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Review article: the nature of oesophageal injury in gastro-oesophageal reflux disease De Hertogh G; Ectors N; Van Eyken P; Geboes KAliment Pharmacol Ther 2006[Sep]; 24 Suppl 2 (ä): 17-26The purpose of this review was to explore issues relating to the nature of oesophageal injury in gastro-oesophageal reflux disease. Several structural and functional elements of the oesophageal epithelium provide for an inherent resistance against refluxed material. It is only when this defence is overcome that reflux-induced damage ensues. The light microscopic changes in reflux oesophagitis are manifold. Early changes are confined to the epithelium and consist of reactive changes and inflammatory cell infiltration. When the epithelial integrity can no longer be maintained, erosions and ulcers develop. Recently, dilatation of the intercellular spaces was described as a sensitive early marker for gastro-oesophageal reflux disease. This parameter was first identified by electron microscopy but can also be assessed by light microscopy in routinely stained tissue sections. Some of the changes occurring in early gastro-oesophageal reflux disease can be reproduced by incubating oesophageal mucosal biopsies in gastrointestinal fluids or their components. Activated pepsin, trypsin and conjugated bile acids at an acidic pH have been identified as probable causes of reflux-induced damage.|Bile/metabolism[MESH]|Biomarkers[MESH]|Eosinophils/pathology[MESH]|Epithelium/pathology[MESH]|Esophagitis, Peptic/pathology[MESH]|Esophagoscopy[MESH]|Esophagus/*injuries/metabolism/pathology[MESH]|Gastroesophageal Reflux/*complications/metabolism/pathology[MESH]|Humans[MESH]|Hyperplasia[MESH]|Lymphocytes/pathology[MESH]|Neutrophils/pathology[MESH]|Pepsin A/metabolism[MESH] |
