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

The publication of the National Institutes of Health Consensus Development Conference guidelines on management of Helicobacter pylori infection in 1994 set a precedence. At present, at least eight European countries have produced national guidelines, and, more recently, the European Helicobacter pylori Study Group also outlined guidelines based on the strength of available evidence. It is generally agreed that H. pylori should be eradicated in peptic ulcer disease. In nonsteroidal anti-inflammatory drug (NSAID)-related ulcers, most countries that considered the issue suggested discontinuing NSAIDs when possible and eradicating H. pylori. The prophylactic eradication of H. pylori was not recommended. A number of panels felt that there was not enough evidence available to recommend eradication of H. pylori in functional dyspepsia, whereas other groups felt that nonulcer dyspepsia, particularly after investigation and with severe or recurrent symptoms, was an indication for eradication therapy. Other conditions (i.e., gastroesophageal reflux disease [GERD] and mucosa-associated lymphoid tissue [MALT] lymphoma) have emerged in this short time as possible indications for H. pylori eradication. There is no evidence that H. pylori infection has a role in the pathogenesis of GERD, but there is evidence suggesting that patients with H. pylori infection who require long-term acid suppression may be at risk of developing atrophic gastritis. The European Helicobacter pylori Study Group has suggested that eradication therapy should be offered to infected family members of patients with gastric cancer. It also recommended that eradication therapy was "strongly recommended" on the basis of "supportive" evidence in gastritis with severe abnormalities and after early resection of early gastric cancer. An "uncertain" recommendation with "equivocal" evidence was given for asymptomatic subjects, extra-alimentary tract disease, the prevention of gastric cancer in the absence of risk factors, and in pediatric patients with recurrent abdominal pain. Despite considerable advances, further research studies are needed to provide definite direction for the treatment of many conditions.
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PMID:Who should be treated for Helicobacter pylori infection? A review of consensus conferences and guidelines. 939 69

Evidence-based medicine combines clinical expertise and the best available evidence from systematic research to aid decision making in patient care. Levels of evidence can be graded from I to V, with level I, the strongest, coming from large randomized controlled trials (RCTs). When a definitive RCT has not been performed, or is impracticable or inappropriate, lesser grades of evidence are used. There is level I evidence supporting the treatment of Helicobacter pylori infection in patients with duodenal or gastric ulcers. Prospective RCTs have shown that cure of the infection is associated with ultimate cure of the ulcer diathesis. Therefore, this is a "grade A" recommendation for treatment. In nonulcer dyspepsia, numerous RCTs have yielded conflicting results regarding the benefits of treatment. Although there are methodological problems with many reported studies, there is some evidence (level II at best) to support treatment--a grade B recommendation. In early gastric cancer and gastric mucosa-associated lymphoid tissue lymphoma, the best available evidence supporting treatment of H. pylori infection is of low quality, i.e., levels III and V. Although these carry only grade C treatment recommendations, treatment is safe and carries at least some evidence of efficacy. It is therefore indicated based on the current best available evidence. No evidence exists to support treating the infection in patients receiving long-term proton pump inhibitors for gastroesophageal reflux disease or in patients with any of the nongastrointestinal conditions that have been tentatively linked to H. pylori.
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PMID:For what conditions is there evidence-based justification for treatment of Helicobacter pylori infection? 939 70

Reflux esophagitis is one of the most common disorders of the upper gastrointestinal tract. It can lead to obstruction through stricture formation, in more severe form to bleeding through ulceration, and to cancer development through the association of Barrett's esophagus. The vast majority of esophagitis can be managed medically. Medical management is separated into two categories: (1) life style modification and (2) drug therapy. Drug therapy includes antacids, prokinetics, sucralfate, H2 receptor antagonists (H2-RAs) and proton pump inhibitors (PPIs). Among these, antisecretory therapy is the mainstay for the treatment. PPIs are shown to be superior to H2-RAs in healing of esophagitis and symptom relief. Recurrence, particularly of erosive esophagitis, is common without maintenance therapy. PPIs are also consistently superior to H2-RAs in maintenance of esophagitis healing. Interestingly, a recent report has suggested that curing Helicobacter pylori infection may provoke reflux esophagitis, raising the possibility that the gastroesophageal reflux diseases become more common in the future. Therefore, treatment strategy for reflux esophagitis needs to be re-established in terms of the future cost-effectiveness evaluation and quality-of-life assessments.
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PMID:[Recent topics in the medical treatment of reflux esophagitis]. 948 79

Symptomatic gastro-oesophageal reflux disease is a common disorder characterized by pathological exposure of the distal oesophagus to acid. The management requires the control of symptoms, prevention of relapse and complications. Proton pump inhibitors are without doubt the most effective agents in the management of gastro-oesophageal reflux disease. In Helicobacter pylori-negative individuals the efficacy of ranitidine, but more pronounced of omeprazole, on the nocturnal intragastric acidity, is less than in Helicobacter pylori-positive patients. Curing the Helicobacter pylori infection in gastro-oesophageal reflux disease patients might, therefore, have the disadvantage of losing efficacy of antisecretory therapy. Conversely, several studies have shown that long-term use of proton pump inhibitors is associated with progression and worsening of body gastritis exclusively in Helicobacter pylori-positives. This observation makes Helicobacter pylori eradication indicated before starting long-term treatment with proton pump inhibitors for gastro-oesophageal reflux disease and other acid-related diseases. The data reported, so far, however, are not conclusive. The Federal Drugs Administration Advisory Committee concluded on available data, that there is no evidence that longterm proton pump inhibitors treatment leads to gastric atrophy, intestinal metaplasia or gastric cancer. Eradication of Helicobacter pylori infection might lead to reduction in the efficacy of antisecretory agents, but might prevent worsening of the gastric corpus gastritis. More data are needed to really answer these clinically relevant questions.
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PMID:Should Helicobacter pylori be eradicated before starting long-term proton pump inhibitors? 951 35

New approaches to the grading of reflux oesophagitis and the definition of reflux disease have been proposed which should improve the precision of descriptions of this common problem. Endoscopy and 24-hour pH monitoring studies, though of great value, have significant limitations for assessment of reflux disease. Only about one third of reflux disease patients have oesophageal mucosal erosion or ulceration. Analysis of symptoms is probably the most useful method for diagnosis. Further research is needed into the best strategies for maximising the potential of symptom analysis. In the pathogenesis of reflux disease, Helicobacter pylori infection is not a major factor but the interaction of H. pylori gastritis and eradication therapy are important areas of great current interest. Troublesome reflux disease arises primarily from abnormally frequent gastro-oesophageal reflux, though heightened oesophageal mucosal sensitivity and defective oesophageal clearance play a role in some patients. Transient lower oesophageal sphincter relaxation appears to be the most important mechanism of reflux. This distinctive, swallow-independent type of lower oesophageal sphincter relaxation has a complex triggering system, apparently located in the brain stem. Medical and surgical treatments of reflux disease are now well characterised and have improved very substantially over recent years. Drugs that inhibit the occurrence of transient lower oesophageal sphincter relaxation are an intriguing possible future therapy.
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PMID:Gastro-oesophageal reflux disease. 970 29

A cross sectional study was designed to elucidate the factors influencing the argyrophil cell population in patients with gastroesophageal reflux disease treated with omeprazole (N = 201) or H2-receptor antagonists (N = 118) and in control patients (N = 215). Fasting gastrinemia and Helicobacter pylori serology were determined. Gastritis, Helicobacter pylori infection, and argyrophil cell density and hyperplasia were evaluated in gastric biopsies. The argyrophil cell density was higher in both treatment groups than in controls (P = 0.002 and P = 0.051), whereas argyrophil cell hyperplasia was similar in the three groups. According to multivariate analysis, positive Helicobacter pylori serology was an independent parameter that decreased both density and grade of hyperplasia of argyrophil cells. Female gender and hypergastrinemia were independent factors increasing argyrophil cell density and hyperplasia, whereas antisecretory therapy, age and active gastritis were not. In addition, atrophic gastritis independently increased argyrophil cell hyperplasia. The prevalence of atrophic gastritis was significantly higher in Helicobacter pylori-positive than in negative patients and lower in the patients treated long-term with omeprazole than in the other groups.
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PMID:Factors influencing corpus argyrophil cell density and hyperplasia in reflux esophagitis patients treated with antisecretory drugs and controls. 972 42

Available evidence would suggest that Helicobacter pylori infection does not contribute to the pathogenesis of gastro-oesophageal reflux disease. The prevalence of H pylori infection in patients with reflux disease is no greater than that in control populations. There are some data suggesting that the organism has a protective role: patients with duodenal ulcers develop reflux disease after H pylori eradication, whereas in patients with oesophageal reflux those with H pylori infection have less severe reflux changes. There is also evidence indicating that the presence of H pylori augments the anti-secretory properties of both the H2 receptor antagonists and proton pump inhibitors (PPIs), suggesting that eradication therapy may not be beneficial. However, the considerable recent interest in the association between H pylori and reflux disease has largely been generated by studies outlining the interactions between H pylori infection and acid suppression in the long term. In H pylori positive patients, therapy with PPIs is associated with a proximal extension of the infection and its associated gastritis. In addition long term PPI therapy is reported to be associated with an accelerated development of atrophic gastritis, suggesting that H pylori should be diagnosed and treated. Although these latter findings in particular need confirmation, H pylori eradication therapy should be considered in this patient group, at least until there is evidence to the contrary.
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PMID:Different management for Helicobacter pylori positive and negative patients with gastro-oesophageal reflux disease? 976 33

To explore the potential contributions of gastroesophageal reflux disease, as opposed to Helicobacter pylori infection, to the development of gastric carditis, we evaluated gastric carditis (using the criteria of the updated Sydney system for the classification of gastritis), clinical and morphologic features of esophagitis, and H. pylori infection (evaluation of Steiner stains) in biopsy specimens from the gastroesophageal squamocolumnar junction. We correlated clinical, endoscopic, and histologic features in an unselected group of 116 patients. Some degree of carditis was found in 107 (92%) of the patients. The mean age of the patients increased with increasing severity of carditis (P < .05). The various groups of patients with different degrees of carditis did not differ significantly in sex ratio, ethnic background, presence of obesity, percentage having symptoms of gastroesophageal reflux disease (such as heartburn, regurgitation, dysphagia, or odynophagia), endoscopic evidence of esophagitis and columnar epithelium in the distal esophagus, or histologic evidence of active esophagitis. The presence, however, of active gastritis and H. pylori infection in the distal stomach and/or in the cardia was significantly associated with carditis. In patients without carditis, H. pylori was not detected in any cardiac or distal gastric biopsy specimen. In contrast, H. pylori was demonstrated in gastric tissue samples (either from the cardia or distally) of patients with carditis, with the prevalence rate increasing with greater degrees of cardiac inflammation. The H. pylori prevalence rate was 12% in the group with mild carditis, 40% in those with moderate carditis, and 57% in patients with marked carditis (P = .0001). In summary, carditis is commonly found in patients with symptoms related to upper gastrointestinal diseases. From analysis of our study cohort, we concluded that carditis was significantly associated with H. pylori infection and active gastritis but not with symptoms or signs of gastroesophageal reflux disease. These findings suggest that carditis with histologic features similar to those of gastritis in the distal stomach was a sequel of H. pylori infection and represented a part of an H. pylori--associated gastric inflammation.
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PMID:Gastroesophageal reflux disease versus Helicobacter pylori infection as the cause of gastric carditis. 979 21

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

The aim of the present review is to summarize the most recent progress in gastroenterological topics, particularly of the upper gastrointestinal tract, which are of special interest in the elderly. The changes in oesophageal function, particularly disorders of motility, may explain, only in part, the unique clinical characteristics of oesophageal pathologies in the elderly. Dysphagia and gastro-oesophageal reflux disease present diagnostic, clinical and therapeutic characteristics that need to be studied with attention to avoid eventual disability, an impairment of nutritional status and a reduction in the quality of life. Aging, per se, does not significantly modify gastric aggressive factors, however, a selective and specific reduction in some gastric defensive mechanisms seems to occur with aging. The prevention of gastric mucosal injury, particularly that due to drugs, requires a better understanding of these age-related changes. Helicobacter pylori infection in the elderly presents peculiar epidemiological aspects particularly for subjects living in nursing homes. An understanding of Helicobacter pylori-related histological modifications of the gastric mucosa, particularly intestinal metaplasia, gastric atrophy and gastric cancer, the incidence of which seems to be both age- and Helicobacter pylori-related, is greatly needed. Moreover, some diagnostic and therapeutic aspects of Helicobacter pylori infection, i.e., the role of serology and the efficacy, side effects and compliance of drug therapies, are specific for the elderly and require a unique clinical approach. Bleeding is dramatically more frequent in this population. The identification of risk factors, i.e., drugs, pathophysiological mechanisms, i.e., the possible relationship between non-steroidal anti-inflammatory drugs and Helicobacter pylori infection, along with the clinical presentation in the elderly patient, must be the foundation of preventive medical care in geriatric gastroenterology.
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PMID:Aging and the gastrointestinal tract. 1036


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