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

2013 ◽  
Vol 04 (01) ◽  
pp. 001-005
Author(s):  
Alexander P C. ◽  
Ramya S. ◽  
Rajkumar Soloman T. ◽  
Raja S. ◽  
Priyadarshini M. ◽  
...  

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)

Medicina ◽  
2010 ◽  
Vol 46 (7) ◽  
pp. 454 ◽  
Author(s):  
Laimas Jonaitis ◽  
Juozas Kupčinskas ◽  
Gediminas Kiudelis ◽  
Limas Kupčinskas

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.


Author(s):  
R. I. Khlynova ◽  
O. M. Khromtsova ◽  
R. B. Berdnikov ◽  
I. B. Khlynov

The aim is to study the effect of Helicobacter pylori infection on risk of developing gastroesophageal reflux disease. Materials and methods - cross-sectional observational study of 1007 patients with dyspepsia syndrome who underwent videoesophagogastroduodenoscopy with biopsy and histological examination of biopsy specimens of the gastric mucosa by OLGA-system. The age, gender, overweight, cigarette smoking, presence of Helicobacter pylori infection and gastritis stage were assessed. Results - the study showed a significant decrease in the incidence of gastroesophageal reflux disease in patients with positive H. Pylori status by 4% (RR 0,68; 95% CI, 0.49-0.94, p=0,041). The risk of developing gastroesophageal reflux disease significantly higher in overweight (RR 2,62; 95% CI 2,0-3,56; р<0,001) men (RR 1,76; 95% CI 1,33-2,32; р=0,0046) who smoked cigarettes (RR 3,23; 95% CI 2,45-4,24; р<0,001) and was not associated with the patient’s age and the stage of gastritis (р>0,05). Conclusion - a significant reduction in the frequency and risk of developing gastroesophageal reflux disease in patients with Helicobacter pylori infection is demonstrated.


2019 ◽  
pp. 014556131989246
Author(s):  
Jerome R. Lechien ◽  
Gersende Debie ◽  
Virginie Mahillon ◽  
Marie-Paule Thill ◽  
Alexandra Rodriguez ◽  
...  

Objectives: To compare the 2 long-term medical strategies in chronic rhinosinusitis without nasal polyps (CRSnNP) and to identify the role of gastroesophageal reflux disease (GERD) and Helicobacter pylori as factors of treatment failure. Material and Methods: Fifty-seven patients with CRSnNP were randomized into 2 therapeutic groups. The first group was treated with 4 weeks of amoxicillin/clavulanate and a short course of oral steroids. The second group received 8 weeks of clarithromycin. Sinonasal Outcome Test-20 (SNOT-20) and Lund and Mackay scores were assessed at baseline and after treatment, and GERD Health-Related Quality of Life (GERD-HRQL) questionnaire was evaluated in all patients. Patients with a GERD-HRQL score >8 received esogastroscopy and H pylori detection. Patients were followed during a 10-year period for clinical course and GERD evolution. The 10-year evolution of patients was described in terms of recurrence, medical, and surgical treatments. Results: Thirty-seven patients completed the study; SNOT-20 and Lund and Mackay scores similarly improved in both groups. Amoxicillin/clavulanate group had significantly more adverse reactions than the clarithromycin group (P = .03). After the therapeutic course, 35% (amoxicillin/clavulanate) and 41% (clarithromycin) of patients needed functional endoscopic sinus surgery (FESS). During the long-term follow-up, 54% (amoxicillin/clavulanate) and 40% (clarithromycin) of patients had late CRSnNP recurrence; FESS was performed in less than 15% of cases of recurrence. Gastroesophageal reflux disease complaint’s severity was associated with late recurrence of CRSnNP. Conclusion: Amoxicillin/clavulanate and clarithromycin would be competitive treatments for CRSnNP. Gastroesophageal reflux disease seems to be a negative factor for treatment response and recurrence.


2004 ◽  
Vol 18 (10) ◽  
pp. 1475-1479 ◽  
Author(s):  
A. Torquati ◽  
H. L. Houston ◽  
J. Kaiser ◽  
M. D. Holzman ◽  
W. O. Richards

2006 ◽  
Vol 43 (2) ◽  
pp. 117-120
Author(s):  
Judite Dietz ◽  
Sílvia Chaves-e-Silva ◽  
Luíse Meurer ◽  
Setsuo Sekine ◽  
Andréa Ribeiro de Souza ◽  
...  

BACKGROUND: Short segment Barrett's esophagus is defined by the presence of <3 cm of columnar-appearing mucosa in the distal esophagus with intestinal metaplasia on histophatological examination. Barrett's esophagus is a risk factor to develop adenocarcinoma of the esophagus. While Barrett's esophagus develops as a result of chronic gastroesophageal reflux disease, intestinal metaplasia in the gastric cardia is a consequence of chronic Helicobacter pylori infection and is associated with distal gastric intestinal metaplasia. It can be difficult to determine whether short-segment columnar epithelium with intestinal metaplasia are lining the esophagus (a condition called short segment Barrett's esophagus) or the proximal stomach (a condition called intestinal metaplasia of the gastric cardia). AIMS: To study the association of short segment Barrett's esophagus (length <3 cm) with gastric intestinal metaplasia (antrum or body) and infection by H. pylori. PATIENTS AND METHODS: Eight-nine patients with short segment columnar-appearing mucosa in the esophagus, length <3 cm, were studied. Symptoms of gastroesophageal reflux disease were recorded. Biopsies were obtained immediately below the squamous-columnar lining, from gastric antrum and gastric corpus for investigation of intestinal metaplasia and H. pylori. RESULTS: Forty-two from 89 (47.2%) patients were diagnosed with esophageal intestinal metaplasia by histopathology. The mean-age was significantly higher in the group with esophageal intestinal metaplasia. The two groups were similar in terms of gender (male: female), gastroesophageal reflux disease symptoms and H. pylori infection. Gastric intestinal metaplasia (antrum or body) was diagnosed in 21 from 42 (50.0%) patients in the group with esophageal intestinal metaplasia and 7 from 47 (14.9%) patients in the group with esophageal columnar appearing mucosa but without intestinal metaplasia. CONCLUSION: Intestinal metaplasia is a frequent finding in patients with <3 cm of columnar-appearing mucosa in the distal esophagus. In the present study, short segment intestinal metaplasia in the esophagus is associated with distal gastric intestinal metaplasia. Gastroesophageal reflux disease symptoms and H. pylori infection did not differ among the two groups studied.


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