Cases reported "Precancerous Conditions"

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1/21. Rapid progression to high-grade dysplasia in Barrett's esophagus after liver transplantation.

    There is an increased incidence of malignancies in transplant recipients. Accelerated progression from a premalignant lesion to carcinoma has been reported in transplant recipients with skin cancer and colon cancer. Whereas Barrett's esophagus is a common premalignant condition in the normal population, rapid progression to severe dysplasia or carcinoma has not been widely reported in transplant recipients. We report on a liver transplant recipient who developed rapid progression from Barrett's esophagus without dysplasia to high-grade dysplasia within 9 months after transplantation.
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2/21. 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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3/21. Heterotopic pancreas of the esophagus masquerading as Boerhaave's syndrome.

    Heterotopic pancreas (HP) of the esophagus is rare. We report a patient with HP of the esophagus and review the presentation, treatment, and results of the nine previously reported cases. Two patients had cancer. This high incidence raises concerns that HP of the esophagus may be premalignant. Because surveillance endoscopy is not possible, all known or suspected esophageal HP should be treated surgically.
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4/21. Total esophageal reconstruction using a tubed parascapular free flap.

    A method for total esophageal reconstruction when intestinal options are no longer available is presented. The technique described utilizes the parascapular microsurgical free flap, which is tubed and interposed between the cervical esophagus and the gastric remnant in the abdomen. The technique involves a well-recognized microsurgical flap and may be added to the armamentarium for total esophageal reconstruction.
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5/21. Columnar-lined lower esophagus: an acquired lesion with malignant predisposition. Report on 140 cases of Barrett's esophagus with 12 adenocarcinomas.

    The analysis of a series of 1,225 cases of reflux esophagitis shows the serious nature of this condition. A liberal use of antireflux operations therefore seems justified. Extensive columnar metaplasia of the distal esophagus, or columnar-lined lower esophagus (CLLE), represents a late irreversible stage of reflux esophagitis. Repeated esophagoscopies demonstrate the acquired nature of the lesion. It is caused by the progressive healing, from below upward, of peptic ulcerations on the squamous epithelium by metaplasia of columnar mucosa. Antireflux operations stop the progressive ascent of heterotopic epithelium and thus stabilize reflux esophagitis and cure complications such as ulcerations and strictures. The premalignant character of this condition is established by a 10 per cent incidence of adenocarcinomas in a series of 140 cases of extensive columnar metaplasia. The transition toward malignancy seems to be irreversible and cannot be arrested by an antireflux operation. Therefore, repeated esophagoscopic controls and biopsies are an absolute necessity in all cases of extensive columnar metaplasia, even after cure of active reflux esophagitis by Nissen fundoplication.
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6/21. Laparoscopic transgastric esophageal mucosal resection for high-grade dysplasia.

    BACKGROUND: High-grade dysplasia of the esophageal mucosa has been shown to be a precursor to adenocarcinoma. In addition to esophagectomy, multiple ablative endoscopic techniques have evolved for the management of this condition. As a surgical alternative to esophagectomy, we describe for the first time a new option in the treatment of high-grade dysplasia. MATERIALS AND methods: Two patients with a history of gastroesophageal reflux disease (GERD) underwent upper gastrointestinal endoscopy which demonstrated high-grade dysplasia of the distal esophagus. The first patient had a short segment (0.5-1.0 cm), and the second patient had a longer (2 cm) segment of dysplasia. The patient is placed in the modified lithotomy position. Five trocars are placed as if to perform a fundoplication. A complete circumferential mobilization of the esophagus is performed. The short gastric vessels are divided with the harmonic scalpel, to free up the fundus of the stomach. An anterior horizontal gastrotomy is performed three to four centimeters below the gastroesophageal junction. A solution of epinephrine and normal saline (1:100,000) is injected into the mucosa at the Z-line and, utilizing specially designed hook electrocautery, the mucosa is incised circumferentially around a lighted bougie. Using blunt dissection the mucosa is undermined, elevated, and excised in four quadrants. Three centimeters of the distal esophageal mucosa are resected. The gastrotomy is then closed using a linear stapler, and a 360 degrees fundoplication is performed around a 50 Fr bougie. RESULTS: High-grade dysplasia was identified in the specimens from both patients; however, neither patient was found to have carcinoma in situ or invasive esophageal cancer. Our first patient has been followed for twenty months, the second for ten months. Both patients underwent routine upper gastrointestinal endoscopy for surveillance of the healing process. At eight months, the mucosa of the first patient showed complete regeneration of squamous epithelium. Our most recent patient appears to be progressing without complications and has also demonstrated normal squamous epithelium at ten months postoperatively, without changes of Barrett's epithelium. CONCLUSION: The technique of laparoscopic transgastric esophageal mucosal resection is feasible and may be proven to be an alternative to esophagectomy for the management of high-grade dysplasia.
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7/21. A "crackleware" oesophagus.

    This case report describes a 70 year old woman with excessive diffuse keratinisation of the oral cavity and oesophagus harbouring a squamous cell carcinoma. This excessive diffuse keratinisation of normally non-keratinised squamous epithelium could not be identified in normally non-keratinised epithelia in other parts of the body (the vagina), arguing against a genetic basis for this disorder. The term "crackleware" oesophagus was used to describe this entity, which has not been described previously in the English literature.
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8/21. Management of Barrett's esophagus: cases and questions.

    gastroesophageal reflux disease and Barrett's esophagus (BE) are associated with increased risk of esophageal adenocarcinoma. However, the majority of patients with adenocarcinoma have no gastroesophageal reflux disease symptoms, and few patients with adenocarcinoma have BE at the time of cancer diagnosis. Furthermore, the annual incidence of cancer in individuals with BE appears to be low. The utility of screening for BE in gastroesophageal reflux disease patients and of routine endoscopic monitoring in BE patients remain unclear. More prospective data on disease progression and an improved knowledge of risk factors are needed to help define optimal management strategies.
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9/21. Corrosive induced carcinoma of esophagus: report of three patients and review of literature.

    patients with corrosive induced esophageal strictures have more than a 1000-fold risk of developing carcinoma of the esophagus. We report three cases of corrosion carcinoma seen by us (a team of gastroenterologists, radiologists and a surgeon) in the last 15 years. Two cases were among 156 patients with corrosive induced strictures on our follow-up, and constituted the only corrosion carcinoma out of 650 esophageal carcinomas operated on by us. Nearly all reported patients with corrosion carcinoma in the published literature had consumed an alkali, but two of our three patients had consumed an acid.
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10/21. Barrett's esophagus with high-grade dysplasia simulating metastatic adenocarcinoma in a fine needle aspiration biopsy.

    An endoscopic ultrasound examination, performed to rule out invasive esophageal carcinoma in a patient with a history of Barrett's esophagus with high-grade dysplasia, disclosed an enlarged paraesophageal lymph node which was aspirated. The aspirate contained markedly atypical clustered large cells that displayed prominent nucleoli and mitoses, as well as lymphoid cells, suggestive of adenocarcinoma metastatic to a lymph node. The neoplastic-appearing cells were, in fact, dysplastic glandular cells that the needle traversed en route to a reactive lymph node. The case represents a rare instance in which Barrett's esophagus with high-grade dysplasia was discerned on fine needle aspiration (FNA) biopsy and highlights a potential pitfall in FNA.
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