CE generally should be considered a complementary test in patients with gastrointestinal bleeding, Crohn's disease, or celiac disease, who have had negative or inconclusive endoscopic or imaging studies.

Capsule endoscopy and double balloon enteroscopy provide similar diagnostic yields in patients with OGIB. However, the diagnostic yield of DBE is significantly higher when performed in patients with a positive CE.

We thank Manno et al. for their letter comparing their experience of single-balloon enteroscopy (SBE) with our results published in this journal [1]. We were glad to see that their findings were in line with our own. Manno et al. performed 72 procedures in 67 patients with no serious complications, including no episodes of acute pancreatitis and no perforations. In the analysis of their own results combined with previously published findings [1 -4], they calculate that the perforation rate during SBE is 0.2 % by suggesting that a perforation that occurred in our cohort was the result of balloon dilation of a stricture and not due to the SBE procedure itself. We disagree with this opinion as we believe that perforations resulting from dilation procedures still have to be counted as a complication of SBE, particularly when a large, multicenter study [5] has demonstrated that the perforation rates for double-balloon enteroscopy (DBE) are notably different for diagnostic (0.1 %) and therapeutic (0.8 %) procedures. Even when our perforation is included, the overall risk during SBE remains low (2 / 484; 0.4 %) and similar to that for DBE (0.3 %) [5]. We were pleased that the authors also had no episodes of acute pancreatitis in their patients. The hypothesized mechanisms for the etiology of postenteroscopy pancreatitis include: an increased intraluminal pressure in the duodenum from balloon inflation causing reflux of duodenal fluids into the pancreatic duct; irritation of the pancreatic sphincter from inflation of the overtube balloon near the papilla; and mechanical strain on the pancreas from the repeated "push-and pull" movements that cause profound stretching of the small intestine. Manno et al. suggest that the main reason for the lowered incidence of acute pancreatitis observed with SBE is the insertion technique that delays balloon inflation until the third part of the duodenum. Therefore, they propose that the primary etiology for pancreatitis is obstruction of the pancreatic duct by inflation of the balloon near the papilla. We also agree with this theory but do not think that this is the only cause for pancreatitis. In our earlier DBE study also published in this journal [6], the occurrence of post-DBE pancreatitis was still 0.7 % despite a modified DBE insertion technique that delayed balloon inflation until after the overtube was distal to the ligament of Treitz and not near the papilla. This suggests that the mechanism for acute pancreatitis after DBE is not entirely due to balloon inflation and must be multifactorial.

Severe acute pancreatitis is often complicated by the development of pancreatic fluid collections (PFCs), which may be associated with significant morbidity and mortality. It is crucial to accurately classify these collections as a pseudocyst or walled-off necrosis (WON) given significant differences in outcomes and management. Interventions for PFCs have increasingly shifted to less invasive strategies, with endoscopic ultrasound (EUS)-guided methods being shown to be safer and equally effective as more invasive surgical techniques. In recent years, many new developments have improved the safety and efficacy of EUS-guided interventions, such as the introduction of lumen-apposing metal stents (LAMS), direct endoscopic necrosectomy (DEN) and multiple other adjunctive techniques. Despite these developments, treatment of PFCs, and infected WON in particular, continues to be associated with significant morbidity and mortality. In this article, we discuss the EUS-guided management of PFCs while reviewing the latest developments and controversies in the field. We end by summarizing our own approach to managing PFCs.

SUMMARY BackgroundTumour necrosis factor-blockade with infliximab has advanced the treatment of Crohn's disease. While infliximab is efficacious, it remains to be determined whether patients who enter clinical remission with an antitumour necrosis factor therapy can have their treatment stopped and retain the state of remission.

Increased small intestinal permeability is a longstanding observation in both Crohn's disease patients and in their healthy, asymptomatic first-degree relatives. However, the significance of this compromised gut barrier function and its place in the pathogenesis of the disease remains poorly understood. The association between abnormal small intestinal permeability and a specific mutation in the NOD2 gene, which functions to modulate both innate and adaptive immune responses to intestinal bacteria, suggests a common, genetically determined pathway by which an abnormal gut barrier could result in chronic intestinal inflammation. Furthermore, rodent colitis models show that gut barrier defects precede the development of inflammatory changes. However, it remains possible that abnormal permeability is simply a consequence of mucosal inflammation. Further insight into whether abnormal barrier function is the cause or consequence of chronic intestinal inflammation will be crucial to understanding the role of intestinal permeability in the pathogenesis of Crohn's disease.

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Gastric antral vascular ectasia (GAVE) is characterized by red, angiomatous lesions in the antrum organized either in stripes or in a diffuse pattern that can be associated with upper gastrointestinal bleeding. Endoscopic band ligation (EBL) has been reported as an effective alternative therapy for patients with GAVE. Consecutive patients with a diagnosis of GAVE were prospectively followed while undergoing EBL every 2 months. Hemoglobin, ferritin, and iron levels were frequently recorded, and clinical follow-up was performed. A total of 21 patients with GAVE were enrolled, and 17 of these patients (81 %) had associated co-morbidities, most frequently cirrhosis and chronic renal failure. A clinical response was achieved in 19 patients (91 %). A significant improvement in the mean hemoglobin level was noted after EBL (P < 0.001), and a significant decrease in blood transfusion requirements per month (P = 0.001). No major complications were observed during the study period. The mean follow-up was 10 months. EBL is an effective and safe treatment for GAVE. Randomized, controlled trials comparing EBL with other endoscopic therapies are warranted.