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Sphincter of Oddi dysfunction (SOD) is a term used to describe a group of heterogenous pain syndromes caused by abnormalities in sphincter contractility. Biliary and pancreatic SOD are each sub-classified as type I, II or III, according to the Milwaukee classification. SOD appears to carry an increased risk of acute pancreatitis as well as rates of post ERCP pancreatitis of over 30%. Various mechanisms have been postulated but the exact role of SOD in the pathophysiology of acute pancreatitis is unknown. There is also an association between SOD and chronic pancreatitis but it is still unclear if this is a cause or effect relationship. Management of SOD is aimed at sphincter ablation, usually by endoscopic sphincterotomy (ES). Patients with type I SOD will benefit from ES in 55%-95% of cases. Sphincter of Oddi manometry is not necessary before ES in type I SOD. For patients with types II and III the benefit of ES is lower. These patients should be more thoroughly evaluated before performing ES. Some researchers have found that manometry and ablation of both the biliary and pancreatic sphincters is required to adequately assess and treat SOD. In pancreatic SOD up to 88% of patients will benefit from sphincterotomy. Therefore, there have been calls from some quarters for the current classification system to be scrapped in favour of an overall system encompassing both biliary and pancreatic types. Future work should be aimed at understanding the mechanisms underlying the relationship between SOD and pancreatitis and identifying patient factors that will help predict benefit from endoscopic therapy.

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AIMS: Patients with upper gastrointestinal haemorrhage (UGIH) are usually admitted to hospital regardless of the severity of the bleed. The aim of this study was to identify patients who could be safely managed without hospitalisation and immediate inpatient endoscopy. METHODS: Based on a literature review, a protocol was devised using clinical and laboratory data regarded as being of prognostic value. A retrospective observational study of consecutive patients who attended the emergency department (ED) with UGIH was conducted during one calendar month. RESULTS: Fifty four patients were identified of whom 44 (81%) were admitted. Twelve suffered an adverse event. One of the 10 patients (10%) initially discharged from the ED was later admitted. Strict implementation of the protocol would have resulted in safe discharge of a further 15 patients, (34% of those admitted), and a saving of an estimated 37 bed days per month. CONCLUSIONS: Patients at low risk from UGIH may be identified in the ED. If validated, this protocol may improve patient management and resource utilisation.

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There is good evidence from faecal occult blood testing trials that detection and removal of non-advanced colorectal neoplasms can achieve a reduction in colorectal cancer mortality. Both colonoscopy and barium enema have potential advantages and disadvantages if implemented for population screening. The relative merits of each are discussed.

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In the past decade, our understanding of the genetic basis, pathogenesis, and natural history of pancreatitis has grown strikingly. In severe acute pancreatitis, intensive medical support and non-surgical intervention for complications keeps patients alive; surgical drainage (necrosectomy) is reserved for patients with infected necrosis for whom supportive measures have failed. Enteral feeding has largely replaced the parenteral route; controversy remains with respect to use of prophylactic antibiotics. Although gene therapy for chronic pancreatitis is years away, our understanding of the roles of gene mutations in hereditary and sporadic pancreatitis offers tantalising clues about the disorder's pathogenesis. The division between acute and chronic pancreatitis has always been blurred: now, genetics of the disorder suggest a continuous range of disease rather than two separate entities. With recognition of pancreatic intraepithelial neoplasia, we see that chronic pancreatitis is a premalignant disorder in some patients. Magnetic resonance cholangiopancreatography and endoscopic ultrasound are destined to replace endoscopic retrograde cholangiopancreatography for many diagnostic indications in pancreatic disease.

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BACKGROUND AND STUDY AIMS: Patients attending for diagnostic oesophagogastroduodenoscopy (OGD) for dyspeptic symptoms are often receiving acid-suppression therapy that has not been discontinued prior to endoscopy, and this may reduce the diagnostic yield of endoscopy. The aim of this study was to compare the diagnostic yield of OGD in uncomplicated dyspepsia in patients receiving no medication, those receiving acid-suppression therapy, and those receiving nonsteroidal anti-inflammatory drugs (NSAIDs) at the time of endoscopy. PATIENTS AND METHODS: A total of 6825 diagnostic OGDs performed in our unit between 1993 and 2001 were analysed. Patients were excluded if they had sinister symptoms, were receiving NSAIDs, or were undergoing repeat or surveillance endoscopy. RESULTS: A total of 4233 OGDs (62 %) fulfilled the criteria for uncomplicated dyspepsia. Of the patients examined in these procedures, 1367 (32 %) were receiving acid-suppression therapy. A total of 724 patients (53 % of those on therapy) were receiving proton-pump inhibitors (PPIs), 393 of whom (54 %) had positive endoscopic findings (oesophagitis 31 %, gastritis 16 %, duodenal ulcer/duodenitis 16 %). A total of 643 (47 % of the patients on therapy) were receiving H 2 -receptor antagonists, 443 of whom (69 % of this group) had positive endoscopic findings (oesophagitis 30 %, gastritis 21 %, duodenal ulcer/duodenitis 31 %). A total of 2866 patients were not receiving acid-suppression therapy, 1805 of whom (63 %) had endoscopic findings (oesophagitis 37 %, gastritis 14 %, duodenal ulcer/duodenitis 24 %). The endoscopic yield was significantly lowest in the PPI group, except for the diagnosis of oesophagitis. Overall, 17 carcinomas were detected in patients referred with simple dyspepsia, and in five of these cases the patients were receiving acid suppression. CONCLUSIONS: The widespread use of acid suppression in the treatment of simple dyspepsia prior to endoscopy leads to a reduction in the endoscopic recognition of mucosal lesions caused by acid-peptic disease, but not to a high healing rate for these lesions, and it may mask malignancy.

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Factors such as poor bowel preparation or obstructing colonic disease may confound the reporting of colonoscopy completion rates, as these factors are outside of the control of the endoscopist performing the procedure. By adjusting for these factors when calculating a colonoscopy completion rate, it may be possible to make a more accurate assessment of a unit's or individuals' competence. Details of two thousand two hundred and sixteen colonoscopies performed by four consultants and their trainees between 1993-2000 were analysed retrospectively from a prospective endoscopy database. Crude (all cases) and adjusted (excluding poor bowel preparation and disease as causes of incompletion) rates were recorded for each sex, and by age according to cause. Overall crude and adjusted completion rates were 77.9% and 85.0% respectively. There was a significant difference between male and female completion rates due to a difference in the incidence of excess looping and intolerance of the procedure (adjusted rate 88.9% in males vs. 81.6% in females, p<0.05). There was a non-significant trend to lower completion rates in patients over 75 years of age compared to younger patients. Completion rates were significantly higher following bowel resection (adjusted rates 93.5% vs. 82.8%, p<0.05). There was no significant difference between completion rates for inpatient and outpatient referrals (P=0.36). Reporting colonoscopy completion rates by adjusting for factors such as poor bowel preparation and obstructing colonic disease allows for direct comparisons of completion rates reported by different units. Reporting completion rates in this way also highlights the effect of inadequate bowel preparation on successful colonoscopy.

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Red cell distribution width (RDW) as measured on modern blood analysers is a sensitive marker of nutritional deficiency affecting red blood cell production and maturation. Such deficiencies are common in coeliac disease and it may therefore be possible indirectly to assess response to a gluten-free diet by monitoring the RDW. We measured RDW, iron, B12, folate and endomysial antibodies (EMA) in 46 newly diagnosed coeliac patients at diagnosis and after a gluten-free diet. RDW was elevated in 76% of patients at diagnosis. There was a significant decrease in RDW (17.3% vs 13.8%) after 12 months of diet, corresponding to sero-conversion of EMA and normalisation of serum iron, B12 and folate levels. We conclude that monitoring RDW is a simple indirect means of assessing response to a gluten-free diet in coeliac disease.

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