Background: Because of the malignant potential of Barrett’s oesophagus, an aim of treatment is to cause the columnar epithelium to regress. A logical approach is to decrease acid reflux which is an important aetiological factor in Barrett’s oesophagus. Treatment with omeprazole 20–80 mg over 1–3 years has yielded conflicting but largely disappointing results. Aim: To determine if treatment of Barrett’s oesophagus with omeprazole 20 mg daily for up to 6 years can cause regression of the Barrett’s epithelium. Patients and Methods: Forty‐seven patients with Barrett’s oesophagus were treated in an open prospective study. Nine patients were treated for 2 years, 12 for 3 years, 10 for 4 years, eight for 5 years and eight for 6 years. Patients were endoscoped at 1–2‐year intervals and endoscoped at the end of the treatment period. Results: No significant shortening of the length of the Barrett’s segment was seen during any treatment period, although omeprazole controlled reflux symptoms and was well tolerated. Macroscopic squamous islands appeared in 55% of patients, mostly in the first 2–3 years although in five patients they appeared later in treatment. Conclusion: Treatment of Barrett’s oesophagus with omeprazole 20 mg daily for periods of up to 6 years did not cause regression in the length of the Barrett’s segment, but it did lead in over half of the patients to partial re‐epithelialization in the form of squamous islands.

Few Barrett's surveillance studies have addressed treatment outcomes and survival. In our study 5% of Barrett's patients undergoing endoscopy have prevalent cancers. If surveillance is performed, 4% per year develop cancer and 2% per year are cured of their cancers. Most surveillance cancers are operable and of those undergoing surgery 70% are cured. Barrett's surveillance is cost-effective compared with other cancer screening or surveillance initiatives.

The transport of triacylglycerol (TG) in mesenteric lymph was studied in rats with duodenal and mesenteric lymphatic cannulas with or without bile fistulas. Rats were infused with 135 mumol glycerol trioleate (TO) for 4 h, followed by 5 h of NaCl infusion. Rats with intact fistulas prefed 20% corn oil had nearly twice the maximum output of TG in lymph as controls. Decay from peak values was zero order for controls and indeterminate for rats prefed corn oil. In rats with bile fistulas, less TG was transported in lymph than in those in which 2 mM phosphatidylcholine (PC) was added to the infusate. The decay from maximum values was zero order for controls and first order for rats infused with PC and TO. Recovery of infused [3H]glycerol trioleate in controls was 43% and increased to 68% on inclusion of PC in the infusate. We conclude that in chow-fed rats lymph TG delivery rates were well below infusion rates, suggesting alternate TG transport routes, TG transport was improved by supplementing the infusate with PC or prefeeding with 20% TG in chow, and PC may be limiting in TG transport in rats with bile fistulas.

Leiomyoma of the oesophagus, although the commonest benign oesophageal tumour, is still rare compared with malignant tumours of the oesophagus. Leiomyomas of the oesophagus are usually diagnosed on barium swallow or histological examination after section. Five cases of leiomyoma of the oesophagus are reported where diagnosis was made by the combination of barium swallow, upper gastrointestinal endoscopy, and computed tomography and all but one patient were followed up for one to four years. The endoscopic biopsy specimens were non-specific in all five patients but none showed any evidence of malignancy. None of the five patients had a history of dysphagia. This paper describes a conservative approach to medical treatment in asymptomatic oesophageal leiomyoma rather than surgical excision as commonly published. It also emphasises the importance of negative endoscopic pinch biopsy specimens and the role of computed tomography in the diagnosis of oesophageal leiomyoma.