SUMMARY BackgroundEndoscopic balloon dilation has been shown to be an alternative to surgery in the treatment of Crohn's symptomatic strictures.

Small-intestinal motility is frequently but not universally abnormal in diarrhea-predominant IBS. The abnormal manometric findings are heterogeneous and range from subtle quantitative changes to severe qualitative abnormalities resembling chronic idiopathic intestinal pseudo-obstruction in a small subset of patients.

Rhythm generation in mature respiratory networks is influenced strongly by synaptic inhibition. In early neonates, GABAA‐receptor‐ and glycine‐receptor‐mediated inhibition is not present, thus the question arises as to whether GABAB‐receptor‐mediated inhibition plays an important role. Using brainstem slices of neonatal mice (postnatal day, P0‐P15), we analysed the role of GABAB‐mediated modulation of GABA and glycine synaptic transmission in the respiratory network. Blockade of GABA uptake by nipecotic acid (0.25–2 mm) reduced the respiratory frequency. This reduction was prevented by the selective GABAB receptor antagonist CGP55845A (CGP) alone at P0‐P3, but by bicuculline as well as CGP at P7‐P15. Blockade of GABAB receptors by CGP increased the respiratory frequency at P0‐P3, whereas it caused a reduction of frequency in older animals. The effect of CGP on respiratory frequency was diminished in the presence of bicuculline and strychnine in older but not in younger animals. The relative contribution of GABAB‐receptor‐mediated pre‐ and postsynaptic modulation was examined by analysing the effect of GABAB receptors on spontaneous and miniature IPSCs. In younger animals (P0‐P3), the GABAB receptor agonist baclofen had no detectable effect on IPSC frequency, but caused a significant decrease in the amplitude. In older animals (P7‐P15), baclofen decreased both the frequency and amplitude of spontaneous and miniature IPSCs. These results demonstrate that GABAB‐receptor‐mediated postsynaptic modulation plays an important role in the respiratory network from P0 on. GABAB‐receptor‐mediated presynaptic modulation develops with a longer postnatal latency, and becomes predominant within the first postnatal week.

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Previous studies have demonstrated an increased gastroesophageal reflux after the ingestion of high-proof alcoholic beverages in normal subjects. Data on gastroesophageal reflux with usual amounts of low-proof alcoholic beverages are not available. The effect of white wine (7.5% v/v, pH 3.2) and beer (7.0% v/v, pH 4.5) was compared with water, a nonalcoholic beverage of pH 3.2, and an ethanol solution (7.5% v/v, pH 7.6) using ambulatory pH measurement in healthy volunteers. The fraction of time at pH < 4 in the first hour after ingestion of 300 ml white wine (median 13.2%) was significantly increased compared with beer (3.6%; P < 0.01), water (0.9%; P < 0.001), ethanol (1.3%; P < 0.001), and the nonalcoholic beverage (0.9%; P < 0.05). Beer provoked significantly more gastroesophageal reflux than water (P < 0.01). It is concluded that white wine and beer induce gastroesophageal reflux, which is neither related to their ethanol content nor to their pH. The mechanism for this effect remains to be identified.

Background: Patients with reflux disease often complain of heartburn after ingestion of coffee. Induction of gastro‐oesophageal reflux has been demonstrated by pH‐metry following the intake of coffee in healthy volunteers. The reflux was reduced when the coffee had undergone a decaffeination process. The aim of this study was to investigate the effect of decaffeination of coffee on reflux in patients with reflux disease. Methods: Seventeen reflux patients underwent two oesophageal 3‐h pH measurements. The patients received, in a double‐blind study design in a randomized order, 300 mL of either regular or decaffeinated coffee together with a standardized breakfast. The fraction time oesophageal pH < 4 was calculated during the three postprandial hours. Results: For regular coffee the fraction time was calculated to a median of 17.9% with a range of 0.7–56.6%. The fraction time was significantly reduced to 3.1% (0–49.9%) after ingestion of decaffeinated coffee. Conclusion: The amount of gastro‐oesophageal reflux induced by the intake of regular coffee in patients with reflux disease can be reduced by the decaffeination of coffee.

Acute ingestion of pure ethanol has been reported to delay gastric emptying and to enhance the propulsive movements of the intestine. The aim of the present study was to investigate the comparative effect of beer (7.0% v/v), white wine (7.5% v/v), ethanol (7.5% v/v), and water on the gastric emptying of a liquid test meal and on the gastrocaecal transit time of lactulose added to the test meal. Gastric liquid emptying was assessed by means of a nasogastric intubation technique using polyethylene glycol 4000 as the non-absorbable marker. The gastrocaecal transit time was evaluated by a hydrogen breath test. Beer (P less than 0.001) and white wine (P less than 0.05) significantly accelerated gastric emptying in comparison with ethanol of the same concentration. The gastrocaecal transit time was significantly shorter when the liquid meal was administered with beer compared with ethanol (P less than 0.005) and water (P less than 0.01). The constituents in beer and white wine responsible for our observations remain to be found.

Background: Coffee and tea are believed to cause gastrooesophageal reflux : however, the effects of these beverages and of their major component, caffeine, have not been quantified. The aim of this study was to evaluate gastro-oesophageal reflux induced by coffee and tea before and after a decaffeination process, and to compare it with water and water-containing caffeine. Methods : Three-hour ambulatory pH-metry was performed on 16 healthy volunteers, who received 300 ml of (i) regular coffee, decaffeinated coffee or tap water ( n = 16), (ii) normal tea, decaffeinated tea, tap water, or coffee adapted to normal tea in caffeine concentration ( n = 6), and (iii) caffeine-free and caffeine-containing water ( n = 8) together with a standardized breakfast.Results: Regular coffee induced a significant ( P < 0.05) gastro-oesophageal reflux compared with tap water and normal tea, which were not different from each other. Decaffeination of coffee significantly ( P < 0.05) diminished gastro-oesophageal reflux, whereas decaffeination of tea or addition of caffeine to water had no effect. Coffee adapted to normal tea in caffeine concentration significantly ( P < 0.05) increased gastro-oesophageal reflux. Conclusions: Coffee, in contrast to tea, increases gastrooesophageal reflux, an effect that is less pronounced after decaffeination. Caffeine does not seem to be responsible for gastro-oesophageal reflux which must be attributed to other components of coffee.