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Specialized Intestinal Metaplasia (specialized + intestinal_metaplasia)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Specialized intestinal metaplasia in patients with gastro-oesophageal reflux disease

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 1 2000
E. 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]

Biologic and clinical variations of adenocarcinoma at the esophago,gastric junction: Relevance of a topographic-anatomic subclassification,

JOURNAL OF SURGICAL ONCOLOGY, Issue 3 2005
J. Rüdiger Siewert
Abstract A topographic-anatomic subclassification of adenocarcinomas of the esophago,gastric junction (AEG) in distal esophageal adenocarcinoma (AEG Type I), true carcinoma of the cardia (AEG Type II), and subcardial gastric cancer (AEG Type III) was introduced in 1987 and is now increasingly accepted and used worldwide. Our experience with now more than 1,300 resected AEG tumors indicates that the subtypes differ markedly in terms of surgical epidemiology, histogenesis and histomorphologic tumor characteristics. While underlying specialized intestinal metaplasia can be found in basically all patients with AEG Type I tumors, this is uncommon in Type II tumors and virtually absent in Type III tumors. Stage distribution and overall long-term survival after surgical resection also shows marked differences between the AEG subtypes. Surgical treatment strategies based on tumor type allow a differentiated approach and result in survival rates superior to those reported with other approaches. The subclassification of AEG tumors thus provides a useful tool for the selection of the surgical procedure and allows a better comparison of treatment results. J. Surg. Oncol. 2005;90:139,146. © 2005 Wiley-Liss, Inc. [source]

Barrett's oesophagus, dysplasia and pharmacologic acid suppression

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2001
R. C. Fitzgerald
Barrett's oesophagus, a significant complication of gastro-oesophageal reflux disease (GERD), is the single most important risk factor for oesophageal adenocarcinoma. The strong association between Barrett's oesophagus and chronic GERD suggests that abnormal oesophageal acid exposure plays an important role in this condition. The progression of Barrett's oesophagus from specialized intestinal metaplasia to dysplasia and finally invasive carcinoma is incompletely understood, but increased and disordered proliferation is a key cellular event. In ex vivo organ culture experiments, cell proliferation is increased after exposure to short pulses of acid, whilst proliferation is reduced in Barrett's oesophagus specimens taken from patients with oesophageal acid exposure normalized by antisecretory therapy. In long-term clinical studies, consistent and profound intra-oesophageal acid suppression with proton pump inhibitors decreases cell proliferation and increases differentiation in Barrett's oesophagus, but the clinical importance of such favourable effects on these surrogate markers is not clear. In clinical practice, proton pump inhibitors relieve symptoms and induce partial regression to squamous epithelium, but abnormal oesophageal acid exposure and the risk for dysplasia or adenocarcinoma persist in many patients. The ability of proton pump inhibitors to suppress acid profoundly and consistently may be critical in the long-term management of Barrett's oesophagus. [source]