamous epithelium of the esophagus substituted by columnar epithelium. The risk factors for development of Barrett's esophagus include frequent gastroesophageal reflux, esophageal stricture, male sex and mental retardation, but there is no report of Barrett's esophagus in children with de lange syndrome. We report a 7-year-old boy who was diagnosed as de lange syndrome shortly after birth and had gastroesophageal reflux since early infancy. Upper gastrointestinal endoscopic examination revealed a cauliflower-like mass and a pink-red velvety mass over the lower third of the esophagus. biopsy showed goblet cells metaplasia, confirming Barrett's esophagus. We suggest surveillance of Barrett's esophagus could be done ahead of schedule in children with long-standing gastroesophageal reflux or with de lange syndrome. ( info) |
16/189. Cytology of small-cell carcinoma arising in Barrett's esophagus. The cytologic and histologic features of a rare case of small-cell carcinoma arising in Barrett's esophagus are reported. The patient presented with progressive dysphagia and an endoscopy revealed a distal esophageal mass with luminal constriction. The brushing smears showed small-cell carcinoma and dysplastic glandular epithelium. The concomitant biopsy confirmed the diagnosis of small-cell carcinoma arising in Barrett's esophagus. ( info) |
17/189. 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. ( info) |
18/189. Frequent c-myc amplification in high-grade dysplasia and adenocarcinoma in barrett esophagus. barrett esophagus (BE) is a condition in which the normal squamous epithelium of the esophagus is replaced by a metaplastic columnar epithelium. BE is a premalignant lesion that represents the initial step in a metaplasia-dysplasia-carcinoma sequence. In the present study, amplification of the proto-oncogene c-myc was determined by means of differential polymerase chain reaction analysis of metaplastic specialized epithelium, low-grade dysplasia, high-grade dysplasia, and invasive adenocarcinoma obtained by microscopic dissection of 43 esophagectomy specimens. Amplification of c-myc was found in none of 29 specialized epithelial specimens, none of 23 low-grade dysplasia specimens, 6 of 24 high-grade dysplasia specimens, and 17 of 39 adenocarcinoma specimens. Our data indicate that amplification of c-myc is a late event in the metaplasia-dysplasia-carcinoma sequence in BE. Furthermore, determination of c-myc amplification may help identify high-risk patients who would benefit from intensified endoscopic surveillance or from immediate treatment. ( info) |
19/189. Pathological documentation of complete elimination of Barrett's metaplasia following endoscopic multipolar electrocoagulation therapy. The previous paradigm that Barrett's is an irreversible premalignant lesion has recently been challenged by a proliferation of reports documenting elimination of Barrett's by a variety of endoscopic techniques. Whether Barrett's is entirely eliminated is unknown as endoscopic biopsy samples the surface of the epithelium only. Numerous reports document underlying specialised columnar epithelium in many of these trials. Until now there have been no reports of pathological examination of the entire oesophagus as a specimen. This case documents complete elimination of intestinal metaplasia from the oesophagus and supports the biological plausibility of these research techniques. ( info) |
| 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. ( info) |