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

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.
 ...
PMID:The role of gastric carditis in metaplasia and neoplasia at the gastroesophageal junction. 1038 31

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.
 ...
PMID:Upper gastrointestinal diseases in the elderly: report of a meeting held at Vicenza, Italy, on 20 March 1998. 1044 4

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.
 ...
PMID:Gastro-oesophageal reflux disease and Helicobacter pylori: an intricate relation. 1045 30

Dyspepsia is a digestive syndrome distinct from (although frequently overlapping with) gastro-oesophageal reflux disease (GORD) and irritable bowel syndrome (IBS), which is characterised by various combinations of painful and non-painful symptoms arising from the epigastrium. Dyspepsia can be secondary to a variety of diseases, but in most instances it is idiopathic. Helicobacter pylori infection is responsible for the majority of peptic ulcers and of other diseases potentially associated with dyspepsia. Nevertheless, a causal role for H pylori infection in symptom occurrence has not been established. Experimental data indicate that H pylori eradication does not improve symptoms in the majority of dyspeptic patients. It has been proposed recently that H pylori negative patients should be managed according to their clinical presentation. Some reports suggest that taking into consideration the most relevant or "predominant" symptom may help to identify distinct subgroups among dyspeptic patients with different underlying pathophysiological abnormalities and different responses to treatment. Well designed and conducted prospective studies are needed to verify whether treatment of H pylori negative dyspeptic patients based on the predominant symptom actually is a cost effective approach.
 ...
PMID:How should Helicobacter pylori negative patients be managed? 1045 34

Currently, the influence of Helicobacter pylori infection on gastro-oesophageal reflux disease is a major focus of attention because it is an issue that is relevant to so many patients. There is accumulating evidence that it is the severity of H. pylori-induced gastritis that determines whether clinically relevant effects occur within individual patients. Several lines of evidence suggest that there is a protective effect against reflux disease if gastritis is severe enough to cause elevation of gastric pH above 3 for significant parts of the 24 h cycle. Conversely, H. pylori eradication would be expected to increase the risk of reflux disease if previously substantially reduced acid secretion recovers significantly as a result of healing of corpus gastritis. This analysis indicates that the interaction of H. pylori and reflux disease should differ for duodenal ulcer patients, who do not have major reductions of acid secretion, and for gastric ulcer or atrophic gastritis patients, who do. Available data that have assessed the effects of H. pylori eradication are especially difficult to interpret in patients with chronic peptic ulcer, because of several important confounding factors. In the case of duodenal ulcer, the available studies are very conflicting, and few have been published in full. For the most relevant patient group, those whose primary problem is reflux disease, there are currently no data available on the effects of H. pylori eradication.
 ...
PMID:Helicobacter pylori and reflux disease. 1050 24

The incidence of adenocarcinoma of the distal esophagus is increasing at an alarming rate. Intestinal metaplasia in the distal esophagus, i.e. Barrett's esophagus, has been identified as the single most important risk factor for these tumors. Barrett's esophagus develops as a consequence of chronic mucosal injury in up to 10% of patients with long-lasting gastroesophageal reflux disease. Experimental and clinical data indicate that adenocarcinoma of the distal esophagus is a direct consequence of mixed (i.e., acid and bile) reflux into the esophagus. Interestingly, Helicobacter pylori infection of the stomach appears to exert a protective effect against the development of esophageal adenocarcinoma. Neither aggressive medical acid suppression nor antireflux surgery can induce a predictable regression of Barrett's esophagus or exert a protective effect against its malignant degeneration. Endoscopic ablation of Barrett's esophagus, although appealing, currently constitutes a potentially dangerous procedure without proven benefit for the patient. Since the development of Barrett's adenocarcinoma follows a multistep process from metaplasia through increasingly severe grades of dysplasia, close endoscopic surveillance with extensive biopsies currently remains the only means to identify patients at risk for malignant degeneration and detect esophageal adenocarcinoma at an early and curable stage.
 ...
PMID:Malignant degeneration of Barrett's esophagus: clinical point of view. 1069 37

AIMS: There is an increasing awareness that short (less than 3 cm) segments of Barrett's epithelium and macroscopically normal cardia epithelium may harbour specialized intestinal metaplasia (SIM), a premalignant phenotype. This was a prospective study of both the prevalence of SIM in an unselected population of patients attending for endoscopy, and the association of SIM with symptoms, lifestyle, medication, endoscopic oesophagitis and carditis. METHODS: Two hundred consecutive patients underwent endoscopy. Biopsies taken from just below the squamocolumnar junction were stained for SIM, and were analysed for carditis and Helicobacter pylori infection. A detailed questionnaire of symptoms, tobacco consumption and the use of proton pump inhibitors was completed. RESULTS: Forty-two patients (21 per cent) had SIM, 19 of 126 (15 per cent) in an endoscopically normal oesophagus, 15 of 63 (24 per cent) in a short segment of Barrett's epithelium and eight of 11 in classical Barrett's oesophagus. Comparative analysis between the SIM positive and negative groups with respect to potential risk factors is outlined below. Table 1. CONCLUSION: SIM is prevalent in patients undergoing endoscopy, does not correlate with symptoms or with H. pylori infection, but is significantly associated with endoscopic and pathological markers of gastro-oesophageal reflux.
 ...
PMID:Specialized intestinal metaplasia: analysis of prevalence, risk factors and association with gastro-oesophageal reflux disease 1071 66

The gastric cardia is a microscopic zone that is normally found in the most proximal portion of the stomach, although cardiac-type mucosa may arise in the distal esophagus as a metaplastic phenomenon secondary to gastroesophageal reflux disease (GERD). Inflammation of the native gastric cardia is strongly associated with Helicobacter pylori infection, although there may be a second form of 'carditis' in which metaplastic cardiac-type mucosa becomes inflamed secondary to GERD. Intestinal metaplasia of the cardia may be difficult to recognize because of the difficulty in accurately identifying the esophagogastric junction by endoscopy and the histologic similarities of intestinal metaplasia in the proximal stomach and distal esophagus. However, cytokeratin 7 and 20 immunoreactivity patterns appear to be useful in distinguishing between these forms of intestinal metaplasia. The preponderance of data suggests that intestinal metaplasia of the cardia is associated with H. pylori infection as opposed to GERD, and preliminary data suggest a lower risk of progression to dysplasia and adenocarcinoma when compared to intestinal metaplasia of the distal esophagus.
 ...
PMID:Inflammation and intestinal metaplasia of the gastric cardia: Helicobacter pylori, gastroesophageal reflux disease, or both. 1072 33

In the MUSE classification of gastroesophageal reflux disease (GERD), esophagitis is assessed by the presence of metaplasia, ulcer, stricture, or erosion, each being graded as absent, mild or severe. Daily reflux symptoms affect about 4 to 7 percent of the population; erosive esophagitis occurs in about 2 percent; the prevalence rate of Barrett's metaplasia is 0.4 percent; and esophageal adenocarcinoma leads to two deaths per million living population. In persons with GERD symptoms, about 20 percent are found to have erosive esophagitis, while ulcers or strictures are found in less than 5 percent of all patients with erosive esophagitis. No clear-cut temporal progression exists between successive grades of disease severity, as the most severe grade of GERD is reached at the onset of the disease. Mild forms of GERD tend to be more common in women than men, while severe GERD characterized by erosive esophagitis, esophageal ulcer, stricture or Barrett's metaplasia are far more common in men than women. All forms of GERD affect Caucasians more often than African Americans or Native Americans. The prevalence of GERD is high among developed countries in North America and Europe and relatively low in developing countries in Africa and Asia. During the past three decades, hospital discharges and mortality rates of gastric cancer, gastric ulcer and duodenal ulcer have declined, while those of esophageal adenocarcinoma and GERD have markedly risen. These opposing time trends suggest that corpus gastritis secondary to Helicobacter pylori infection protects against GERD. This hypothesis is consistent with the geographic and ethnic distributions of GERD. Case-control studies also indicate that cases with erosive esophagitis are less likely to harbor active or chronic corpus gastritis than controls without esophagitis.
 ...
PMID:Clinical epidemiology and natural history of gastroesophageal reflux disease. 1078 May 69

Our knowledge of Helicobacter pylori infection is now changing the way in which we investigate patients presenting with dyspepsia, with noninvasive H. pylori testing replacing endoscopy. Non-invasive H. pylori testing has been shown to be useful in predicting the underlying diagnosis in patients presenting with dyspepsia. Several studies have shown that 20-50% of dyspeptic patients with a positive H. pylori test will have evidence of underlying ulcer disease or duodenitis. In contrast, less than 5% of dyspeptic patients with a negative H. pylori test will have evidence of ulcer disease and in these subjects, the likeliest diagnosis is gastroesophageal reflux disease. This has led to many groups recommending that noninvasive H. pylori testing should be used in place of endoscopy, with all those testing positive being given anti-H. pylori therapy and those testing negative being treated symptomatically. One concern about nonendoscopic management of dyspeptic patients is the possibility of missing underlying malignancy but studies have shown that in western countries this is rare in patients less than 55 years of age presenting with dyspepsia in the absence of sinister symptoms. There is increasing evidence supporting eradication of H. pylori infection in dyspeptic patients without ulcer disease. Meta-analysis of four prospective randomized trials indicates that such treatment is superior to placebo in about 10% of subjects. H. pylori-positive dyspeptic patients are also recognized to have an increased risk of developing ulcer disease in the future which will be removed by treating the infection. Another justification for eradicating the infection in the absence of ulcer disease is the fact that H. pylori infection is now proven to be a risk factor for gastric cancer. Prospective randomized studies comparing endoscopy with noninvasive H. pylori testing in the management of dyspeptic patients indicate that managing dyspepsia by noninvasive H. pylori testing is at least as effective as endoscopic-based management in producing symptomatic resolution and saves a substantial number of endoscopic procedures. There is therefore now substantial evidence indicating that noninvasive H. pylori testing should be used in place of endoscopy to determine the management of younger dyspeptic patients without sinister symptoms and who are not taking nonsteroidal anti-inflammatory drugs.
 ...
PMID:Should non-invasive Helicobacter pylori testing replace endoscopy in investigation of dyspepsia? 1082 49


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>