Lenglinger et al

Reply: I appreciate the important opinion of Professor Riegler and co-workers concerning the adequate biopsy sampling for exclusion of columnar-lined esophagus in the obese. They correctly say that the “best” site for biopsy sampling in order to detect intestinal metaplasia in a short-segment of columnar-lined esophagus is at the squamo-columnar junction or just distal to it, and I agree completely with them. I have been interested in the early detection or cardiac intestinal metaplasia (CIM) and short-segment Barrett’s esophagus (BE) for many years, and my personal policy when doing upper endoscopy in asymptomatic or symptomatic patients, is to take routine biopsy samples just at the site or 4 to 5 mm distal to the squamo-columnar junction. In the first study, we took 139 control subjects without GERD symptoms and 372 patients with symptoms of chronic GE reflux.1 We found that 2% of controls, 12.4% of patients with GE reflux without esophagitis, and 11.7% of patients with esophagitis showed the presence of IM just distal to the squamo-columnar junction. This is the only study performed in asymptomatic patients. In a second study,2 we demonstrated, as clearly stated by Chandrasoma3 and also by Riegler, that IM always arose in cardiac epithelium or “carditis”. In a third study, in 134 control asymptomatic patients, fundic mucosa was present distal to the squamocolumnar junction in 59%, while cardiac mucosa was present in 41%.4 On the contrary among patients with GE symptoms with normal endoscopy, cardiac mucosa was present in 63%, while among patients with erosive esophagitis, cardiac mucosa was present in 74% of the cases. In a fourth study,5 we determined the clinical symptoms, manometric studies and 24-h acid and bile monitoring among 48 patients with carditis, 105 patients with CIM and 78 patients with short-segment BE and 69 patients with long-segment BE. Later, we determined the prevalence of BE by endoscopic and histologic studies in 306 control subjects and 376 patients with GERD symptoms.6 Again, control subjects had 1.6% of IM at the squamocolumnar junction, while patients with symptoms showed 18% of CIM, with 17% of them having even low-grade dysplasia. A later study determined the prevalence of IM according to the length of the endoscopic columnar-lined esophagus, showing that short-segment BE is 3 times more frequent than long-segment BE, and the prevalence of IM increases parallel to the length of the columnar-lined segment.7 In all these studies, biopsy samples were taken 4 to 5 mm distal to the squamo-columnar junction. As Professor Riegler and his group state, obese patients have not been adequately evaluated before surgery by routine endoscopic and histologic samples. We have no clear explanation why obese patients showed IM in only 2.6%.

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It could be sampling error which I cannot exclude, but the important point is that already 5.8% of the obese patients had a BE.8 At 1 year after surgery, there is a regression of IM to cardiac mucosa in 2 out of 3 patients with CIM and in 57% of patients with short-segment BE. Therefore, according to our findings9 and according to the hypothesis of Professor Riegler and his group, I believe that routine endoscopic and histologic sampling at the squamocolumnar junction or just distal to it should be a routine preoperative investigation. I thank the group from Vienna for the important points discussed.

Prof Dr. Attila Csendes, FACS Chairman Department of Surgery Clinical Hospital University of Chile E-mail: [email protected]

References 1. Csendes A, Smok G, Sagastume H et al. Endoscopic assessment of the prevalence of gastro-esophageal junction intestinal metaplasia in gastroesophageal reflux. Rev Méd Chile 1998; 126: 155-61. 2. Csendes A, Smok G, Burdiles P et al. “Carditis” an objective histological marker for pathologic gastroesophageal reflux disease. Dis Esophagus 1998; 11: 103-5. 3. Chandrasoma PT. Columnar lined esophagus: what it is and what it tells us. Eur Surg 2006; 38: 197-209. 4. Csendes A, Smok G, Christensen H et al. Prevalence of cardial or fundic mucosa and Helicobacter pylori infection in patients with chronic gastroesophageal reflux. Rev Méd Chile 1999; 127: 1439-46. 5. Csendes A, Smok G, Flores N et al. Comparison of clinical, endoscopic and functional findings in patients with intestinal metaplasia at the cardia, carditis and short-segment columnar epithelium of the distal esophagus with and without intestinal metaplasia. Dis Esophagus 2000; 13: 61-8. 6. Csendes A, Smok G, Burdiles P et al. Prevalence of Barrett’s esophagus by endoscopy and histologic studies: a prospective evaluation of 306 control subjects and 376 patients with symptoms of gastroesophageal reflux. Dis Esophagus 2000; 13: 5-11. 7. Csendes A, Smok G, Burdiles P et al. Prevalence of intestinal metaplasia according to the length of the specialized columnar epithelium lining the distal esophagus in patients with gastroesophageal reflux. Dis Esophagus 2003; 16: 24-8. 8. Csendes A, Burgos AM, Smok G et al. Effect of gastric bypass on Barrett’s esophagus and intestinal metaplasia of the cardia in patients with morbid obesity. J Gastrointest Surg 2006; 10: 259-64. 9. Csendes A, Burgos AM, Smok G et al. Endoscopic and histologic findings of the foregut in 426 patients with morbid obesity. Obes Surg 2007; 17: 28-34.