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

Helicobacter pylori, the most common source of chronic infection worldwide, is a principal aetiological agent of type B gastritis, gastric and duodenal ulcers, and mucosa-associated lymphoid tissue lymphomas; the presence of this pathogen is also associated with gastric carcinoma. Infection with H. pylori is prevalent in patients with gastro-oesophageal reflux disease (GORD) even though it does not appear to play an important role in GORD pathophysiology. However, epidemiological studies have shown that colonization with cagA-positive H. pylori provides significant protection against the development of GORD and its long-term complications. Whereas clinical trial results indicate that the presence of H. pylori has little influence on the effectiveness of antisecretory therapy with a proton pump inhibitor (PPI) in patients with GORD, the meta-analysis of results from long-term studies suggests that risk of GORD relapse may be reduced in the presence of H. pylori infection. Several investigators have raised concerns about increased risk for gastric neoplasia in H. pylori-positive patients treated with PPIs. However, long-term follow-up of such patients indicates neither significant risk of neoplasia nor accelerated development of gastric glandular atrophy. Thus, the excellent safety record of these compounds seems not to be compromised by the presence of H. pylori.
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PMID:Gastro-oesophageal reflux disease and Helicobacter pylori or gastro-oesophageal reflux disease from Helicobacter pylori? 1143 May 5

The Maastricht 2 Consensus Report features evidence-based recommendations for the management of Helicobacter pylori infection. Strongly recommended indications for H. pylori eradication include duodenal and gastric ulcer, mucosa-associated lymphoid tissue lymphoma, atrophic gastritis, post gastric cancer resection, first-degree relation to gastric cancer patients, and patient's wishes. Advisable indications include functional dyspepsia, with the statement that eradication can lead to long-term improvement of symptoms in a subset of patients. Because H. pylori eradication does not cause gastro-oesophageal reflux disease (GORD) in most patients, or exacerbate existing GORD, H. pylori should be eradicated in patients requiring long-term acid suppression. Also advisable is H. pylori eradication before administration of non-steroidal anti-inflammatory drugs (NSAIDs), although this alone may be insufficient to reduce recurrent bleeding or enhance ulcer healing in patients receiving antisecretory therapy who continue to take NSAIDs. Maastricht 2 also introduced the concept of the 'treatment package' that considers first- and second-line eradication therapies together. A 'search and treat' strategy should be considered in patients with peptic ulcers; for patients with uncomplicated duodenal ulcer, administration of proton pump inhibitors can be limited to the period of antibiotic treatment.
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PMID:Key points from the revised Maastricht Consensus Report: the impact on general practice. 1168 30

Significant progress and new insights have been gained in the 4 years since the first Maastricht Consensus Report, necessitating an update of the original guidelines. To achieve this, the European Helicobacter Pylori Study Group organized a meeting of specialists and experts from around the world, representatives from National Gastroenterology Societies and general practitioners from Europe to establish updated guidelines on the current management of Helicobacter pylori infection. The meeting took place on 21-22 September 2000. A "test and treat" approach is recommended in adult patients under the age of 45 years (the age cut-off may vary locally) presenting in primary care with persistent dyspepsia, having excluded those with predominantly gastro-oesophageal reflux disease symptoms, non-steroidal anti-inflammatory drug users and those with alarm symptoms. Diagnosis of infection should be by urea breath test or stool antigen test. As in the previous guidelines, the eradication of H. pylori is strongly recommended in all patients with peptic ulcer, including those with complications, in those with low-grade gastric mucosa-associated lymphoid tissue lymphoma, in those with atrophic gastritis and following gastric cancer resection. It is also strongly recommended in patients who are first-degree relatives of gastric cancer patients and according to patients' wishes after full consultation. It is advised that H. pylori eradication is considered to be an appropriate option in infected patients with functional dyspepsia, as it leads to long-term symptom improvement in a subset of patients. There was consensus that the eradication of H. pylori is not associated with the development of gastro-oesophageal reflux disease in most cases, and does not exacerbate existing gastro-oesophageal reflux disease. It was agreed that the eradication of H. pylori prior to the use of non-steroidal anti-inflammatory drugs reduces the incidence of peptic ulcer, but does not enhance the healing of gastric or duodenal ulcer in patients receiving antisecretory therapy who continue to take non-steroidal anti-inflammatory drugs. Treatment should be thought of as a package which considers first- and second-line eradication therapies together. First-line therapy should be with triple therapy using a proton pump inhibitor or ranitidine bismuth citrate, combined with clarithromycin and amoxicillin or metronidazole. Second-line therapy should use quadruple therapy with a proton pump inhibitor, bismuth, metronidazole and tetracycline. Where bismuth is not available, second-line therapy should be with proton pump inhibitor-based triple therapy. If second-line quadruple therapy fails in primary care, patients should be referred to a specialist. Subsequent failures should be handled on a case-by-case basis by the specialist. In patients with uncomplicated duodenal ulcer, eradication therapy does not need to be followed by further antisecretory treatment. Successful eradication should always be confirmed by urea breath test or an endoscopy-based test if endoscopy is clinically indicated. Stool antigen test is the alternative if urea breath test is not available.
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PMID:Current concepts in the management of Helicobacter pylori infection--the Maastricht 2-2000 Consensus Report. 1186 Mar 99

Helicobacter pylori (H. p.) causes active chronic antrum gastritis in all infected patients. In a relatively small percentage complications of H. p.-gastritis including duodenal ulcer, gastric ulcer, giant fold gastritis, lymphocytic gastritis, autoimmune gastritis, gastric carcinoma and gastric MALT lymphoma may develop. Strongly recommended indications for eradication therapy include gastroduodenal ulcer disease, giant fold gastritis, lymphocytic gastritis, autoimmune gastritis, gastric MALT lymphoma, atrophic gastritis, corpus-predominant gastritis, post gastric cancer resection and patients who are first degree relatives of gastric cancer patients. Eradication therapy is controversial in patients with gastroesophageal reflux disease, functional dyspepsia and in patients in whom treatment with nonsteroidal antiinflammatory drugs (NSAID) or long-term treatment with proton pump inhibitors (PPI) is planned.
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PMID:[Helicobacter pylori infection--clinical aspects and indications for treatment]. 1199 61

Helicobacter pylori is a gastric pathogen that is a major cause of peptic ulcer disease, has a role in mucosa-associated lymphoid tissue (MALT) lymphoma and is associated with gastric cancer. Yet, in a large proportion of the human population, H. pylori infection has no apparent adverse clinical consequences. Furthermore, recent research suggests that H. pylori may even confer protection against gastroesophageal reflux disease. The conflicting evidence surrounding H. pylori infection was discussed at a sponsored symposium in Helsinki, introduced by Professor P. Malfertheiner, with papers presented by Dr H. J. O'Connor, Professor R. M. Genta, Dr P. Unge and Professor A. T. R. Axon. Emerging epidemiological and retrospective evidence suggests that the presence of H. pylori infection may provide some protection against gastroesophageal reflux disease, but there is other evidence that shows no benefit of H. pylori for the protection of the oesophagus. It was felt that prospective, multicentre studies are needed to explore the H. pylori-gastroesophageal disease relationship further, to avoid confusing potential benefits with known risks. Following the symposium, a discussion on the relative risks and benefits for H. pylori eradication was provided by Professor Axon and Professor Blaser. Eradication of H. pylori has been recommended in a series of management guidelines issued by consensus groups. However, accurate estimates of the relative risks and benefits of H. pylori infection in the general population, as well as in specific patient groups, is essential in order to develop a management strategy.
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PMID:Symposium: Helicobacter pylori and clinical risks--focus on gastro-oesophageal reflux disease. 1200 Mar 12

Treatment recommendations for H. pylori infection are peptic ulcer disease, MALT lymphoma, atrophic gastritis and following gastric cancer resection as well as first degree relatives of gastric cancer patients. Advisable situations are functional dyspepsia, before introduction of NSAID's or intended long-term proton-pump inhibitor treatment. It is thought that eradication therapy is not associated with gastro-esophageal reflux disease and does not enhance NSAID induced peptic ulcer healing. Therapy should be given as a package which considers first and second line eradication therapies together; in uncomplicated duodenal ulcer patients, eradication therapy does not need to be followed by further antisecretory treatment. First line therapy should be with triple therapy using a proton pump inhibitor (PPI), combined with clarithromycin and amoxycilline or metronidazole. Second-line therapy should use a quadruple therapy with a PPI, bismuth, metronidazole and tetracycline. Where bismuth is not available, second line therapy should be with a PPI triple therapy. If second line quadruple therapy fails in primary care, patients should be referred to the specialist and handled on a case by case basis. Successful eradication should always be confirmed by urea breath test (UBT), or endoscopy-based tests if endoscopy is clinically indicated. Stool antigen test is the alternative if UBT is not available. A 'test and treat' approach based on non-invasive testing can be offered to adult patients presenting in primary care with persistent dyspepsia under the age of 45 years (the age cut-off may vary locally), having excluded those with predominantly gastroesophageal reflux disease (GERD) symptoms, NSAID users, and patients with alarm symptoms.
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PMID:[Helicobacter pylori--2002]. 1207 Oct 78

Since the initial report 20 years ago by Marshall and Warren of an unidentified curved bacillus located on the gastric epithelium of patients with chronic active gastritis, the discovery of Helicobacter pylori and its association with a number of gastrointestinal diseases has revolutionized the field of gastroenterology. Although the association of H. pylori infection with peptic ulcer disease, chronic gastritis, mucosa-associated lymphoid tissue lymphoma, and gastric adenocarcinoma has been well documented over the past two decades, other areas remain less clear, including the role of H. pylori in gastropathy associated with nonsteroidal anti-inflammatory drugs, gastroesophageal reflux disease, and both uninvestigated and nonulcer dyspepsia. Although these areas still remain somewhat controversial, recent reports further clarify the role of H. pylori in these conditions. A review of the recent literature regarding H. pylori-associated diseases is presented along with recommendations for diagnosis and treatment of H. pylori infection.
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PMID:Helicobacter pylori-Associated Diseases. 1244 Oct 33

Helicobacter pylori infection has been recognized as the most important pathogenetic principal of peptic ulcer disease, atrophic gastritis, gastric adenocarcinoma and MALT lymphoma. At the moment efforts are made to clarify it's role in functional dyspepsia, and gastro-esophageal reflux disease. The complex interactions between H. pylori infection and NSAIDs is another field of ongoing research. Diagnosis and eradication therapy are standardized. Established indications are peptic ulcer disease, low-grade gastric MALT lymphoma, early gastric cancer treated by mucosal resection and partial gastrectomy for gastric cancer. Atrophic gastritis, known to be a precancerous lesion, as well as first degree relatives of patients with gastric cancer is another widely accepted indication for eradication therapy. The recommended eradication regimens combine a proton pump inhibitor with clarithromycin and either amoxicillin or metronidazole--for a week.
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PMID:[Helicobacter pylori. Update 2002]. 1250 73

Helicobacter Pylori infection has been identified as a pathogenic factor in a number of gastroduodenal diseases, most importantly in gastric and duodenal ulcer disease. This association and the development of H. PYLORI eradication therapies has had a tremendous influence on the surgical therapy for these disorders. Decades ago, surgery was the therapy of choice for gastric and duodenal ulcers. Now, however, the first line of therapy includes treatment of H. PYLORI infection, suppression of gastric acid secretion, and protection of gastric mucosal barriers combined with a range of endoscopic procedures. These developments have had a major impact on the indications for surgery in benign gastroduodenal diseases. In addition, advances in our understanding of the pathogenetic mechanisms of H. PYLORI infection have also changed our views of gastric mucosa-associated lymphoid tissue lymphoma, gastric cancer, and gastroesophageal reflux disease.
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PMID:How Helicobacter Pylori changed the life of surgeons. 1268 75

Dyspepsia is a common clinical problem. Its causes include peptic ulcer disease, gastroesophageal reflux, and functional (nonulcer) dyspepsia. A detailed clinical description of pain does not reliably differentiate the cause. Approximately 80% of gastroscopies are performed for the investigation of dyspepsia. "Gastritis" is diagnosed endoscopically in 59% of all stomachs, although in only 3% are the changes severe. Pathologic examination of unselected gastric biopsy specimens reveals that abnormalities are present in 62-73%, but there is only a weak correlation between endoscopic and histologic findings. For these reasons, it is recommended that endoscopic examination should always be accompanied by biopsy. Ideally, biopsies should be taken in a systematic fashion to include sampling of antrum and corpus. Recent evidence suggests that gastric infection by Helicobacter pylori initially presents as a superficial gastritis. Later it may become atrophic with development of intestinal metaplasia. The onset of atrophic changes may be related to the duration of infection, the strain of the infecting organism, associated dietary factors, or as-yet undefined host factors related to immunity. Persistent superficial gastritis predisposes to duodenal ulcer and gastric mucosa-associated lymphoid tissue lymphoma. Atrophic gastritis predisposes to gastric ulcer and adenocarcinoma. Evidence is accumulating that in some patients, pernicious anemia may be an end result of H. pylori-induced atrophic gastritis. Reactive gastropathy is a relatively common finding in gastric biopsies; in most instances it is associated with either reflux of duodenal contents or therapy with nonsteroidal anti-inflammatory drugs. Lymphocytic gastritis, eosinophilic gastritis, and the gastritis associated with Crohn's disease are distinct morphologic entities. Lymphocytic gastritis and eosinophilic gastritis have a variety of clinical associations. Carditis is a controversial topic: currently opinions are divided as to whether it is the result of gastroesophageal reflux or a proximal extension of H. pylori infection from the remainder of the stomach.
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PMID:Gastritis and carditis. 1269 98


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