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

A variety of abnormalities contribute to the development of gastroesophageal reflux disease (GERD) including transient lower esophageal sphincter relaxation, low esophageal sphincter pressure, presence of a hiatal hernia, diminished esophageal clearance of refluxed gastric contents, and alterations in esophageal mucosal resistance. Helicobacter pylori infection clearly plays a role in the pathogenesis of peptic ulcer disease and mucosa associated lymphoma of the stomach and is a definite risk factor for distal gastric cancer. The role of H. pylori infection in GERD remains controversial and incompletely understood. Although H. pylori infection does not cause reflux disease, circumstantial evidence suggests that it may protect against the development of GERD and its complications in some patients. The most likely mechanism whereby H. pylori infection protects against GERD is by decreasing the potency of the gastric refluxate in patients with corpus predominant gastritis. A variety of implications of H. pylori infection on GERD treatment have also arisen in recent years. These focus on the risk of gastric atrophy while on proton pump inhibitor therapy and the efficacy of proton pump inhibitors before and after eradication of H. pylori. This article puts into perspective our current understanding of the complex, incompletely understood relationship between H. pylori infection and GERD.
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PMID:The possible role of Helicobacter pylori in GERD. 1147 51

This review article refers to the impact which Helicobacter pylori infection has on the management of dyspepsia. The answer to the question of whether H. pylori eradication is clinically useful in dyspeptic patients or not remains a controversial and debatable subject. Nonetheless, the recent Maastricht 2 - 2000 Consensus Report, taking into account all the available data so far, concluded that a 'test-and-treat' approach to dyspepsia should be used in adult patients with persistent dyspepsia under the age of 45 years (the cutoff age may vary locally), having excluded those with predominantly gastroesophageal reflux disease symptoms, nonsteroidal anti-inflammatory drug users, and patients with alarm symptoms or a family history of gastric cancer.
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PMID:Impact of H. pylori infection on the management of dyspepsia. 1154 21

The prevalence of Helicobacter pylori infection is steadily decreasing in developing countries, and this has been paralleled by an increasing incidence of gastroesophageal reflux disease (GERD) and adenocarcinomas of the esophagus and of the esophagogastric junction. The prevalence of H. pylori infection, which is on the decline in Europe and in the United States, is probably related to improvements in sanitary conditions and socioeconomic status. These epidemiological data do not support a role for H. pylori in the pathogenesis of GERD, but at the same time suggest a negative association with the rising incidence in esophageal diseases. While H. pylori infection clearly does not cause GERD, it may protect certain susceptible individuals from the development of GERD and its complications. There are conflicting reports that GERD can develop after H. pylori eradication and that proton pump inhibitors are less effective in suppressing intragastric acidity in H. pylori negative patients--reasons not to eradicate H. pylori in GERD patients. On the contrary, other data suggest an increase in the development of atrophic gastritis in GERD patients (H. pylori positive) on long-term proton pump inhibitor therapy - a reason to eradicate H. pylori. Preexisting lower esophageal sphincter dysfunction, susceptibility to GERD, unmasking of latent GERD, and patterns and severity of gastritis may be important factors contributing to the development of GERD rather than just the presence or absence of infection with H. pylori.
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PMID:Helicobacter pylori: a debated factor in gastroesophageal reflux disease. 1154 22

Epidemiological evidence has clearly shown a highly significant relationship between Helicobacter pylori infection and the development of duodenal ulcer and distal gastric adenocarcinoma. Despite H. pylori being a common aetiological factor for both disorders, the two disease phenotypes are virtually mutually exclusive. This indicates that the host response to infection has a pivotal role in determining outcome; these disease phenotypes relate to the effect of infection on gastric acid secretion, duodenal ulcer being closely related to sustained acid secretion whereas gastric cancer follows gastric atrophy and impaired gastric acid secretion. Cancer at the oesophageal junction and that associated with Barrett's oesophagus is now the most rapidly increasing tumour in the gastrointestinal tract. The challenge for the next millennium, therefore, is to try and develop methods for identifying patients at risk of developing oesophagogastric cancer. A common feature in the pathogenesis of both gastric and oesophageal adenocarcinoma is inflammation presenting clinically as gastritis and oesophagitis. The pathway from gastritis to gastric atrophy, dysplasia and carcinoma is thought to be a multi-step process, probably triggered by free radicals within the gastric epithelium and increased exposure to luminal carcinogens. However, it has been unclear as to which aspect of the host response determines whether an individual will move along the neoplasia pathway. Recent work has shown that qualitative aspects of the immune environment in the stomach may account for a substantial part of the phenotypic divergence following H. pylori infection. Interleukin-1 beta polymorphisms relate closely to the propensity for an individual to develop distal gastric cancer and maybe useful for predicting risk in family members. In Barrett's oesophagus, we have recently shown that the immune environment may also be important in determining whether an individual will develop cancer. Although we did not find that Barrett's oesophagus was a profoundly inflammatory condition (unlike esophagitis in the squamous epithelium), where there was evidence of inflammation it was qualitatively different from that of oesophagitis in that a Th-2 response with increased expression of IL-4 predominated in Barrett's, whereas a Th-1 proinflammatory response characterised oesophagitis in squamous epithelium. It seems likely that the specific immune environment within Barrett's metaplasia may be an important driver towards dysplasia and carcinoma. Thus, the immune environment in the stomach and esophagus may be critical in determining whether an individual is at risk of developing neoplastic complications of H. pylori infection and gastroesophageal reflux. Identification of the genetic factors which underpin these responses may ultimately result in development of methods to identify individuals at high risk.
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PMID:Acid, helicobacter and immunity: a new paradigm for oesophagogastric cancer. 1159 70

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

The availability of clinic-based diagnostic tests means that screening for and the eradication of Helicobacter pylori can be done by primary care physicians. However, confusion still exists regarding indication and treatment regimens. It is universally accepted that patients with Helicobacter pylori infection and peptic ulcer disease require eradication therapy. But the benefits of Helicobacter pylori eradication in gastro-oesophageal reflux disease, non-steroidal anti-inflammatory drug-related peptic ulceration, and non-ulcer dyspepsia remain unclear. There is no evidence that the elimination of Helicobacter pylori is beneficial for asymptomatic patients or in preventing gastric cancer. One-week triple therapy with a proton pump inhibitor or ranitidine bismuth citrate in combination with clarithromycin/metronidazole and amoxycillin is the recommended first-line treatment for Helicobacter pylori infection. Problems with patient compliance and the development of antibiotic resistance are the two most important factors to consider when choosing the treatment regimen. The optimal retreatment therapy for treatment failure is still unknown, and quadruple therapy is best reserved for these cases.
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PMID:Treatment of Helicobacter pylori infection. 1182 83

In patients with diseases known to be associated with Helicobacter pylori infection, such as peptic ulcer, treatment of the underlying infection is the standard of care. However, in most major consensus management guidelines, including those published in Canada, widespread testing for H pylori infection is not recommended. This practice is not encouraged because of insufficient evidence of cost-benefit in gastric cancer prevention, the potential for increases in antibiotic resistance and the controversial hypothesis of potential negative effects of eradication in certain clinical entities. For example, there is insufficient evidence to recommend against eradicating H pylori discovered in a patient with symptoms of gastroesophageal reflux disease. The management guidelines designed specifically in Canada should, therefore, continue to be applied, with H pylori diagnosed and treated in appropriately selected patients.
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PMID:Risks and benefits of Helicobacter pylori eradication: current status. 1182 40

Gastro-oesophageal reflux disease (GERD) and Helicobacter pylori infection are common conditions that frequently coexist. Controversy continues regarding the role of H. pylori infection in GERD. The results of some studies suggest that eradication of H. pylori may increase the risk for developing GERD, and some experts have suggested that chronic H. pylori infection may be of benefit. This article reviews the data on H. pylori infection and GERD and its treatment.
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PMID:Review article: gastro-oesophageal reflux disease and Helicobacter pylori infection. 1184 28

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

The management of Helicobacter pylori infection is still surrounded by controversy and uncertainties. Indications and correct application of current regimens for Helicobacter pylori infection are still considered a matter of debate. Regarding indications, only peptic ulcer and mucosa associated lymphoid tissue lymphoma are considered clear indications for treatment. In other conditions, such as atrophic gastritis, post gastric cancer resection, first-degree relatives of gastric cancer patients, dyspeptic patients, patients with gastro-oesophageal reflux disease and non-steroidal anti-inflammatory drug users, the value of Helicobacter pylori eradication is still controversial. The regimens for first-line and second-line treatment of Helicobacter pylori infection have been recommended by the Maastricht 2 Consensus Report. Although all the treatments are considered to be effective, physicians still do not agree on what first-line regimen should be used. Furthermore, a consensus on the duration of the antibiotic treatment is still lacking, although Maastricht guidelines for treatment of Helicobacter pylori infection recommend a one-week therapy. Also regimens, as a third-line treatment, and methods to improve compliance and clinical outcome are still a matter of debate. All these points will be considered in the present review
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PMID:Treatment of Helicobacter pylori infection. Indications and regimens: an update. 1192 76


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