Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An algorithmic approach to evaluation of dyspepsia or abdominal discomfort begins with differentiation between peptic ulcer disease and gastroesophageal reflux disease as well as recognition of alarm signs and symptoms for gastric cancer, which are indications for early endoscopy. In the absence of alarm symptoms, most patients should undergo noninvasive testing for H pylori infection with a serologic, urea breath, or stool antigen test. Factors to consider in selection of appropriate testing include reliability, specificity, sensitivity, cost, and local access and expertise. As a general rule, physicians should choose a test that has the best accuracy for the level of testing expertise available. The basic principle underlying testing for H pylori is that patients should not undergo testing unless the physician is willing to treat on the basis of a positive test result. In patients who receive treatment, confirmation of cure is important for preventing further morbidity and reducing risk of transmission of infection.
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PMID:Recognizing peptic ulcer disease. Keys to clinical and laboratory diagnosis. 1008 37

Cancer of the distal stomach, both of the intestinal and diffuse type, is strongly associated with Helicobacter pylori colonization. This bacterium causes chronic active inflammation of the gastric mucosa in the majority of colonized subjects. In a considerable number of them, this will eventually lead to a loss of gastric glands, and thus the establishment of atrophic gastritis, which is associated with the development of intestinal metaplasia and dysplasia. Development of atrophy and metaplasia of the gastric mucosa are thus strongly associated with H. pylori infection, instead of a direct and inevitable consequence of ageing. Approximately 40-50% of infected subjects develop these conditions, but they are rare in non-infected subjects. The presence of these consecutive disorders leads to a 5-90-fold increased risk for cancer of the distal stomach, in particular of the intestinal type. This sequence explains the increased risk for gastric cancer in H. pylori-infected subjects, as has been shown in various cross-sectional and longitudinal studies. In a combined analysis of three longitudinal studies, a significant trend was observed towards an increased odds ratio with longer intervals between (retrospective) serological diagnosis of H. pylori infection and observation of gastric cancer, this risk being more than eight-fold increased if the interval had been at least 15 years. This is thought to reflect development of atrophic gastritis and intestinal metaplasia with loss of H. pylori colonization in the years prior to development of cancer. Atrophic gastritis and gastric cancer thus appear closely associated with the presence of H. pylori, yet not all infected subjects will eventually develop atrophy and only a small minority develop gastric cancer. Factors that influence the risks for atrophy and cancer in the presence of infection may be related to the time that infection occurred and to characteristics of the bacterial strain and the host. Evidence for the role of these factors is now increasing. Recognition of the causal role of H. pylori in the induction of gastric cancer theoretically presents tools for cancer prevention. The efficacy of screening and bacterial eradication for prevention of distal gastric cancer is being studied in a number of large-scale intervention studies in different populations. It is hoped that these studies will also provide answers to the potential preventive role of H. pylori colonization in the development of gastro-oesophageal reflux disease and associated conditions, in particular development of cancer of the proximal stomach. Infection with H. pylori plays an important role in the aetiology of atrophic gastritis and gastric cancer. Studies suggest an eight-fold increased risk for both conditions in the presence of infection. Factors that influence the risk for both conditions in the presence of infection are the age at which infection occurred and the presence of cagA as a marker for more pathogenetic H. pylori strains. The efficacy and side-effects of intervention for the prevention of distal gastric cancer has yet to be established.
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PMID:Review article: exploring the link between Helicobacter pylori and gastric cancer. 1020 81

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

Helicobacter pylori has apparently colonized the human stomach since time immemorial and is superbly adapted for persistence. Several genotypes, including cag+, are associated with increased risk of gastric and duodenal diseases. With modern life, for probably the first time in human history, there are large numbers of noncolonized persons. Duodenal ulceration has been present essentially for only 200 years; that its incidence rose just as H. pylori was waning is best explained by changes in gastric microecology. As H. pylori is disappearing, duodenal ulceration and gastric cancer rates are falling. However, more proximal diseases, gastroesophageal reflux (GERD), Barrett's esophagus, and adenocarcinomas of the gastric cardia and lower esophagus, are increasing; colonization with cag+ H. pylori strains appears protective against these diseases. Thus, in the 21st century, the continuing decline in H. pylori may lead to the disappearance of duodenal ulcers and distal gastric cancers and toward a marked increase in GERD, Barrett's esophagus, and esophageal adenocarcinoma.
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PMID:Hypothesis: the changing relationships of Helicobacter pylori and humans: implications for health and disease. 1066 87

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

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

Helicobacter pylori is now considered a major pathogen of the upper gastrointestinal tract. It is seen as an important cause of peptic ulceration not associated with NSAID use. It is also increasingly linked to other diseases of the GI tract, although the relationship between the organism and conditions such as gastric cancer, non-ulcer dyspepsia and gastroesophageal reflux disease is not as clear as is the case in peptic ulcer disease. This is probably because of a lack of well-performed, statistically powerful, prospective therapeutic trials that indicate that H. pylori eradication is of benefit in these diseases. The high infection rate without overt disease seen in many populations, especially from developing countries, probably contributes to this "credibility gap." While we have excellent therapeutic regimens available at this time, rational targeting requires that the objective evidence in favor of therapeutic intervention in upper GI disease, as well as the local H. pylori epidemiology, needs to be considered.
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PMID:Helicobacter pylori: therapeutic targets. 1037 56

The aim of this article is to summarize the recent progress in geriatric/gastroenterological topics, particularly of the upper gastrointestinal tract, which were the focus of the First International Meeting on Upper Gastrointestinal Diseases in the Elderly, held in Vicenza, Italy, in March 1998. The Meeting was divided into three sections: gastro-oesophageal reflux disease (GORD) in the elderly, Helicobacter pylori infection in the elderly, and nonsteroidal anti-inflammatory drugs (NSAIDs) and the upper gastrointestinal tract in the elderly. GORD presents unique clinical features in elderly patients. The changes in oesophageal function, particularly disorders of motility, only partially explain its unique clinical manifestation. The diagnostic, clinical and therapeutic characteristics of GORD in the elderly need to be studied with attention to avoid its severe local complications, i.e. bleeding, stenosis and Barrett's oesophagus, as well as the more generalized risks of disability, impairment of nutritional status and reduction in the quality of life. Epidemiological studies have demonstrated that the prevalence of H. pylori infection increases with ageing and that subjects living in nursing homes have discrete epidemiological characteristics which render them a high-risk group. The incidence of some histological modifications of the gastric mucosa, particularly intestinal metaplasia, gastric atrophy and gastric cancer, seems to be both age- and H. pylori-related; their study in elderly subjects could give the key to understanding the pathophysiological mechanisms of H. pylori gastric damage. NSAID-related gastroduodenal damage, particularly haemorrhage, increases with age. Ageing, per se, does not modify significantly gastric aggressive factors, such as acid and pepsin secretions; however, a selective and specific reduction in some gastric defensive mechanisms seems to occur with ageing. Clinical studies on prevention of NSAID damage have rarely been performed in an elderly population, and meta-analyses of published data can lead to conflicting conclusions from a pharmaco-economic perspective. The identification of risk factors of NSAID-related gastroduodenal damage must be the foundation of preventive medical care for elderly subjects.
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PMID:Upper gastrointestinal diseases in the elderly: report of a meeting held at Vicenza, Italy, on 20 March 1998. 1044 4

Dyspepsia, according to the internationally accepted Rome criteria, refers to pain or discomfort centred in the upper abdomen; patients with predominant heartburn are excluded from this group, although minor or infrequent heartburn is commonly associated with dyspepsia. It is an important condition not only because it is common and costly, but because it may indicate the presence of serious disease such as peptic ulcer or gastric cancer. However, the most frequent causes of dyspepsia are functional dyspepsia and gastro-oesophageal reflux disease. The discovery of Helicobacter pylori has resulted in important advances in the management of dyspepsia. The clinician faced with a patient who has persistent or recurrent dyspepsia needs to differentiate clearly those patients who have not been previously investigated from patients documented to have functional dyspepsia after investigation (fig 1). Here, the management of H pylori positive dyspeptic patients who have and have not been fully investigated will be reviewed.
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PMID:How should Helicobacter pylori positive dyspeptic patients be managed? 1045 33

Although the incidence of gastric cancer has declined in the past few decades in developed countries, it has remained one of the most frequent malignomas with high mortality. Epidemiological, clinical and basic research studies confirm the role of Helicobacter pylori in the pathogenesis of the tumors of the distal stomach and low-grade MALT lymphomas. On the contrary more and more data suggest a possible protective role of the infection in the gastro-oesophageal reflux disease, tumors of the cardia and adenocarcinoma of the distal oesophagus. The intensive research being done in the past few years prove our previous concept, that the pathogenesis of gastric cancer is a multifactorial process, which is affected by Helicobacter pylori ("a major environmental factor") together with distinct environmental, social and genetic factors. The interaction of these factors and the importance of them urge further investigations, which may differ in different populations.
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PMID:[Helicobacter pylori infection and cancer of the stomach]. 1058 16


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