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)

The prevalence of Helicobacter pylori infection increases with age world-wide, reaching levels of 40-60% in asymptomatic elderly subjects and over 70% in elderly patients with gastroduodenal diseases. However, the percentage of H. pylori-positive elderly patients who are treated for their infection remains very low. Data are now available that demonstrate the benefit of curing H. pylori infection in elderly patients with H. pylori-associated peptic ulcer disease and severe chronic gastritis. Furthermore, the cure of H. pylori may prevent the progression of intestinal metaplasia and gastric atrophy. New studies are needed to clarify the role of eradication in elderly patients with non-ulcer dyspepsia and gastro-oesophageal reflux disease and in those who use non-steroidal anti-inflammatory drugs. H. pylori infection may be easily diagnosed by histological evaluation, rapid urease test or culture performed on gastric biopsies taken during endoscopy. However, the biopsy site must be carefully selected in elderly patients. For non-invasive monitoring of H. pylori infection after treatment, the 13C-urea breath test has significantly higher accuracy than serology in the elderly; further studies are needed to clarify the role of the H. pylori stool antigen test in old age. One-week proton pump inhibitor-based triple therapy regimens, including clarithromycin, amoxicillin and/or nitroimidazoles, are highly effective and well tolerated in elderly patients. Low doses of both proton pump inhibitors and clarithromycin (in combination with standard doses of amoxicillin or nitroimidazoles) are sufficient. Low compliance and antibiotic resistance are the main factors related to treatment failure in old age.
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PMID:Review article: an approach to Helicobacter pylori infection in the elderly. 1192 85

Gastro-oesophageal reflux disease is a multifactorial disorder in which the pathophysiological mechanisms are variably combined in different patients. Motor dysfunction of the lower oesophageal sphincter (LOS) and, possibly, the proximal stomach is a major cause of the increase in the number of reflux episodes. Transient LOS relaxation is the main mechanism of reflux in many patients with endoscopically negative disease, whereas a hypotensive LOS becomes relevant only in patients with oesophagitis. Alterations in primary and secondary peristalsis contribute to the increased oesophageal acid exposure by delaying clearance. The presence of a hiatus hernia, especially when voluminous and/or non-reducible, increases the number of reflux episodes by mechanically weakening the oesophago-gastric junction, and impairs oesophageal clearance. Hypersensitivity to acid is often present and contributes to the clinical manifestations of the disease, whereas oesophageal hypersensitivity, both to chemical and mechanical stimuli, plays a predominant role in a subset of patients. Increased concentrations of noxious compounds in the oesophageal refluxate may contribute to the development of anatomical lesions, but this is still a matter for debate. The clinical relevance of Helicobacter pylori infection and of mucosal defensive factors still needs to be fully elucidated.
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PMID:Review article: gastro-oesophageal reflux disease--pathophysiological issues of clinical relevance. 1204 63

The incidence and mortality related to esophageal adenocarcinoma (EAC) have been increasing in the United States, several European countries, and Oceania for the past 2 to 3 decades. Survival remains dismal, with little improvement during the same time period. Variations in the coding, classification, and detection of gastroesophageal malignancy may have contributed partially to the observed trends. Remarkable differences related to gender, ethnicity, and geography characterize the epidemiology of EAC. Gastroesophageal reflux disease (GERD) is the main risk factor for Barrett's esophagus, which is the only known precursor lesion for EAC. Several risk factors that promote the development of GERD and/or Barrett's esophagus have been proposed to explain these rising trends; these factors include the declining rates of Helicobacter pylori infection, obesity, dietary factors, and certain drugs.
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PMID:The epidemic of esophageal adenocarcinoma. 1213 11

Considering that the role of Helicobacter pylori infection in gastroesophageal reflux and reflux esophagitis (GERD) is still controversial and that the role of virulence markers of the bacterium has not been evaluated in most studies of GERD, we investigated the association among H. pylori infection with cagA-positive and -negative strains, corpus gastritis, and GERD in a large group of patients by controlling for confounding factors. We studied prospectively 281 consecutive adult patients: 93 with GERD and 188 controls. H. pylori infection status was diagnosed by culture, by the preformed urease test, with a carbolfuchsin-stained smear, and by histology. The cagA status was determined by PCR of H. pylori isolates and gastric biopsy specimens. H. pylori infection was diagnosed in 191 (68.0%) of 281 patients. Among the 93 patients with GERD, 84 presented with mild or moderate esophagitis and 9 presented with severe esophagitis. In the multivariate analysis, the age of the patients and the degree of oxyntic gastritis were associated with GERD. Among the strains isolated from patients with GERD and from the control group, 24.4 and 66.9%, respectively, were positive for cagA (P < 0.001). Compared to infection with cagA-negative strains, infection with cagA-positive H. pylori strains was associated with a more intense gastritis in the corpus (P = 0.001). cagA status (odds ratio [OR] = 0.16, 95% confidence interval [CI] = 0.07 to 0.40), gastritis of the corpus (OR = 0.69, 95% CI = 0.48 to 0.99), and age (OR = 1.04, 95% CI = 1.01 to 1.07) were associated with GERD. In conclusion, the study provides evidence supporting the independent protective roles of cagA-positive H. pylori strains and the degree of corpus gastritis against GERD.
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PMID:Role of corpus gastritis and cagA-positive Helicobacter pylori infection in reflux esophagitis. 1214 41

Helicobacter pylori infection is recognized to be a pathogen of various gastroduodenal disease. Eradication therapy of H. pylori reduces the recurrence of gastro-duodenal ulcer, improves histological gastritis, and is suggested to act a certain role in protection against gastric carcinogenesis. Although, several studies show uncomfortable results arise after H. pylori infection was cured. These studies suggest that gastro-esophageal reflux disease (GERD) and gastro-duodenal erosion may increase after successful eradication of H. pylori. Recently, adenocarcinoma of the gastric cardia and esophagus increase in incidence. Reflux esophagitis and Barrett's esophagus are recognized as precancerous lesion of esophageal adenocarcinoma. It is uncertain the association of newly occurrence of GERD after H. pylori eradication and increase of esophageal adenocarcinoma. GERD may cause adenocarcinoma development, though long term observations is necessary after H. pylori eradication.
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PMID:[Occurrence of upper gastrointestinal tract disease after Helicobacter pylori eradication]. 1218 64

The prevalence of Helicobacter pylori infection increases with age worldwide. However, the percentage of H. pylori-positive elderly patients who are tested and treated for their infection remains very low. We now have data that demonstrate the benefit of curing H. pylori infection in elderly patients with H. pylori-associated peptic ulcer disease and severe chronic gastritis. Furthermore, the cure of H. pylori may prevent progression of intestinal metaplasia and gastric atrophy. Studies are needed to clarify the role of eradication for elderly patients who have nonulcer dyspepsia, gastroesophageal reflux disease and who use nonsteroidal anti-inflammatory drugs. H. pylori infection may be easily diagnosed by histological evaluation, rapid urease test or culture performed on gastric biopsies taken during endoscopy. However, the biopsy site must be carefully selected in elderly patients. For noninvasive monitoring of H. pylori infection after treatment, the 13C-urea breath test has significantly higher accuracy than serology in the elderly. The role of the H. pylori stool antigen test in old age still needs to be clarified. One-week PPI-based triple therapy regimens including clarithromycin, amoxycillin and/or nitroimidazoles are highly effective and well tolerated in elderly patients. Low doses of both PPIs and clarithromycin (in combination with standard doses of amoxycillin or nitroimidazoles) are sufficient. Antibiotic resistance and low compliance are the main factors related to treatment failure at any age.
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PMID:Helicobacter pylori infection in geriatrics. 1219 11

Helicobacter pylori infection has been recognized as the most important pathogenetic principal of peptic ulcer disease, atrophic gastritis, gastric adenocarcinoma and MALT lymphoma. At the moment efforts are made to clarify it's role in functional dyspepsia, and gastro-esophageal reflux disease. The complex interactions between H. pylori infection and NSAIDs is another field of ongoing research. Diagnosis and eradication therapy are standardized. Established indications are peptic ulcer disease, low-grade gastric MALT lymphoma, early gastric cancer treated by mucosal resection and partial gastrectomy for gastric cancer. Atrophic gastritis, known to be a precancerous lesion, as well as first degree relatives of patients with gastric cancer is another widely accepted indication for eradication therapy. The recommended eradication regimens combine a proton pump inhibitor with clarithromycin and either amoxicillin or metronidazole--for a week.
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PMID:[Helicobacter pylori. Update 2002]. 1250 73

Gastroesophageal reflux disease (GORD) represents an illness which reflects a syndrome caused by returning of acid gastric, alkaline pancreatic and bowels content into the oesophagus, which is in the stomach, because of the protective mechanisms of oesophageal loss. The aim of this study was that this prospective study should explain the role of Helicobacter pylori infection in modification of GORD, respectively whether the Helicobacter pylori infection acts protectively or by deterioration of the disease. According to the settled rules, the inquiry was performed as well as the selection of 97 candidates to undergo research in this study. Helicobacter pylori infection has been proved by immunoassay in all pts in the beginning of this study. Endoscopy has been performed in all pts, the degree of gastroesophageal reflux disease by Sawary-Miller was done. The main group consisted of 50 candidates in whom the eradication of Helicobacter pylori infection was done with triple therapy, pantoprazol + amoxycilin + klaritromicin, which was proven by an immunoassay test. Two groups of pts were formed: the main one with eradicated Helicobacter infection, and a controlled one with a Helicobacter positive infection, which was subject to modification of life style. During 12 months, this study consisted of endoscopic evaluations and monthly evaluation of pts daily difficulties. The eradication of Helicobacter pylori infection acts on the improvement of gastroesophageal disease course by improvement of endoscopic findings by Sawary-Miller, and by decreasing daily acid symptoms. The eradication of Helicobacter pylori infection in gastroesophageal reflux disease does it act at the symptoms such as heartburn, weekly acid symptoms and chest pain.
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PMID:[Effect of eradication of Helicobacter pylori infection on endoscopic findings and symptoms of gastroesophageal reflux]. 1251 34

The falling prevalence of Helicobacter pylori infection and related diseases (peptic ulcer disease, gastric cancer) in developed countries has been paralleled by an increased recognition of gastro-oesophageal reflux and its complications. These epidemiological data do not support a role for H. pylori in the pathogenesis of reflux disease, but suggest a negative association with the increasing incidence of oesophageal diseases. This has led some investigators to propose a 'protective' role of H. pylori infection against the development of oesophageal diseases. In these patients, pre-existing lower oesophageal sphincter dysfunction, susceptibility to reflux, unmasking of latent reflux and the patterns and severity of gastritis are probably important factors contributing to the development of oesophageal diseases. The most likely mechanism by which H. pylori infection may protect against reflux is by decreasing the potency of the gastric refluxate in patients with corpus-predominant gastritis. The prevalence of H. pylori infection in patients with reflux disease is probably no greater than that in those without reflux, and there are conflicting data indicating that reflux symptoms or erosive oesophagitis develop after H. pylori eradication. It is also unclear whether H. pylori augments the antisecretory effects of proton pump inhibitors or accelerates the development of atrophic gastritis.
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PMID:Review article: Helicobacter pylori and reflux disease. 1256 42

Gastroesophageal reflux disease (GERD) is one of the common diseases of the upper gastrointestinal system. It is present in the whole world population, especially frequent in the developed countries. It evolves from pathological reflux which exposes the esophagus to the gastric contents which must overcome esophageal defense system. Many factors have been found to be involved in the pathogenesis of GERD; the most important one is the relaxation of the lower esophageal sphincter. Intensity of the disease is proportional to the amount of gastric contents refluxing from the stomach and the duration of esophageal exposure to this contents. GERD is currently in the spotlight because of its special significance in the development of very specific disease in the lower part of the esophagus--Barrett's esophagus, as well as esophageal adenocarcinoma which has lately been increasing in prevalence. Today, unrecognized and inadequately cured GERD is known to be a high risk factor for adenocarcinoma of the esophagus. In recent years the relation between GERD and Helicobacter pylori infection has been the topic of investigation by many prominent researchers. Therapy of GERD is based on inhibition of acid secretion. There are many different therapeutic agents available, however, proton pump inhibitors (PPI) are considered to be the most effective in the treatment of this disease.
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PMID:[Gastroesophageal reflux disease and Helicobacter pylori infection]. 1259 18


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