Shyam Menon

Antimotility during ERCP.

We read with great interest the article by Kulling et al reporting on 27,061 endoscopic procedures performed with propofol in two private gastroenterology practices in Switzerland, using only 1 endoscopy nurse, clinical patient assessment, and pulse oxymetry. We share the authors’ enthusiasm about the potential of propofol to allow highquality sedation in gastroenterology, provided that titration is the cornerstone of drug application. The cumulative reported experience of propofol sedation by non-anesthetists of approximately 125,000 endoscopic proceduresdwithout a single case requiring endotracheal intubationdis indeed impressive; we must, however, be aware that gastroenterologists will have to compare favorably, with an extremely low complication rate in anesthetic procedures and a mortality of approximately 0.69/100,000 cases in surgery. A much greater number of patients will need to be investigated before a definitive statement on safety can be made. We recently reported that the use of propofol significantly increased the need for staff members in the endoscopy suite. Studies showing that endoscopy can be performed with only 1 nurse in private practice are, therefore, extremely significant in terms of cost effectiveness. We would, however, caution our colleagues that additional electronic monitoring such as capnography (in addition to oxymetry) may be extremely beneficial and reassuring in the private practice setting, despite the absence of proof that these devices decrease morbidity and mortality. This proof would again require a very large number of patients to be studied and has, therefore, never been established for any electronic monitoring device in GI endoscopy. Relying solely on oxymetry does not allow the assessment of patient ventilation. Capnography was developed to measure end-tidal CO in intubated patients and allows endoscopists an early qualitative recognition of (generally short) episodes of apnea in their nonintubated patients, without aiming to replace clinical assessment. We believe that routine use of capnography would facilitate the monitoring of ventilation and be an additional ‘‘political’’ argument in favor of ‘‘one-nurse endoscopy.’’ Further, capnography is now available at a reasonably low cost. Propofol has become a topic of passionate discussion throughout the world, creating ‘‘believers’’ and ‘‘nonbelievers.’’ With use of capnography in the GI suite, our critical colleagues in anesthesiology would recognize that gastroenterologists are indeed able to differentiate between oxygenation and ventilation. We would very strongly caution colleagues who intend to start using propofol to first collaborate with their local anesthesia team; indeed, collaboration increases security, teamwork, and fun! Florian Froehlich, MD Gastroenterology Unit Hôpital du Jura Porrentruy/Delémont, Switzerland and Department of Gastroenterology University of Basle Basle, Switzerland Nicolas Milliet, MD Department of Anesthesia Hôpital du Jura Porrentruy/Delémont, Switzerland

Endoloop ligation of large polyps

Am J Gastroenterol 1991;86:935-8. 5. Hajiro K, Yamamoto H, Matsui H, et al. Endoscopic diagnosis and excision of intraluminal duodenal diverticulum. Gastrointest Endosc 1979; 25:151-4. 6. Hiraoka T, Nakamura M, Ohno K, et al. Endoscopic excision of intraluminal duodenal diverticulum. Dig Dis Sci 1985;30:274-81. 7. Ravi J, Joson PM, Ashok PS. Endoscopic incision of intraluminal duodenal diverticulum. Dig Dis Sci 1993;38:762-6. 8. Van Os EC, Petersen BT, Kelly DG, et al. Endoscopic management of an intraluminal duodenal diverticulum. Gastrointest Endosc 1996;44:494-7.

Colonoscopic surveillance in ulcerative colitis

1. Rubin DT. The changing face of colorectal cancer in inflammatory bowel disease: progress at last!. Gastroenterology 2006;130:1350-2. 2. Leighton JA, Shen B, Baron TH, et al. ASGE guideline: endoscopy in the diagnosis and treatment of inflammatory bowel disease. Gastrointest Endosc 2006;63:558-65. 3. Kiesslich R, Neurath MF. Which new techniques will replace classical surveillance?. In: Gasche C, Gassull M, Herrerı́as Gutiérrez JM, et al, editors. Intestinal inflammation and colorectal cancer, Falk Symposium 158. Dordrecht, The Netherlands: Springer; 2007. p. 131-51. 4. Lichtenstein GR, Cohen R, Yamashita B, et al. Quality of life after proctocolectomy with ileoanal anastomosis for patients with ulcerative colitis. J Clin Gastroenterol 2006;40:669-77. 5. Rubin DT, Rothe JA, Hetzel JT, et al. Are dysplasia and colorectal cancer endoscopically visible in patients with ulcerative colitis? Gastrointest Endosc 2007;65:998-1004. 6. Rutter MD, Saunders BP, Wilkinson KH, et al. Most dysplasia in ulcerative colitis is visible at colonoscopy. Gastrointest Endosc 2004;60:334-9.

Electronic Clinical Challenges and Images in GI

t I uestion. A 67-year-old man with a 2-month history of iredness and abdominal discomfort was found to have a icrocytic anemia with an hemoglobin of 6.7 g/dL. He ad no history of weight loss, hematemesis, or melena. is past medical history was significant for mitral reguritation secondary to a previous episode of bacterial ndocarditis and epilepsy, which was well controlled on henytoin and phenobarbital. Clinical examination revealed a soft, nontender, moile central abdominal mass; rectal examination was noral. Abdominal computed tomography (CT) was perormed Figures A and B). See the GASTROENTEROLOGY web site (www. astrojournal.org) for more information on submiting your favorite image to Clinical Challenges and mages in GI.

Primary Prophylaxis of SBP

been reported that H felis infection in C57BL/6 mice induces chronic active gastritis that mimics the pathologic features observed in H pylori-induced gastritis in humans7,8 and results in the development of gastric cancer.9 We found that PP deficiency severely impaired both the development of Helicobacter-induced gastritis mediated by interferon (IFN)–producing CD4 T cells and the production of antiHelicobacter antibodies despite marked bacterial colonization in the gastric mucosa.3 Thus, the data by Nagai et al and our data suggest that PPs have an important role not only in the cell-mediated immunity, but also in the specific humoral immunity against Helicobacter. In the Selected Summary,1 Gewirtz and Sitaraman raised certain questions. What signals drive the priming of CD4 T cells in PPs, and what direct these cells to migrate to the stomach and then to the site of infection? Nagai et al and we have demonstrated that Helicobacter antigens are taken up by dendritic cells (DCs) in PPs.2,3 It has been reported that DCs in PPs instruct naïve T cells to differentiate into gut-homing T cells that express guthoming chemokine receptors, such as integrin 4 7, and CC chemokine receptor 9 (CCR9).10 Indeed, we demonstrated that PP deficiency impairs differentiation of Helicobacter-specific IFN–producing CD4 T cells into CCR9-expressing cells.3 Furthermore, by transfer of splenic T cells from normal mice infected with Helicobacter into immunodeficient RAG2 knockout mice, we found that infiltration of Helicobacter-specific CD4 T cells into the gastric mucosa depends on Helicobacter colonization in the stomach.3 Finally, we showed the expression of CCR9-ligand, TECK/CCL25 in Helicobacterinduced inflamed gastric mucosa.3 From these data, it is tempting to speculate that DCs in PPs taking up Helicobacter antigens prime CD4 T cells to differentiate into Helicobacter-specific CD4 T cells expressing gut-homing chemokine receptors, and interaction between bacteria and epithelial cells in the gastric mucosa triggers the recruitment of Helicobacter-specific CD4 T cells that express gut-homing chemokine receptors into the infection sites.