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Query: UMLS:C0017168 (gastroesophageal reflux disease)
11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Currently, the influence of Helicobacter pylori infection on gastro-oesophageal reflux disease is a major focus of attention because it is an issue that is relevant to so many patients. There is accumulating evidence that it is the severity of H. pylori-induced gastritis that determines whether clinically relevant effects occur within individual patients. Several lines of evidence suggest that there is a protective effect against reflux disease if gastritis is severe enough to cause elevation of gastric pH above 3 for significant parts of the 24 h cycle. Conversely, H. pylori eradication would be expected to increase the risk of reflux disease if previously substantially reduced acid secretion recovers significantly as a result of healing of corpus gastritis. This analysis indicates that the interaction of H. pylori and reflux disease should differ for duodenal ulcer patients, who do not have major reductions of acid secretion, and for gastric ulcer or atrophic gastritis patients, who do. Available data that have assessed the effects of H. pylori eradication are especially difficult to interpret in patients with chronic peptic ulcer, because of several important confounding factors. In the case of duodenal ulcer, the available studies are very conflicting, and few have been published in full. For the most relevant patient group, those whose primary problem is reflux disease, there are currently no data available on the effects of H. pylori eradication.
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PMID:Helicobacter pylori and reflux disease. 1050 24

Increased intragastric alkaline reflux has been documented in patients with reflux esophagitis; however, the effect on gastric histology has not been investigated in this population. We examined gastric biopsies from 72 non-acid-suppressed patients with gastroesophageal reflux disease (GERD) for changes of reflux gastritis or other forms of gastritis. In the Helicobacter pylori-negative GERD patients (n = 52) using the Dixon scoring system for reflux gastritis with a threshold score of >/=11, reflux gastritis was found in 15% (three of 20) of GERD patients with erosions and in no GERD patients without erosions. When the reflux gastropathy threshold score was changed to more than 8, 90% (18 of 20) of GERD patients with erosions and 19% (six of 32) of GERD patients without erosions were classified as having reflux gastritis. Regardless of the reflux gastritis threshold used, only 14% (seven of 52) of the H pylori-negative GERD patients exhibited normal gastric histology. Inactive chronic gastritis or nonspecific reactive changes were histologic findings in those gastric biopsies not classified as reflux gastritis or normal. All H pylori-positive GERD patients (n = 20) had active chronic gastritis. We conclude that most GERD patients will exhibit some form of gastric pathology: either reflux gastritis, chronic gastritis, or nonspecific reactive changes, depending on what reflux threshold score is applied and the presence of H pylori. Studies to define the intragastric alkaline content in conjunction with gastric histopathology need to be performed to further define those reflux esophagitis patients with reflux gastritis.
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PMID:Reflux gastritis in gastroesophageal reflux disease: A histopathological study. 1055 74

Gastric cardia inflammation and intestinal metaplasia are the subjects of recent investigation. Some authors have found associations with gastroesophageal reflux disease, whereas others have identified relationships with Helicobacter pylori (HP). We studied 150 consecutive patients who underwent upper endoscopy, had normal gastroesophageal anatomy, and had biopsies of the antrum, cardia, and lower esophagus, to evaluate relationships between reflux esophagitis, cardia inflammation, intestinal metaplasia, and HP gastritis. Forty-two patients had HP infection. Cardia inflammation was significantly related to esophageal squamous inflammation in the non-HP-infected patient group and to antral inflammation and cardia HP infection in the HP-infected patient group. The differences between the patient groups was most apparent in the patients with moderate or marked inflammation. Twenty-seven percent of patients had cardia intestinal metaplasia that was related to cardia inflammation. Cardia inflammation and intestinal metaplasia probably have multiple causes. Pathologists should refrain from applying the term Barrett's esophagus for biopsies procured from the cardia that show intestinal metaplasia in patients with a normal squamocolumnar junction.
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PMID:Gastric cardia inflammation and intestinal metaplasia: associations with reflux esophagitis and Helicobacter pylori. 1057 98

Colonisation with Helicobacter pylori exerts several effects on the production of acid. The bacterium does not play a direct role in the pathogenesis of gastroesophageal reflux disease (GORD). Successful eradication of H. pylori in patients with ulcer disease appears to be followed by an increase in incidence of GORD. It has been postulated that the infection could protect against the development of GORD. H. pylori ulcers and gastritis should be treated by eradication therapy. It is unclear yet what is the best treatment in patients with H. pylori infection without an ulcus or gastritis.
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PMID:[Eradication of Helicobacter pylori possibly followed by gastroesophageal reflux disease]. 1062 50

The nature of the relationship between Helicobacter pylori (Hp) infection and gastroesophageal reflux disease (GERD) remains unclear. This article reviews the current body of knowledge regarding the association between these two common entities. The authors examine the potential interactions of Hp and GERD from epidemiologic and pathophysiologic viewpoints and summarize and critique the prevalence and eradication studies that have been performed to date. Special consideration is given to the possible effects that long-term use of proton pump inhibitors may have on Hp gastritis.
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PMID:Helicobacter pylori and gastroesophageal reflux disease. 1069 12

In biopsy interpretation of GERD demonstration or exclusion of Barrett's esophagus and its complications (dysplasia and carcinoma) is the main task, especially in its differentiation to cardiac gastritis with intestinal metaplasia. Despite of all molecular-biological examinations till today no biomarker exists for the malignant potential of Barrett's esophagus, therefore regular surveillance is necessary. Differentiation of Barrett's esophagus from cardiac mucosa with intestinal metaplasia is not yet possible by using immunochemistry, also there is no marker for the differential diagnosis of low grade dysplasia versus reactive atypia and high grade dysplasia versus early cancer of mucosa type.
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PMID:[Biopsy differential diagnosis of gastroesophageal reflux (GERD)]. 1071 91

Symptomatic gastroesophageal reflux disease is common in our experience after vertical banded gastroplasty. Our aim was to determine the safety and efficacy of Roux-en-Y gastric bypass in the treatment of symptomatic gastroesophageal reflux disease complicating vertical banded gastroplasty. We evaluated prospectively collected data on 25 patients who underwent revisional bariatric surgery because of severe gastroesophageal reflux disease after vertical banded gastroplasty. Only 4 of 25 patients had gastroesophageal reflux disease symptoms prior to vertical banded gastroplasty. Endoscopic findings in 24 patients included esophagitis (58%), Barrett's esophagus (28%), pouchitis (29%), and gastritis (21%);7 (28%) of 25 patients had evidence of stenosis at the pouch outlet. Mean follow-up (complete in all 25) after Roux-en-Y gastric bypass was 37 +/- 7 months (range 3 to 102 months). There were no deaths. Postoperative complications occurred in six patients: pneumonia in two, wound infection in two, prolonged drainage of the defunctionalized stomach via gastrostomy in one, and fever in one. Median hospitalization was 7 days (range 5 to 43 days). At follow-up (37 +/- 7 months), 24 (96%) of 25 are completely or almost completely symptom free. Body mass index was 33 +/- 2 kg/m(2) before and 28 +/- 2 kg/m(2) after Roux-en-Y gastric bypass (P = 0. 001). Symptoms of gastroesophageal reflux disease are common after vertical banded gastroplasty. Conversion to Roux-en-Y gastric bypass is safe, relieves gastroesophageal reflux disease, and promotes further weight loss. Moreover, maladaptive eating (vomiting, and so forth) induced by vertical banded gastroplasty is relieved.
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PMID:Gastroesophageal reflux after intact vertical banded gastroplasty: correction by conversion to Roux-en-Y gastric bypass. 1076 90

In the MUSE classification of gastroesophageal reflux disease (GERD), esophagitis is assessed by the presence of metaplasia, ulcer, stricture, or erosion, each being graded as absent, mild or severe. Daily reflux symptoms affect about 4 to 7 percent of the population; erosive esophagitis occurs in about 2 percent; the prevalence rate of Barrett's metaplasia is 0.4 percent; and esophageal adenocarcinoma leads to two deaths per million living population. In persons with GERD symptoms, about 20 percent are found to have erosive esophagitis, while ulcers or strictures are found in less than 5 percent of all patients with erosive esophagitis. No clear-cut temporal progression exists between successive grades of disease severity, as the most severe grade of GERD is reached at the onset of the disease. Mild forms of GERD tend to be more common in women than men, while severe GERD characterized by erosive esophagitis, esophageal ulcer, stricture or Barrett's metaplasia are far more common in men than women. All forms of GERD affect Caucasians more often than African Americans or Native Americans. The prevalence of GERD is high among developed countries in North America and Europe and relatively low in developing countries in Africa and Asia. During the past three decades, hospital discharges and mortality rates of gastric cancer, gastric ulcer and duodenal ulcer have declined, while those of esophageal adenocarcinoma and GERD have markedly risen. These opposing time trends suggest that corpus gastritis secondary to Helicobacter pylori infection protects against GERD. This hypothesis is consistent with the geographic and ethnic distributions of GERD. Case-control studies also indicate that cases with erosive esophagitis are less likely to harbor active or chronic corpus gastritis than controls without esophagitis.
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PMID:Clinical epidemiology and natural history of gastroesophageal reflux disease. 1078 May 69

Proton pump inhibitors have become of pivotal importance for the treatment of GERD. The purpose of this paper is to review the interaction between Helicobacter pylori and PPIs in the treatment of GERD. H. pylori exaggerates the acid suppressive effects of PPIs. During treatment with these drugs, H. pylori-positive subjects thus have a higher intragastric pH than H. pylori-negative subjects. The mechanism for this phenomenon remains to be elucidated. We hypothesize that it is related to H. pylori-induced corpus gastritis, which impairs parietal cell function. The available evidence suggests that this phenomenon has no clinical relevance for the treatment of GERD. The 24-hr esophageal pH during PPI treatment does not depend on the H. pylori status, nor does the medication dose needed for maintenance therapy or the number of clinical relapses during such therapy depend on the H. pylori status. PPIs, on the other hand, also affect H. pylori. During treatment with these drugs, the pattern of bacterial colonization and associated gastritis shifts proximally. The increased gastritis of the body mucosa is associated with a more rapid development of atrophic gastritis, a condition characterized by a loss of gastric glands and associated with an increased cancer risk. For these reasons, one has to consider H. pylori eradication in infected GERD patients in need of PPI maintenance therapy.
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PMID:Helicobacter pylori, proton pump inhibitors and gastroesophageal reflux disease. 1078 May 83

The relationship between Helicobacter pylori (HP) and gastroesophageal reflux disease (GERD) is very complex and still not well understood. However, many issues, even those as basic as whether HP induces or protects against GERD, are still controversial. The gastritis location could play also a role in the induction of GERD. Some investigators suggested that infection by the Cag A strain of HP seems to have a positive association with reflux esophagitis. Therefore, the aim of this study was to investigate the relationship between GERD, gastritis location, HP infection and Cag A positivity.
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PMID:[Gastritis localization and GERD incidence in patients with Cag A(+) and Cag A(-) Helicobacter pylori infection]. 1083 11


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