Problem A retrospective audit of surveillance for Barrett 's oesophagus 1996-2001 Effects of change Disseminating guidelines had little effect on practice. Six months after surveillance coordinators were introduced, adherence to the planned surveillance interval increased from 17% to 92% and the number of endoscopies at which sufficient biopsies were collected increased from 45% to 83%. These changes have been maintained. Lessons learnt Disseminating guidelines and results of an audit on endoscopic surveillance in Barrett's oesophagus had no effect on practice. Introducing coordinators who proactively managed the process greatly improved adherence to guidelines. ContextBarrett's oesophagus is a premalignant condition in which damage to the oesophageal mucosa from gastro-oesophageal reflux leads to replacement of normal squamous oesophageal epithelium by columnar epithelium. The presence of columnar epithelium increases the risk of oesophageal adenocarcinoma, which occurs at a rate of 0.5-1% each year.

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These data implicate a role for galanin in AP and suggest a potential clinical application for galanin antagonists in treatment.

PFR is a physical therapy that should be considered as the initial treatment in patients with fecal incontinence. An improvement can be expected in up to 67 percent of patients. Initial good results can predict overall outcome.

Background-Sphincter of Oddi dysfunction has been implicated as a cause of various forms of acute pancreatitis. However, there is no direct evidence to show that sphincter of Oddi dysfunction can cause obstruction of trans-sphincteric flow resulting in acute pancreatitis. Aims-To determine if induced sphincter of Oddi spasm can produce transsphincteric obstruction and, in combination with stimulated pancreatic secretion, induce acute pancreatitis. Methods-In anaesthetised possums, the pancreatic duct was ligated and pancreatic exocrine secretion stimulated by cholecystokinin octapeptide/secretin to induce acute pancreatitis. In separate animals, carbachol was applied topically to the sphincter of Oddi to cause transient sphincter obstruction. Sphincter of Oddi motility, trans-sphincteric flow, pancreatic duct pressure, pancreatic exocrine secretion, plasma amylase levels, and pancreatic tissue damage (histology score) were studied and compared with variables in ligation models. Results-Acute pancreatitis developed following stimulation of pancreatic exocrine secretion with peptides after pancreatic duct ligation (p<0.05). Neither pancreatic duct ligation nor stimulation of pancreatic exocrine secretion with cholecystokinin octapeptide/secretin alone resulted in acute pancreatitis. Topical carbachol stimulated sphincter of Oddi motility abolished trans-sphincteric flow, and increased pancreatic exocrine secretion (p<0.05) and pancreatic duct pressure to levels comparable with pancreatic duct ligation (p<0.001). Carbachol application (with or without combined peptide stimulation) elevated plasma amylase levels (p<0.01) and produced pancreatic tissue damage (p<0.05). Decompression of pancreatic duct ameliorated these effects (p<0.05). Conclusion-Induced sphincter of Oddi dysfunction when coupled with stimulated pancreatic secretion causes acute pancreatitis. This may be an important pathophysiological mechanism causing various forms of acute pancreatitis. (Gut 2000;47:539-545)