Leg raise increases pressure in lower and upper esophageal sphincter among patients with gastroesophageal reflux disease.

The purpose of this study was to determine the relation between posturally increased intra-abdominal pressure and lower/upper esophageal sphincter pressure changes in patients with gastroesophageal reflux disease. We used high resolution manometry to measure pressure changes in lower and upper esophageal sphincter during bilateral leg rise. We also examined whether the rate of lower and upper esophageal sphincter pressure would increase during leg raise differentially in individuals with versus without normal resting pressure. Fifty eight patients with gastroesophageal reflux disease participated in the study. High resolution manometry was performed in relaxed supine position, then lower and upper esophageal sphincter pressure was measured. Finally, the subjects were instructed to keep their legs lifted while performing 90-degree flexion at the hips and knees and the pressure was measured again. Paired t-test and independent samples t-test were used. There was a significant increase in both lower (P < 0.001) and upper esophageal sphincter pressure (P = 0.034) during leg raise compared to the initial resting position. Individuals with initially higher pressure in lower esophageal sphincter (>10 mmHg) exhibited a greater pressure increase during leg raise than those with initially lower pressure (pressure ≤10 mmHg; P = 0.002). Similarly individuals with higher resting upper esophageal sphincter pressure (>44 mmHg) showed a greater pressure increase during leg raise than those with lower resting pressure (≤44 mmHg; P < 0.001). The results illustrate the influence of postural leg activities on intraesophageal pressure in patients with gastroesophageal reflux disease, indicating by means of high resolution manometry that diaphragmatic postural and sphincter function are likely interrelated in this population.

Is there any relationship between functional dyspepsia and chronic gastritis associated with Helicobacter pylori infection?

BACKGROUND/AIMS: The relationship between functional dyspepsia, H. pylori infection and chronic gastritis is controversial. Our aims were 1) To determine the prevalence of symptoms and the degree of association between symptoms and histopathological findings in different topographical gastric regions in patients with functional dyspepsia and H. pylori infection; 2) To determine the effect of eradication treatment on functional dyspepsia symptoms. METHODOLOGY: Prospective randomized study. 251 consecutive patients with dyspepsia (141 women and 110 men), mean age 48.08, SD 16.68 (without ulcer, gastric malignancy or reflux esophageal disease as determined by endoscopy), and with H. pylori infection, underwent upper endoscopy accompanied by the obtaining of 6 biopsies (cardia, corpus, antrum) at baseline, 3 and 6 months after treatment (pantoprazole 40 mg, once daily, amoxycillin 100 mg b.i.d., clarithromycine 500 mg b.i.d.). Inflammation, activity, H. pylori presence and other mucosal alterations were evaluated semi-quantitatively according to the Sydney system, before treatment and 6 months following treatment. An interview that was carried out before, and 6 months following the treatment, determined seven symptoms (scored as 0-3); epigastric burning and pressure, pain after meal, nausea, vomiting, bloating and belching, pain on empty stomach and anorexia. 95% confidence intervals were calculated for mean values of the symptoms and histological findings. The association between symptoms and histological findings was determined by the Kendall tau-b (K tau-b). Using the t test on a 5% level of significance we tested the null hypothesis that symptoms and histological findings were independent variables. RESULTS: The effectiveness of eradication after 3 months was 87.3% and after 6 months 92.0%. Reinfection rate after 6 months was 6.4% and the overall failure of eradication was 1.6%. Significant decline of chronic inflammation, activity and H. pylori was found in cardia, corpus and antrum (P = 0.001). Glandular atrophy was found to be lower in corpus and antrum (P = 0.001), whereas in cardia an increase was found. Intestinal metaplasia remained unchanged in all gastric regions, whereas a higher degree of foveolar hyperplasia was found, which was most pronounced in corpus and antrum (P = 0.01). There was a significant regression of lymphoid follicles in cardia and antrum (P = 0.001). On the first visit, the mean significant association between symptoms and histological findings was higher, with lower variation of K tau values as compared with the visit 6 months after treatment (K tau-b 0.171, SD 0.05, variation coefficient 30.5% vs. K tau-b 0.167, SD 0.07, variation coefficient 41.5%). According to the topographic distribution of gastritis at the time of the first visit, the mean significant association between symptoms and findings was found to be highest in antrum and corpus as opposed to the visit 6 months after treatment, where the values of association were found to be highest for variables from cardia and lowest for those in gastric corpus. After 6 months both the number of patients complaining of symptoms and dyspepsia score were lower (Wilcoxon P = 0.000). CONCLUSIONS: Advanced morphological changes of gastric mucosa were found to be significantly associated with symptoms of dysmotility. Pain on an empty stomach is predictive of antral inflammation. Cardia showed higher values of mean association with symptoms 6 months after therapy. Eradication treatment results in an improvement of both inflammatory changes and symptoms. In some patients persisting dysmotility symptoms were associated with persistent inflammation in cardia, which was also true for antrum, however to a lesser degree.