Barrett’s esophagus following treatment of achalasia with botulinum toxin英文文献资料.docVIP

Open Journal of Gastroenterology, 2012, 2, 168-171 OJGas /10.4236/ojgas.2012.24032 Published Online November 2012 (http://www.SciRP.org/journal/ojgas/) Barrett’s esophagus following treatment of achalasia with botulinum toxin Christopher D. Wells , Susanne Carpenter , Kevin L. Huguet , Daniel J. Krochmal , 1 2 2 2 2* David E. Fleischer 1 , Kristi L. Harold 1 2 Division of Gastroenterology, Mayo Clinic, Rochester, USA Department of Surgery, Mayo Clinic, Rochester, USA Email: harold.kristi@ * Received 21 July 2012; revised 22 August 2012; accepted 30 August 2012 ABSTRACT thirds of the esophagus and incomplete relaxation of the LES [2]. Pathologically, there is a marked decrease or even absence of myenteric ganglion cells in the eso- phageal body as well as collagen replacement of myen- teric nerves [3]. Similar findings are noted at the LES. Excitatory neurons (predominantly cholinergic) are un- affected while inhibitory neurons are dramatically re- duced in number [4]. Barrett’s esophagus (BE) is characterized by the re- placement of the normal squamous epithelium in the distal esophagus by columnar epithelium which demon- strates specialized intestinal metaplasia. This condition seems to occur most often as a consequence of gastroe- sophageal reflux disease (GERD). Repeated acid expo- sure leads to a chronic inflammatory state prompted by cycles of mucosal injury and healing which ultimately initiates a metaplastic process whereby columnar cells replace squamous cells [5]. This epithelium is character- ized by mucin-containing goblet cells, and it is only with these pathologic changes that a diagnosis of BE can be made. BE is a concerning finding given the risk of pro- gression to dysplasia and adenocarcinoma [6]. Acha