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Squamocolumnar Junction (squamocolumnar + junction)
Selected AbstractsLower esophageal palisade vessels and the definition of Barrett's esophagusDISEASES OF THE ESOPHAGUS, Issue 7 2008K. Ogiya SUMMARY., The designated area of the columnar-lined esophagus (CLE) is anatomically defined by the distal limit of the lower esophageal palisade vessels (LEPV) and the term ,Barrett's esophagus' is equally used along with the name CLE in Japan. The aim of this study was to investigate the actual prevalence of CLE based on the Japanese criteria and to evaluate the criteria per se. A total of 42 esophagi consecutively resected at this institute were included. All subjects underwent a surgical resection for squamous cell carcinoma of the esophagus. The position of the LEPV, squamocolumnar junction, the prevalence of CLE and intestinal metaplasia were investigated both pre- and postoperatively. Preoperative endoscopy revealed CLE based on the Japanese criteria in half of all patients. In the resected specimens the distal limit of LEPV was lower than the squamocolumnar junction in 95.2%. In other words, almost all cases had CLE (equivalent to Barrett's mucosa in Japanese criteria). However, most of the CLE areas were very short and their average maximum length was only about 5 mm. In addition, no intestinal metaplasia was observed in any of the CLE cases. Almost all individuals might therefore be diagnosed to have CLE or Barrett's mucosa based on precise endoscopic observations in Japan. The CLE located in a small area, e.g. less than 5 mm, defined according to the LEPV criteria without any other factor concerning typical Barrett's esophagus such as signs of gastroesophageal reflux should therefore be excluded from consideration as a high-risk mucosa. [source] In GERD patients, mucosal repair associated genes are upregulated in non-inflamed oesophageal epitheliumJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 5 2009D. R. De Vries Abstract Previous studies addressing the effects of acid reflux and PPI therapy on gene expression in oesophageal epithelium concentrated on inflamed tissue. We aimed to determine changes in gene expression in non-inflamed oesophageal epithelium of GERD patients. Therefore, we included 20 GERD patients with pathological total 24-hr acid exposure of 6,12% and SAP , 95%. Ten patients discontinued PPI treatment (PPI-), 10 took pantoprazole 40 mg bid (PPI+). Ten age/sex-matched healthy controls were recruited. Biopsies were taken from non-inflamed mucosa 6 cm and 16 cm proximal to the squamocolumnar junction (SCJ). Gene expression profiling of biopsies from 6 cm was performed on Human Genome U133 Plus 2.0 arrays (Affymetrix). Genes exhibiting a fold change >1.4 (t-test P -value < 1E, 4) were considered differentially expressed. Results were confirmed by real-time RT-PCR. In PPI- patients, 92 microarray probesets were deregulated. The majority of the corresponding genes were associated with cell,cell contacts, cytoskeletal reorganization and cellular motility, suggesting facilitation of a migratory phenotype. Genes encoding proteins with anti-apoptotic or anti-proliferative functions or stress-protective functions were also deregulated. No probesets were deregulated in PPI+ patients. QPCR analysis of 20 selected genes confirmed most of the deregulations in PPI- patients, and showed several deregulated genes in PPI+ patients as well. In the biopsies taken at 16 cm QPCR revealed no deregulations of the selected genes. We conclude that upon acid exposure, oesophageal epithelial cells activate a process globally known as epithelial restitution: up-regulation of anti-apoptotic, anti-oxidant and migration associated genes. Possibly this process helps maintaining barrier function. [source] An electron microscopic study,Correlation of gastroesophageal reflux disease and laryngopharyngeal reflux,THE LARYNGOSCOPE, Issue 7 2010Sanghoon Park MD Abstract Objectives/Hypothesis: Laryngopharyngeal reflux (LPR) originates from regurgitation of gastric contents, a mechanism seemingly identical to gastroesophageal reflux disease (GERD). Some researchers postulate a connection between LPR and GERD, whereas some assert LPR is a disease apart from GERD. We examined symptoms of GERD from LPR patients, and performed gastrointestinal endoscopy and transmission electron microscopy (TEM) to evaluate GERD findings from these patients. Study Design: Prospective study at an academic tertiary care center. Methods: Control subjects had no symptoms or signs of LPR/GERD. LPR was diagnosed with a Reflux Symptom Index >13 and Reflux Finding Score >7, and were questioned for GERD-related symptoms and examined with esophagogastroduodenoscopy, then allocated into either an LPR without GERD or LPR with GERD group. Esophageal tissues were obtained from the squamocolumnar junction and managed for TEM, and the intercellular space (IS) was measured to find dilatation, a characteristic GERD finding. Results: About 30% (8/26) of LPR patients showed GERD-related symptoms, connecting LPR with the GERD group. Most of the LPR patients showed grossly normal endoscopic findings. On TEM, IS of control group (n = 15) was measured as 0.35 ± 0.27 ,m, whereas the LPR without GERD group (n = 18) and LPR with GERD group (n = 8) revealed a dilated IS of 0.61 ± 0.47 ,m and 0.95 ± 0.44 ,m, respectively. This difference was statistically significant compared to the control group (P < .05). Conclusions: The mean IS of LPR was significantly increased, suggesting common pathogenesis between LPR and GERD. Laryngoscope, 2010 [source] Specialized intestinal metaplasia in patients with gastro-oesophageal reflux diseaseBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 1 2000E. Carton Background: There is an increasing awareness that short (less than 3 cm) segments of Barrett's epithelium and macroscopically normal cardia epithelium may harbour specialized intestinal metaplasia (SIM), a premalignant phenotype. The prevalence of SIM was studied prospectively in an unselected population of patients attending for endoscopy, and the association of SIM with symptoms, lifestyle, medication, endoscopic oesophagitis and carditis was investigated. Methods: Two hundred consecutive patients underwent endoscopy. Biopsies taken from just below the squamocolumnar junction were stained for SIM, and were analysed for carditis and Helicobacter pylori infection. A detailed questionnaire of symptoms, tobacco consumption and the use of proton pump inhibitors was completed. Results: Forty-two patients (21 per cent) had SIM: 19 (15 per cent) of 126 in an endoscopically normal oesophagus, 15 (24 per cent) of 63 in a short segment of Barrett's epithelium and eight of 11 in classical Barrett's oesophagus. There was a significant association between SIM and carditis (P < 0·0001) and endoscopic oesophagitis (P = 0·03). Conclusion: SIM is prevalent in patients undergoing endoscopy, does not correlate with symptoms or H. pylori infection, but is significantly associated with endoscopic and pathological markers of gastro-oesophageal reflux. © 2000 British Journal of Surgery Society Ltd [source] | ||||||||||