A Prospective Randomized Trial of Sham, Single Dose Stretta and Double Dose Stretta for the Treatment of Gastroesophageal Reflux Disease (GERD): One Year Follow-Up

It remains unclear whether the Helicobacter pylori eradication may cause or provoke gastroesophageal reflux disease. Therefore, we aimed to elucidate the role of H. pylori eradication and other factors in the development of erosive esophagitis in patients with duodenal ulcer. Materials and methods. We enrolled 183 H. pylori-positive duodenal ulcer patients without erosive esophagitis. Final endoscopy was performed 12 months later or in case if ulcer relapse was suspected. H. pylori was diagnosed by the urease test and histology if the results of at least one of the tests were positive. A total of 142 patients were assigned to the eradication treatment. The control group included 41 volunteers – 20-mg omeprazole b.i.d. for 4 weeks was administered. Results. A total of 150 patients completed the study. Of the 119 patients, 70 (58.8%) were cured from H. pylori, and in 49 (41.2%) of patients, treatment of H. pylori was unsuccessful. All 31 controls remained H. pylori-positive. At the final endoscopy, erosive esophagitis was found in 19 (12.7%) patients. Erosive esophagitis developed in 8 (11.4%) successfully eradicated patients, in 9 (18.4%) unsuccessfully treated patients, and in 2 (6.5%) controls (P>0.05 comparing the groups). Multivariate logistic regression analysis revealed 3 factors at baseline, which were significant (P<0.05) in predicting the occurrence of erosive esophagitis: age more than 43 years (OR, 4.96; 95% CI, 1.47–16.71), nonerosive gastroesophageal reflux disease (OR, 3.96; 95% CI, 1.34–11.68), and smoking (OR, 3.17; 95% CI, 1.01–9.17). Conclusions. H. pylori eradication did not influence the incidence of erosive esophagitis in patients with duodenal ulcer during a one-year follow-up period. Pre-existing nonerosive gastroesophageal reflux disease, smoking, and older age are important predictors of de novo development of erosive esophagitis.

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Effects of long-term acid suppressants with ranitidine and omeprazole on gastric mucosa

Journal of Digestive Endoscopy ◽

10.1055/s-0039-1700260 ◽

2013 ◽

Vol 04 (01) ◽

pp. 001-005

Author(s):

Alexander P C. ◽

Ramya S. ◽

Rajkumar Soloman T. ◽

Raja S. ◽

Priyadarshini M. ◽

...

Keyword(s):

Gastroesophageal Reflux Disease ◽

Gastric Mucosa ◽

Gastroesophageal Reflux ◽

Intestinal Metaplasia ◽

Reflux Disease ◽

Chronic Active Gastritis ◽

H Pylori ◽

One Year

ABSTRACT Background and objectives: Proton pump inhibitors are used widely for gastroesophageal reflux disease and ulcer type dyspepsia. Majority of the patients require long term medication. H2 receptor antagonist are also used for relief of symptoms. Though tachyphylaxis has been reported, symptom response is seen with long term use. The aim of the present study was to study the effects of long-term acid suppressants on gastric antral histology. Methods: Patients who received long-term acid suppressants such as ranitidine and omeprazole for gastroesophageal reflux disease or dyspepsia were included. All of them had an antral biopsy for histology and H. pylori status at baseline, at 6 months and 12 months. Patients on acid suppressants for less than a year or on long-term non-steroidal anti inflammatory drugs were excluded from the study. The grading of gastritis was classified as chronic active gastritis, atrophic gastritis, intestinal metaplasia and dysplasia. Results: Thirty patients received ranitidine and 28 omeprazole. In H. pylori positive group, the median duration of ranitidine and omeprazole were 3 years (1.5 to 8 years) and 4 years (1 to 10 years) respectively. Two thirds of patients had chronic active gastritis (ranitidine: 35.5% omeprazole:26.6%); 10 had gastric atrophy (ranitidine: 6.6% omeprazole:15.5%) and 7 had intestinal metaplasia (ranitidine4.4% omeprazole11.1%). Four of the 10 patients on omeprazole showed progression of histology as against only one of the 13 patients on ranitidine at one year of follow up. In omeprazole pylori negative patients, the median duration of ranitidine and omeprazole was 2.5 years (range 1 to 6 years) and 3 years (range 2 to 7 years) respectively. Irrespective of the acid suppressants, the baseline histology was either chronic active gastritis (78.5%) or gastric atrophy (21.5%). None had intestinal metaplasia. Also there was no progression in histology staging during the follow up. Conclusions: Long-term acid suppressants irrespective of the H. pylori status are not associated with significant histological changes in gastric mucosa. Despite a significant drop out of cases, among the cases followed up no significant progression in histological staging was seen during a one year follow-up. (J Dig Endosc 2013;4(1):1–5)

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