Abstract

Background: Following a meal proximal gastric relaxation enable the stomach to maintain a low balanced pressure and adapt its volume to the size of the ingested meal. Patients with GastroEsophageal Reflux Disease are known to have delayed gastric emptying. Enhanced postprandial distension facilitates gastroesophageal reflux events and generates symptoms via stimulation of subcardiac receptors. The aim of this study was to investigate the gastric accommodation in patients with moderate erosive esophagitis and Barrett's esophagus in relation to the symptoms generated by a test meal. Patients and methods: Twenty-one patients with short segment Barrett's esophagus (BE), 17 patients with moderate erosive esophagitis (EE) (10 LA-A; 7 LA-B), and 19 control persons with no history of dyspepsia or reflux symptoms were enrolled into the study. After an overnight fast the subjects ingested a test soup of 500ml. Using ultrasonography the proximal sagittal area (pSA) and the frontal oblique diameter were measured and the approximate proximal gastric volume (aGV) was calculated. Participants were asked to score their abdominal symptoms before and after the test meal on a visual analogue scale. Results: Both in patients with EE and BE the aGV was significantly higher than that in the control persons. Pain and discomfort were significantly greater before testing in patient with EE and with BE than those in control persons. EE patients experienced significantly more postprandial fullness than patients with BE or the control persons. There was a significant correlation between the pSA and postprandial fullness in the EE group, but not in the patients with BE or in the control group. Conclusion: proximal gastric dysfunction may have a pathogenetic role both in EE and in BE. The difference in the postprandial fullness between the two subgroups of patients with reflux disease as well as the lack of correlation with the pSA are in agreement with the clinical observation that patients with Barrett's oesophagus are relatively less symptomatic. Grant support: ETT 340/01 and TÁMOP-4.2.1/B-09/1/KONV-2010–0005

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