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Lower Oesophagus (lower + oesophagus)
Selected AbstractsBarrett's oesophagus,a pathologist's viewHISTOPATHOLOGY, Issue 1 2007J-F Fléjou Barrett's oesophagus, a precancerous condition for oesophageal adenocarcinoma, detected on endoscopy and confirmed on histology, shows intestinal metaplasia of the lower oesophagus. The significance of microscopic foci of intestinal metaplasia at the gastro,oesophageal junction, corresponding either to so-called ,ultrashort' segment Barrett's oesophagus, or to carditis with intestinal metaplasia, is still a matter of debate. The surveillance of patients with Barrett's oesophagus is still based on systematic biopsy sampling of Barrett's mucosa on endoscopy, looking for dysplasia. Although well-established classifications of dysplasia are now used by most pathologists, there remain numerous problems with this subjective marker (sampling, diagnostic reproducibility, natural history, etc). Therefore, many alternative biomarkers have been proposed, but only DNA aneuploidy, proliferation markers and p53 loss of heterozygosity/overexpression have been shown to be of some use at the present time. Some endoscopic improvements already allow a better selection of biopsies, and it may be that in future new technologies will allow ,virtual biopsies'. On the other hand, the role of pathologists now extends to the evaluation of new therapeutic modalities of early neoplastic lesions in Barrett's oesophagus, especially endoscopic mucosal resection. [source] Megaoesophagus in Rassf1a -null miceINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 2 2009Louise Van Der Weyden Summary Megaoesophagus, or oesophageal achalasia, is a neuromuscular disorder characterized by an absence of peristalsis and flaccid dilatation of the oesophagus, resulting in the retention of ingesta in the dilated segment. The aetiology and pathogenesis of idiopathic (or primary) megaoesophagus are still poorly understood and very little is known about the genetic causes of megaoesophagus in humans. Attempts to develop animal models of this condition have been largely unsuccessful and although the ICRC/HiCri strain of mice spontaneously develop megaoesophagus, the underlying genetic cause remains unknown. In this report, we show that aged Rassf1a -null mice have an enhanced susceptibility to megaoesophagus compared with wild-type littermates (,20%vs. ,2% incidence respectively; P = 0.01). Histological examination of the dilated oesophaguses shows a reduction in the numbers of nerve cells (both ganglia and nerve fibres) in the myenteric plexus of the dilated mid and lower oesophagus that was confirmed by S100 immunohistochemistry. There was also a chronic inflammatory infiltrate and subsequent fibrosis of the myenteric plexus and the muscle layers. These appearances closely mimic the gross and histopathological findings in human cases of megaoesophagus/achalasia, thus demonstrating that this is a representative mouse model of the disease. Thus, we have identified a genetic cause of the development of megaoesophagus/achalasia that could be screened for in patients, and may eventually facilitate the development of therapies that could prevent further progression of the disease once it is diagnosed at an early stage. [source] Fatal pneumoperitoneum caused by nasopharyngeal oxygen delivery after transoesophageal echocardiography for cardiac surgeryACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2009G. MOURISSOUX We report a case of fatal post-operative pneumoperitoneum in a patient who had undergone urgent mitral valve surgery. In the absence of a proven cause of the pneumoperitoneum (refusal by the family of an autopsy), we can only propose a hypothesis for its origin. The most probable one is that forceful or sustained retrograde flexion of the transoesophageal echocardiographic probe created a lower oesophagus or gastric rupture and that oxygen flow administered by the nasal cannula went straight to the abdominal cavity, leading to tension pneumoperitoneum. [source] Modulation of salivation and heartburn in response to the site of acid infusion in the human oesophagusALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2010S. K. Dutta Summary Background, The pathogenesis of gastro-oesophageal reflux disease includes increased acid reflux, reduced salivation and impaired peristalsis. This may depend upon the height of acid wave and magnitude of oesophageal mucosal exposure. Interestingly, the effect of site of acid infusion upon salivary secretion and heartburn has not been examined in any detail. Aim, To examine whether acid infusion in the upper oesophagus may cause increased salivation and heartburn as compared with acid infusion in the lower oesophagus. Methods, Twelve healthy male subjects (mean age 30) received infusions of HCl, citric acid and acetic acid at 10 and 20 cm above the lower oesophageal sphincter (LES) for fixed time periods. Parotid saliva collected periodically and heartburn severity scored using standardized scale. Standard statistical methods (paired t -tests, analysis of variance) were used to determine the significance of results. Results, Acid infusion in the upper oesophagus increased parotid flow rate as compared with that in the lower oesophagus (P < 0.05). Likewise, there was a significantly increased heartburn score at 20 cm as well as 10 cm above LES (P < 0.05) as compared with that in the stomach. Conclusion, These data suggest a significant increase in salivation and heartburn in response to acid infusion in the upper vs. lower part of the oesophagus. [source] Lobar torsion following thoraco-abdominal oesophagogastrectomyANAESTHESIA, Issue 10 2009V. Felmine Summary Following thoraco-abdominal oesophagogastrectomy for an adenocarcinoma of the lower oesophagus, an 81-year-old female with no pre-existing respiratory disease could not be weaned from mechanical ventilation. Right upper and middle lobe torsion were found at thoracotomy on the 14th postoperative day. Both lobes were resected. The patient was discharged from hospital after several postoperative complications. Pulmonary torsion is a rare, potentially life-threatening complication of thoraco-abdominal oesophagogastrectomy. Differentiation from the more common postoesophagectomy pulmonary complications can be difficult. Early post-thoracotomy lung opacification, in the absence of the expected degree of hypoxaemia, should trigger a suspicion of pulmonary torsion. [source] New classification of oesophageal and gastric carcinomasBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 3 2001K. Dolan Background: The current International Classification of Diseases (ICD)-O classification of carcinomas of the oesophagus and stomach causes epidemiological and clinical confusion, particularly the use of the term cardia and the overlapping subsites described in the stomach. This study compared the epidemiological and clinical features of each subtype and subsite of carcinoma of the oesophagus and stomach to assess requirements for a new classification of these carcinomas. Methods: Data were extracted with appropriate validity checks on all cases of oesophageal and gastric carcinoma identified throughout the period 1974,1993 by the Merseyside and Cheshire Cancer Registry, which covers a population of 2·5 million. Comparison of all identifiable epidemiological and clinical features of adenocarcinomas at four different subsites, namely the upper two-thirds of the oesophagus, the lower third of the oesophagus, cardia and subcardia of the stomach, was performed. Results: There were 5322 primary carcinomas of the oesophagus and 10 535 carcinomas of the stomach registered between 1974 and 1993. The incidence of adenocarcinoma of the lower oesophagus and cardia trebled in males and doubled in females, whereas adenocarcinoma of the subcardia region of the stomach declined in both sexes. The incidence of adenocarcinoma of the lower oesophagus and of the cardia was similar for median age at diagnosis, male: female ratio, percentage of patients who smoked, and survival; both were significantly different from values for carcinoma of the subcardia in these respects. Conclusion: These data suggest that there is considerable overlap between adenocarcinomas of the lower oesophagus and adenocarcinomas currently classified as of the cardia. The authors believe this is due to the group of carcinomas classified as cardia consisting mainly of carcinomas that traverse the gastro-oesophageal junction. These carcinomas were different in all studied parameters from carcinomas of the stomach and should be classified separately from gastric carcinomas. A new subsite classification of oesophageal and gastric carcinomas is proposed that includes the gastro-oesophageal junction as a subsite of the oesophagus and that simplifies the subsite classification of the stomach into proximal, distal and overlapping. © 2001 British Journal of Surgery Society Ltd [source] Barrett's esophagus and Cornelia de Lange SyndromeACTA PAEDIATRICA, Issue 9 2010Francesco Macchini Abstract Aim:, To review the records of Cornelia de Lange Syndrome (CDLS) children, affected by Gastro-oesophageal reflux disease (GERD), to detect the presence of Barrett's Esophagus (BE). Methods:, A total of 62 CDLS patients were investigated for GERD (1 month,35 years). In all of them a pH-metry, an upper endoscopy with multiple biopsies and a complete radiologic digestive evaluation were carried out. BE was diagnosed in case of replacement of oesophageal mucosa by specialized intestinal-type columnar mucosa. Anti-reflux surgery was considered in case of persistence of BE after medical therapy. Follow-up (mean 3.5 years) consisted in endoscopy every 6 months . Results:, Gastro-oesophageal reflux disease was found in 50 CDLS patients (80%) and BE in six of them (12% of the GERD group, 9.6% of the entire population, mean age 17 years, range 6,32 years). A short segment BE was observed in three patients, a long one in two patients and an infiltrating adenocarcinoma of the lower oesophagus in one patient. Conclusions:, A higher frequency of BE in CDLS patients than in a normal population is found. A delayed diagnosis because of atypical GERD symptoms and an altered intestinal motility as a result of neurological impairment can be recognized as the main cause. [source] | ||||||||||