Helicobacter pylori may induce bile reflux: link between H pylori and bile induced injury to gastric epithelium.

Helicobacter pylori and duodenogastric reflux are both recognised as playing aetiological roles in chronic gastritis. This study investigated whether H pylori colonisation of the antral mucosa and duodenogastric reflux are independent phenomena or have a causal relationship. Thirty eight patients (15 men, 23 women) aged (mean (SD)) 48 (17) years participated. Each patient underwent gastroscopy. Antral biopsy specimens were taken to investigate H pylori colonisation. In addition BrIDA-99mTc/111In-DTPA scintigraphy was used to quantify duodenogastric reflux. H pylori positive patients who were found to have duodenogastric reflux were treated with amoxycillin (1 g/d) and metronidazole (1.5 g/d) for seven days and four tablets of bismuth subcitrate daily for four weeks. Follow up antral biopsies and scintigraphy were repeated at six months. Duodenogastric reflux could not be found in 18 patients, including eight (44%) who were H pylori positive. Ten of the 11 patients who had duodenogastric reflux (reflux % 11.6 (9.2)), however, were H pylori positive (chi 2 = 6.26, p = 0.01). These 10 patients were given eradication treatment. At six months, in six patients who became H pylori negative, duodenogastric reflux was significantly reduced from a pretreatment value of 14.3% to 3.3% (two tail, paired t = 2.57, p = 0.016). These data suggest that H pylori may induced duodenogastric reflux which may be important in the pathogenesis of H pylori gastritis or carcinogenesis, or both.

Tuberculous esophagitis. Report of a case and review of modern approaches to diagnosis and treatment.

We describe a patient with tuberculous esophagitis who was referred to us with low-grade fever, but no esophageal symptoms. The diagnosis was established in biopsies obtained from a deep midesophageal ulcer seen on endoscopy. Investigation of the patient failed to identify any extra-esophageal tuberculous foci, but a computed tomography scan revealed mediastinal lymphadenopathy without lung involvement. Primary infection of the esophagus by tuberculosis is questioned, and widespread use of computed tomography may show it to be a fiction.

The clinical need for sphincter of Oddi manometry in gastrointestinal endoscopy units.

The clinical need for sphincter of Oddi manometry (SOM) was investigated by retrospective analysis of 736 consecutive endoscopic retrograde cholangiopancreatography (ERCP) referrals (1985-89). During this period SOM was not performed in any unit in Greece including our own. Assuming a conservative or a more liberal policy in the utilization of SOM, a biliary and a pancreatic group of patients were established respectively, depending on the clinical presentation. ERCP was diagnostic in 168/194 (86.6%) of patients referred for post-cholecystectomy symptoms, but SOM was considered to be necessary to establish a diagnosis in the remaining 26 (13.4%) patients (biliary group). ERCP revealed pancreatic and/or biliary pathology in 46/69 (66.7%) patients, referred for symptoms attributed to pancreatitis, but 11/69 (15.9%) patients with pancreas divisum and 12/69 (17.4%) with acute recurrent idiopathic pancreatitis may have benefitted from SOM for planning endoscopic therapy (pancreatic group). Thus, only 5 patients from each group per 147 ERCP annual referrals were candidates for SOM. When taking into account that to run a SOM service the minimum annual number of investigations should be 50 and that the provision of ERCP in the UK is 50 per 100,000 of population per year, it is extrapolated that such a Gastrointestinal Endoscopy Unit should serve a population of 1.5 to 3 million.