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1.
Article in English | IMSEAR | ID: sea-141251

ABSTRACT

Background and aim The relationship between gastroesophageal reflux disease (GERD) and Helicobacter pylori is controversial. We evaluated endoscopic, 24-h gastric and esophageal acid profile among patients with GERD in relation to H. pylori, as the latter might alter gastric acid secretion. Methods Patients with GERD (n=123), who were not on acid-suppressive drugs, and had not received anti-H. pylori therapy, underwent gastroduodenoscopy and tests for H. pylori detection. Esophageal manometry, 24-h pH metry, serum pepsinogen-I (PG-I), PG-II and gastrin-17 ELISA were done in all these patients. Univariate and multivariate analyses were performed to assess independent predictors for erosive esophagitis (EE). Results Of 123 patients (mean age 40.5 [13.1] years, 85 [69.1%] men), 59 (47.9%) had H. pylori infection. EE was more common in H. pylori non-infected than infected (49 vs. 32, p<0.001). Among patients older than 40 years, absence of H. pylori was associated with lower esophageal pH and longer reflux (p=0.02 and p<0.001, respectively). PG-I/PG-II ratio was lower in H. pylori infected subjects (p <0.001). In patients with higher LA grade of esophagitis, elevated PG-I levels and PG-I/PG-II ratio were associated with more acidic stomach (p=0.04 and p=0.01, respectively). Multivariate analyses showed low gastrin-17 (p=0.016), higher age (p=0.013), hiatus hernia (p=0.004) and absence of H. pylori (p=0.03) were independent predictors for risk of EE. Conclusion H. pylori infection is associated with less acidic stomach and less severe GERD. Low gastrin-17, higher age, hiatus hernia and absence of H. pylori were the best predictors for EE risk.

2.
Basic & Clinical Medicine ; (12)2006.
Article in Chinese | WPRIM | ID: wpr-591311

ABSTRACT

Objective To determine the postprandial acid distributions in patients with gastroesophageal reflux disease (GERD), and their potential relationship with esophageal acid exposure. Methods Esophageal and gastric pH were recorded in a 1 h fasting segment and a 4 h postprandial segments using a triple-channel pH catheter with three antimony electrodes, which were positioned 5 cm proximal to the upper margin of LES(LES-5 cm), 5 cm and 10 cm distal to the upper margin of LES(LES+5 cm and LES+10 cm), respectively. Esophageal acid exposure and gastric integrated acidity (IA) were calculated for each ambulatory pH study. Ten healthy subjects (HS) and 10 patients with GERD were enrolled. Results (1) Total postprandial IA had a trend to be lower at LES+5 cm than at LES+10 cm in HS, but there was no significant difference between the two positions in patients with GERD. (2)Two hours after meal, there was no significant difference of gastric IAs and baseline in HS. Whereas gastric IAs in patients with GERD returned back to a higher level than baseline: LES+5 cm: 5.4 (1.8-6.8) mmol/L?h vs 1.8(0.3-3.1) mmol/L?h (P

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