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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 gastritis (i.e. H. pylori infection and complications) is a focus of tremendous research activity today. Besides peptic ulcer disease, a large number of reports suggest that other diseases are associated with H. pylori. The International Agency for Research on Cancer sponsored by the World Health organization classified the bacterium as a group I carcinogen in 1994. Population-based studies of H. pylori and gastric cancer in 1991 showed an increased odds ratio, of 3-6, in infected patients, and a calculation of odds ratios in different age groups showed a markedly increased odds ratio, to about 20, in younger ages. Studies of non-ulcer dyspepsia and the effect of cure of H. pylori show either none, small, or significant symptom relief, suggesting a positive effect in a subgroup of non-ulcer dyspepsia patients. Mucosa-associated lymphoid tissue-lymphoma caused by H. pylori could be eradicated, at least in its mild forms. Barrett's ulcer is a possible H. pylori-associated disease as well as gastroesophageal reflux disease. Normal feedback in the acid regulation system is changed in infected patients, which may facilitate an increased gastroesophageal acidic reflux. Gastropathy and/or peptic ulcer due to use of nonsteroidal antiinflammatory drugs is probably aggravated by the infection. The infectious disease H. pylori gastritis is associated with a large number of complications, some of which are serious. There are no data showing any advantages of the infection. Giving anti-H. pylori therapy to infected patients should be regarded as essential.
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PMID:Are there more clinically important complications of Helicobacter pylori infection than peptic ulcer disease? A review of current literature. 984 18

Heretofore regarded as a strict pathogen, recent identification of multiple mutants of H. pylori, varying in pathogenicity, genomic composition, antigenic structure and other characteristics, has led to speculation that not all strains of the organism merit elimination. Affecting half the world's population, H. pylori appears to cause clinically significant disease in <20% of cases. The costs of eradicating harmless infection in over 2 billion people are prohibitive, particularly in countries lacking resources, and are questionable even in advanced countries where infection, gastritis and related diseases are declining as social conditions improve. Major controversies surround empiric eradication of helicobacter infection in patients with asymptomatic gastritis or non-specific dyspepsia. Apart from cost, and feasibility, there are concerns that widespread campaigns to eradicate H. pylori might cause major increases in esophageal reflux disease and esophageal adenocarcinoma, while causing some serious iatrogenic illness and increasing antibiotic resistance, with uncertain consequences to affected populations.
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PMID:H. pylori infection in non-ulcer patients--to treat or not to treat. The case against treatment. 1002 59

A significant proportion of patients with gastro-oesophageal reflux disease (GERD) have Helicobacter pylori infection, but it is unclear whether or not H. pylori should be treated in this clinical setting. The aim of this review was to critically assess the relationship between H. pylori and GERD and its potential implications for the management of GERD. Data for this review were gathered from the following sources up to April 1998-the biomedical database MEDLINE, a detailed review of medical journals, and a review of abstracts submitted to relevant international meetings. On average, 40% of GERD patients carry H. pylori infection, with a reported infection prevalence ranging from 16% to 88%. To date, there has been no reported controlled trial of effective H. pylori therapy in GERD. GERD has been reported to develop de novo following the cure of H. pylori in peptic ulcer disease. In the presence of H. pylori, proton pump inhibitor therapy appears to accelerate the development of atrophic corpus gastritis, a potentially precancerous condition. Conversely, proton pump inhibitor therapy seems to become less effective after cure of H. pylori. The mechanisms underlying these important contrasting phenomena are poorly understood. The relationship between H. pylori and GERD is complex, and it is difficult to give definitive guidelines on the management of H. pylori infection in GERD. Controlled trials of H. pylori therapy in GERD are urgently needed, as well as further long-term data on both the natural history of gastric histopathological changes in the H. pylori-positive GERD patient treated with proton pump inhibitors, and the impact of H. pylori status on the clinical efficacy of antisecretory therapy. Pending these data, it is perhaps advisable to advocate cure of H. pylori in young patients with proton pump inhibitor-dependent GERD who, in the absence of anti-reflux surgery, are faced with the likelihood of long-term medical therapy.
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PMID:Review article: Helicobacter pylori and gastro-oesophageal reflux disease-clinical implications and management. 1010 40

As in previous years, developments in the field of ulcers and gastritis have been dominated by new findings related to Helicobacter pylori. With the decrease in the frequency of H. pylori infection, the relative proportion of non-H. pylori ulcers has increased. Attempts to reduce the endoscopy workload by H. pylori or CagA screening have not been successful, and are probably ill-advised. It has become increasingly clear that curing H. pylori infection will not automatically lead to complete relief of symptoms in patients with duodenal ulcer disease. Post-therapy confirmation of cure will probably become the norm. Studies comparing omeprazole to misoprostol or ranitidine for nonsteroidal anti-inflammatory drug (NSAID) ulcer prevention in true NSAID ulcers have shown that omeprazole is equal to full-dose misoprostol for ulcer healing and to the lowest useful dose of misoprostol for ulcer prevention. H2-receptor antagonists cannot be recommended for NSAID ulcer healing or prevention. Elimination of H. pylori increases the prevalence of gastroesophageal reflux disease in a population in such a way that superficially, there appears to be a choice between more gastroesophageal reflux disease or multifocal atrophic gastritis. The risk of developing adenocarcinoma of the esophagogastric junction is many times (10-fold to 60-fold) less than the risk of developing gastric cancer from CagA-positive H. pylori infection with multifocal atrophic gastritis - the "protective" lesion.
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PMID:Ulcer and gastritis. 1022 77

Since Helicobacter pylori (Hp) was first isolated in 1983, much work has been carried out on the pathogenic effects of this organism. Hp infection is common in humans and currently is the most important etiologic agent in the development of chronic active gastritis, gastric and duodenal ulcers, carcinoma and Malt-lymphoma of the stomach. Moreover Hp infection has also been associated with various extradigestive diseases. At present, a role of Hp infection in dyspepsia is discussed. Dyspepsia is defined by persistence of pain, burning or discomfort localised to the upper abdomen; some authors include in dyspepsia symptoms such as belching, bloating, alitosis, nausea, postprandial repletion, vomiting and regurgitation. In absence of any underlying pathologies, such as peptic ulcer, gastroesophageal reflux, pancreatitis, biliary tract disease or others, dyspepsia is defined as functional or idiopathic dyspepsia. Functional dyspepsia may be distinct in ulcer, reflux or dysmotility-like dyspepsia and unspecified dyspepsia. Hp infection is common in dyspeptic patients and a role of this bacterium has been postulated mostly in ulcer-like dyspepsia. Mechanisms by when Hp induces dyspeptic symptoms are uncertain; bacterial cytotoxins, phlogosis mediators, activity of chronic gastritis Helicobacter-related and host immune response probably play an important role in pathogenesis of functional dyspepsia. However, dyspepsia is not present only in infected patients; therefore other pathogenic factors may be implicated in expression of dyspeptic symptoms in uninfected subjects, such as gastric dysmotility, modifications of gastric output or altered visceral sensibility, psychological factors, gastroesophageal reflux and irritable bowel.
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PMID:[Dyspepsia and Helicobacter pylori]. 1036 46

Gastroesophageal reflux disease (GERD) is responsible for a high proportion of digestive symptoms attributable to the upper gastrointestinal tract. Helicobacter pylori (H. pylori) is the main etiologic factor in chronic gastritis and gastroduodenal ulcer disease, but its relation with GERD has not yet been established. The aim of this paper is to review the relationship between H. pylori and GERD, trying to answer the question whether a nexus of "friendship" or "hate" exists between them. Although H. pylori may, in theory, represent a cause for GERD, available data suggest that the infection is not a risk factor for the development of GERD, and the microorganism could even represent a protective factor against this disease. The antisecretory effect of proton pump inhibitors (PPIs) seems to depend on the presence of the infection and H. pylori eradication has, therefore, negative consequences on the efficacy of antisecretory drugs (although its possible clinical relevance, precisely in patients with GERD, remains unknown). Moreover, H. pylori eradication in patients with duodenal ulcer disease is associated in some studies, but not in others, with a higher incidence of GERD, although the reported reflux esophagitis is usually mild. It can be concluded, from these data, that investigating or treating H. pylori infection is not recommended in patients with GERD (when these patients do not need PPI maintenance therapy). Finally, it has recently been recommended to eradicate H. pylori infection in those patients with GERD needing long-term treatment with omeprazole, as some studies have reported that this drug induces, in presence of the microorganism, an atrophic gastritis, with the consequent theoretic risk of gastric cancer. However, several arguments against this attitude can be postulated, and noteworthy are the following: many studies suffer important methodological defects, several authors report contrary results, and the possibility that H. pylori could play, as previously mentioned, a protective role against GERD. It may be concluded, therefore, that the indication of eradicating H. pylori in patients with GERD and maintenance therapy with PPIs, although supported by several arguments, cannot be considered as definitively established. In conclusion, H. pylori and GERD seem to have, in any case, a "friendly" relationship, although it may be transformed into one of "hate" when PPIs enter the scene.
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PMID:Helicobacter pylori and gastroesophageal reflux disease: friends or foes? 1037 Jun 61

Adenocarcinomas at the gastroesophageal junction appear to arise from foci of intestinal metaplasia that develop either in the distal esophagus or the proximal stomach (the gastric cardia). Metaplasia is usually a consequence of chronic inflammation, and it is logical to assume that intestinal metaplasia at the gastroesophageal junction develops as a result of chronic inflammation in the epithelia that normally line the junction region. Intestinal metaplasia in the esophagus is known to be a sequela of chronic inflammation in squamous epithelium caused by gastroesophageal reflux disease, whereas intestinal metaplasia in the distal stomach is often a consequence of chronic gastritis caused by Helicobacter pylori infection. For the gastric cardia, the contributions of gastroesophageal reflux disease, H. pylori infection, and other factors to inflammation, metaplasia, and neoplasia are not clear. If physicians are to develop meaningful preventive strategies and specific therapies for tumors of the proximal stomach, a clear understanding of pathogenesis is important. Recent studies on pathogenetic factors for inflammation in cardiac epithelium (gastric carditis) have yielded contradictory results, perhaps because of fundamental differences in the techniques used by different investigators for identifying and sampling the gastric cardia. This report explores the roots of the controversy regarding the role of gastric carditis in the development of metaplasia and neoplasia at the gastroesophageal junction and suggests practical guidelines for biopsy protocols to be used in future studies that will be necessary to resolve these disputes.
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PMID:The role of gastric carditis in metaplasia and neoplasia at the gastroesophageal junction. 1038 31

Antacids are commonly used self-prescribed medications. They consist of calcium carbonate and magnesium and aluminum salts in various compounds or combinations. The effect of antacids on the stomach is due to partial neutralisation of gastric hydrochloric acid and inhibition of the proteolytic enzyme, pepsin. Each cation salt has its own pharmacological characteristics that are important for determination of which product can be used for certain indications. Antacids have been used for duodenal and gastric ulcers, stress gastritis, gastro-oesophageal reflux disease, pancreatic insufficiency, non-ulcer dyspepsia, bile acid mediated diarrhoea, biliary reflux, constipation, osteoporosis, urinary alkalinisation and chronic renal failure as a dietary phosphate binder. The development of histamine H2-receptor antagonists and proton pump inhibitors has significantly reduced usage for duodenal and gastric ulcers and gastro-oesophageal reflux disease. However, antacids can still be useful for stress gastritis and non-ulcer dyspepsia. The recent release of proprietary H2 antagonists has likely further reduced antacid use for non-ulcer dyspepsia. Other indications are still valid but represent minor uses. Antacid drug interactions are well noted, but can be avoided by rescheduling medication administration times. This can be inconvenient and discourage compliance with other medications. All antacids can produce drug interactions by changing gastric pH, thus altering drug dissolution of dosage forms, reduction of gastric acid hydrolysis of drugs, or alter drug elimination by changing urinary pH. Most antacids, except sodium bicarbonate, may decrease drug absorption by adsorption or chelation of other drugs. Most adverse effects from antacids are minor with periodic use of small amounts. However, when large doses are taken for long periods of time, significant adverse effects may occur especially patients with underlying diseases such as chronic renal failure. These adverse effects can be reduced by monitoring of electrolyte status and avoiding aluminum-containing antacids to bind dietary phosphate in chronic renal failure. Antacids, although effective for discussed indications of duodenal and gastric ulcer and gastro-oesophageal reflux disease, have been replaced by newer, more effective agents that are more palatable to patients. Antacids are likely to continue to be used for non-ulcer dyspepsia, minor episodes of heartburn (gastro-oesophageal reflux disease) and other clear indications. Although their wide-spread use may decline, these drugs will still be used, and clinicians should be aware of their potential drug interactions and adverse effects.
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PMID:Antacids revisited: a review of their clinical pharmacology and recommended therapeutic use. 1040 Apr 1

Heartburn is a common symptom affecting 21-44% of the adult population on a monthly basis. Oesophagitis is less common, affecting 2% of individuals. Epidemiological studies have shown that patients with gastro-oesophageal reflux disease (GORD) have similar incidence rates of Helicobacter pylori infection as do controls. Some groups have reported that there is a lower incidence, deducing that infection does not cause, and in some way confers protection against GORD. Additional supportive evidence is available from reports of GORD development following successful H pylori eradication. The mechanisms involved are complicated. Individuals with H pylori induced pangastritis and subsequent hypochlorhydria may be protected whereas those with an antral predominant gastritis, as in duodenal ulcer disease, with an increased acid output may be prone to development of GORD. Recent evidence has linked H pylori infection with the development of inflammation of the gastric cardia---carditis. Reports are available which show that carditis is a frequent finding in patients with GORD. The incidence of both cardia and oesophageal carcinoma is increasing. The relation between GORD, carditis, intestinal metaplasia, and cardia carcinoma is unclear. Intestinal metaplasia may result from multifocal atrophic gastritis, linked to H pylori infection or from GORD and the development of Barrett's oesophagus. Long term follow up studies will be required to assess the malignant potential of these histological entities and whether or not H pylori infection has an aetiological role.
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PMID:Gastro-oesophageal reflux disease and Helicobacter pylori: an intricate relation. 1045 30

Helicobacter pylori is a worldwide infection. In gastro-duodenal ulcer disease no doubt remains about the necessity of H. pylori eradication. Controversies subsisting in other pathologies such gastro-esophageal reflux, dyspepsia, gastritis, gastric adenocarcinoma or MALT lymphoma are reviewed. Multiple drug combinations have been proposed to cure the infection. These are discussed in the clinical setting of Belgian practice.
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PMID:[Controversies in the treatment of Helicobacter pylori]. 1049 76


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