Regeneration of canine oesophageal mucosa was studied under basal conditions and in the presence of gastro-oesophageal reflux. In normal circumstances mucosal defects in the oesophagus regenerate by squamous epithelium. In the presence of gastro-oesophageal reflux of either acid or a combination of acid and bile, regeneration was frequently by columnar epithelium (Barrett's oesophagus). This columnar regeneration was not seen with bile reflux alone. By the use of squamous barriers to proximal migration of columnar epithelium in the stomach, it was demonstrated that columnar re-epithelialization may occur from cells intrinsic to the oesophagus and is not dependent on proximal migration of cardiac columnar epithelium. The cell of origin of this epithelium may be located in oesophageal gland ducts and is likely to be a multipotential stem cell since the regenerated columnar epithelium may contain goblet and parietal cells not normally found in the oesophagus. This epithelium is morphologically distinct on mucin histochemistry from cardiac columnar epithelium. These findings support the concept that Barrett's epithelium is metaplastic.

Fasting and postprandial intragastric bile acid concentrations have been estimated and compared in patients with complications of Barrett's oesophagus, patients with Barrett's oesophagus without complications, patients with oesophagitis and a group of normal subjects who acted as controls. There was no significant difference in fasting intragastric bile acid concentrations between the groups. Postprandial bile acid concentrations were significantly greater in the patients with complications of Barrett's than in the remaining groups at 60, 90 and 120 min. Significant concentrations of bile acids were seen in gastric juice of unaltered pH and may be undetected on intra-oesophageal pH monitoring. Duodenogastric reflux may be implicated in the pathogenesis of complications of Barrett's oesophagus.

The development of Barrett's epithelium is frequent after esophagectomy, is time-related, reflecting chronic acid and bile exposure, and is not specific for adenocarcinoma or the presence of previous Barrett's epithelium. This model may represent a useful in vivo model of the pathogenesis of Barrett's metaplasia and tumorigenesis.

Symptomatic patients with endoscopicaily verified reflux oesophagitis were randomised to a double blind trial in which they received either omeprazole (20 mg once daily) or cimetidine (400 mg four times daily) for four, and if necessary, eight weeks. In an 'intention to treat' analysis, oesophagitis was found to have healed after four weeks in 77 of 137 (56%)

Background: Heparin therapy may be effective in steroid resistant inflammatory bowel disease. Aim: A randomized pilot study, to compare unfractionated heparin as a first‐line therapy with corticosteroids in colonic inflammatory bowel disease. Methods: Twenty patients with severe inflammatory bowel disease (ulcerative colitis, n=17; Crohn’s colitis, n=3) were randomized to either intravenous heparin for 5 days, followed by subcutaneous heparin for 5 weeks (n=8), or high‐dose intravenous hydrocortisone for 5 days followed by oral prednisolone 40 mg daily, reducing by 5 mg per day each week (n=12). After 5 days, non‐responders in each treatment group were commenced on combination therapy. Response to therapy was monitored by: clinical disease activity (ulcerative colitis: Truelove and Witt Index; Crohn’s colitis: Harvey and Bradshaw Index), stool frequency, serum C‐reactive protein and α1 acid glycoprotein, endoscopic and histopathological grading. Results: The response rates were similar in both treatment groups: clinical activity index (heparin vs. steroid; 75% vs. 67%; P=0.23), stool frequency (75% vs. 67%; P=0.61), endoscopic (75% vs. 67%; P=0.4) and histopathological grading (63% vs. 50%; P=0.67). Both treatments were well‐tolerated with no serious adverse events. Conclusion: Heparin as a first line therapy is as effective as corticosteroids in the treatment of colonic inflammatory bowel disease. Large multicentre randomized comparative studies are required to determine the role of heparin in the management of inflammatory bowel disease.