ABSTRACT
UNLABELLED: The oesophageal inflammation during gastrointestinal reflux disease (GERD) has been considered to be an acid and pepsine related disorder. The oesophagus remains under the prolonged exposure of gastric acid, which damages the mucosa and causes an esophagitis. Amongst the most important pathogenetic factors of GERD, the delayed gastric emptying and transient episodes of low esophageal sphincter (LES) relaxation have been described. The examinations like electrogastrography (EGG) and 24-hours pH-metry are useful for the evaluation of these disturbances. AIM: The aim of the study was to confirm the co-existence among the abnormal gastric myoelectric activity and the esophageal pH changes in patients with GERD. METHODS: Ten patients (8 m., 2 f.) 20-61 years of age (mean 46 +/- 15.3 years) with GERD were examined. The EGG recording lasted one hour: 30 min. in fasting state and 30 min. after a standard meal. The 24-hours pH-metry measurement, five cm above the upper edge of LES, was done on separate days. A control group, matched for number and age, for the comparison of the EGG recording, was recruited. RESULTS: Amongst the patients suffering from GERD the results of fasting EGG showed the lower normogastria (mean 45.3 +/- 21.9% vs. 86.5 +/- 8.8%: p < 0.01) and the high dysrrhytmia time period (mean 54.7 +/- 21.9% vs. 13.5 +/- 9.6%: p < 0.01), than in the control group. After the meal, the dysrrhytmia persisted (mean 43.5 +/- 24.3% vs. 9.6 +/- 11.5%: p < 0.01). The mean increase of the slow waves amplitude after the meal was 0 +/- 55% vs. 80 +/- 146%; p < 0.05. The recording of the 24-hours pH-metry showed an increase of the pH < 4 episodes number (mean 329 +/- 246) and time percentage (mean 12.2 +/- 6.6%). The patients obtained mean 65.5 +/- 61 points in the De Meester and Johnson scoring. A significant correlation among the postprandial dysrrhytmia and reflux episodes time percentages was observed (p < 0.05). CONCLUSIONS: The results of our studies suggest the importance of the gastric myoelectric activity disturbances in pathogenesis of GERD.
