Background-Barrett's oesophagus, columnar metaplasia of the epithelium, is a premalignant condition with a 50-100-fold increased risk of cancer. The condition is caused by chronic gastro-oesophageal reflux. Regression of metaplasia may decrease the cancer risk. Aims-To determine whether elimination of acid gastro-oesophageal reflux induces a regression of metaplastic epithelium. Methods-Sixty eight patients with acid reflux and proven Barrett's oesophagus were included in a prospective, randomised, double blind study with parallel groups, and were treated with profound acid secretion suppression with omeprazole 40 mg twice daily, or with mild acid secretion suppression with ranitidine 150 mg twice daily, for 24 months. Endoscopy was performed at 0, 3, 9, 15, and 24 months with measurement of length and surface area of Barrett's oesophagus; pH-metry was performed at 0 and 3 months. Per protocol analysis was performed on 26 patients treated with omeprazole, and 27 patients treated with ranitidine. Results-Omeprazole reduced reflux to 0.1%, ranitidine to 9.4% per 24 hours. Symptoms were ameliorated in both groups. There was a small, but statistically significant regression of Barrett's oesophagus in the omeprazole group, both in length and in area. No change was observed in the ranitidine group. The diVerence between the regression in the omeprazole and ranitidine group was statistically significant for the area of Barrett's oesophagus (p=0.02), and showed a trend in the same direction for the length of Barrett's oesophagus (p=0.06). Conclusions-Profound suppression of acid secretion, leading to elimination of acid reflux, induces partial regression of Barrett's oesophagus. (Gut 1999;45:489-494)

Short-lasting gastric air distension 1) provokes TLESRs but does not differentiate GERD patients from controls, 2) reveals impaired belching capacity in patients after complete fundoplication, and 3) shows that common cavities do not exclusively occur during TLESRs.

Isocaloric and isovolemic amounts of protein (casein), fat (intralipid) and carbohydrate (saccharose) and an isovolemic control solution of water were administered intragastrically to conscious rats. The plasma CCK levels, determined by a sensitive and specific radioimmunoassay, showed an increment of 6.3 +/- 0.6, 2.7 +/- 0.5, 1.7 +/- 0.4 and -0.9 +/- 0.4 pM, respectively (basal value 2.5 +/- 0.3 pM). The threshold increment of plasma CCK to stimulate pancreatic enzyme secretion by exogenous CCK was found to be 1.5 pM. It is therefore concluded that casein is a potent stimulus for CCK secretion and pancreatic secretion, but that fat and even carbohydrate, although less potent, also produce a CCK increment above the threshold for pancreatic secretion.

Rectal motor characteristics are not different between patients with constipation-predominant IBS, patients with STC and healthy controls while during isobaric distensions, sensations of urge were reduced in STC and sensations of pain were increased in IBS. Rectal visceroperception testing may help distinguish groups of patients with different subtypes of constipation.

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