continues to be said that medicine is an art that must

continues to be said that medicine is an art that must be practiced before it is completely understood. and short-segment Barrett’s esophagus and includes 101 patients enrolled over 18 years (1982-2000). Barrett’s esophagus is an acquired abnormality occurring in 10% to 15% of patients with gastroesophageal reflux disease. It is defined by the presence of an endoscopic segment of columnar-lined esophagus that has intestinal metaplasia (goblet cells) on biopsy. For reasons that are not entirely clear its prevalence has exploded in the past 25 years increasing from an average of 1/1 0 upper endoscopies in the early 1980s to 10/1 0 in late 1980s and over 55 to 60/1 0 in the late 1990s. 2 3 Patients with Barrett’s esophagus are characterized by long-standing severe reflux symptoms often beginning at a relatively young age 4 and accompanied by severe anatomic and physiologic defects including high esophageal acid A 922500 exposure large hiatal hernias 5 and virtually absent lower esophageal sphincter and often poor esophageal body contractility. 6 Esophagitis stricture and ulceration commonly accompany the Barrett’s segment. There are two treatment options in patients with Barrett’s esophagus (lifelong proton pump inhibitors [PPIs] and antireflux surgery) with success reflected by two distinct outcomes: the clinical control of reflux and the prevention of esophageal adenocarcinoma. Although most gastroenterologists and surgeons believe they know how to treat Barrett’s esophagus there are surprisingly few data A 922500 to indicate the optimal treatment. 7 When evaluating studies of Barrett’s esophagus experience has shown that the details are important. In the Parrilla study medical therapy consisted of 20 mg omeprazole (PPI) twice daily since 1992 in all medically treated patients. Surgical therapy consisted of an open 1.5- to 3.0-cm Nissen over a 48 to 50 French bougie with short gastric division in 39% of patients and crural closure in all. On the surface outcome in the two groups was nearly identical although esophagitis and/or stricture persisted in 20% of the medically treated patients compared to only 3% to 7% of those following antireflux surgery. Fifteen percent of patients had abnormal acid exposure after surgery emphasizing the importance of reporting both mean/median and prevalence data. This is consistent with two other recent reports A 922500 of the long-term outcome of antireflux Agt surgery in patients with Barrett’s esophagus in which approximately 20% of patients continued to reflux despite antireflux surgery. 8 9 It is unfortunate that pH data were not routinely collected in patients on PPI therapy. In the subgroup of 12 patients who did have 24-hour monitoring on treatment 3 of 12 (25%) had persistently high esophageal acid exposure and most (75%) had persistently high bilirubin exposure. Perhaps most importantly the paper addresses one of the main unanswered queries in the pathophysiology of esophageal adenocarcinoma: Will antireflux treatment alter the organic background of Barrett’s esophagus? Considering that gastroesophageal reflux definitely causes Barrett’s esophagus the chance that halting reflux will prevent development or even result in regression can be an essential question that must definitely be answered. Even though the advancement of dysplasia and adenocarcinoma was no different general the subgroup of operative patients with regular postoperative pH research developed considerably less dysplasia and got no adenocarcinoma. This observation ought never to be ignored. Furthermore both operative patients who created cancer were proven to possess recurrent reflux. The info strongly support the idea that eradication of reflux may certainly prevent development of neoplasia and will go a step beyond most by including data in the efficiency of antireflux medical procedures. In this respect it is a noticable difference within the Spechler et al. paper to which it could be likened. 10 One miracles if Norman Barrett 11 got any insight in to the quagmire he was unleashing along with his preliminary description from the esophageal condition that bears his name. Dilemma encircling the columnar-lined esophagus started with Barrett himself (he thought it to be always a congenitally brief esophagus) 12 and is continuing to grow greater and even more medically relevant with each transferring decade. As we have now stand some 50 years afterwards virtually every element of the condition we make reference to as Barrett’s esophagus is certainly controversial and sometimes debated. 13 This consists of its description 14 pathophysiology 15 prevalence 16 significance 17 and treatment 18 A 922500 up to and.