Dept. of Gastroenterology and Hepatology, NC22, Cleveland Clinic Foundation; 9500 Euclid Ave., Cleveland, OH, 44195.
Am J Physiol Gastrointest Liver Physiol. 2010 May;298(5):G571-81. doi: 10.1152/ajpgi.00454.2009. Epub 2010 Mar 18.
Gastroesophageal reflux disease (GERD) is one of the most common problems in clinical practice today. It is widely believed that functional and structural abnormalities of the gastroesophageal junction as well as an abnormal exposure to gastroduodenal contents are the main contributors to its pathogenesis. Novel findings of the inflammatory process in GERD suggest a far more complex process involving multifaceted inflammatory mechanisms. This review summarizes knowledge about the expression of inflammatory mediators in GERD and their potential cellular sources and provides an integrated concept of disease pathogenesis. In addition we evaluate the contribution of inflammatory mediators to well-known complications of GERD, namely motility abnormalities, fibrosis, and carcinogenesis. Novel findings regarding the pathophysiology of esophageal inflammation should enhance our understanding of GERD and its complications and provide new treatment insights.
胃食管反流病（GERD）是当今临床实践中最常见的问题之一。人们普遍认为，胃食管交界处的功能和结构异常以及胃十二指肠内容物的异常暴露是其发病机制的主要原因。GERD 中炎症过程的新发现表明，涉及多方面炎症机制的过程要复杂得多。这篇综述总结了 GERD 中炎症介质的表达及其潜在的细胞来源，并提供了疾病发病机制的综合概念。此外，我们评估了炎症介质对 GERD 的众所周知的并发症，即运动异常、纤维化和癌变的贡献。有关食管炎症病理生理学的新发现应增强我们对 GERD 及其并发症的理解，并提供新的治疗见解。
