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

Alkaline gastroesophageal reflux (GER) is a controversial concept for the pathogenesis of non-infectious esophagitis in the absence of measurable acid GER. Excessive duodenogastric reflux, as it can be seen in antroduodenal motility disorders, seems to be prerequisite. Yet, bile acids, a marker for duodenal secretions, are more frequently found during acid than during alkaline GER. Moreover, it has not been possible to show mucosal toxicity by bile acids or trypsin when tested at concentrations similar to those measured in esophageal refluxate. It remains therefore questionable as to whether alkaline pH measured in the esophagus results from reflux of duodenal contents or if it is a sign of increased salivary or esophageal secretions, and if the analogy of gastritis and esophagitis secondary to biliary reflux is allowed. Alkaline GER more probably is an erroneous pathogenic concept for esophagitis which requires intensified antacid therapy.
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PMID:[Is alkaline gastroesophageal reflux an etiology for esophagitis?]. 948 42

Next to headache recurrent gastro-intestinal complaints constitute the most common reason for medical consultation among daycare and school children. The use of more sophisticated examination methods has shown that in up to 50 per cent of cases the cause of the gastric complaints is a treatable disease or a functional anomaly of the gastro-intestinal tract. The commonest conditions are lactose intolerance, gluten sensitivity, gastro-oesophageal reflux, and gastritis. In some cases stomach pain is triggered by psychosomatic mechanisms. Depending upon the child's age, aetiological indications can sometimes be derived from history taking. In many cases the investigations can be made in the out-patient clinic. The cornerstones of treatment are various kinds of dietary elimination regimens, prokinetic agents, and antibiotics. Recently, the investigation of neuroendocrinological and neurophysiological processes related to psychosomatic causes of gastric complaints has once again become common.
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PMID:[Recurrent stomach complaints in children]. 965 64

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

The pattern of Helicobacter pylori gastritis depends on acid secretion. Profound acid suppressive therapy with proton pump inhibitors leads to a decrease of antral gastritis, but an increased severity of corpus gastritis. As such, maintenance therapy with these drugs for gastroesophageal reflux disease has consistently been associated with an increased incidence of atrophic gastritis in H. pylori infected patients. For this reason, the preventive effect of H. pylori eradication in these patients needs to be considered; this is being studied in prospective trials.
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PMID:[Reflux esophagitis; is the preventive eradication of Helicobacter pylori needed in patients on omeprazole?]. 962 81

H. pylori is found in the stomach of patients with chronic gastritis. The infection is usually transmitted by the gastro-oral route and bacteria could be identified in saliva and dental plaque. An essential cause of chronic laryngitis is gastroesophageal reflux. The aim of the study was to evaluate if a H.pylori-associated chronic laryngitis exists. 38 patients with chronic laryngitis underwent gastroscopy. Biopsies were taken from the gastric antrum and body, lower, middle and upper esophagus. H. pylori was diagnosed by rapid urease test and histology. 14 of the patients (36.8%) were H.pylori-positive, but the bacteria could not be identified between stomach and larynx. 24 patients were H. pylori-negative. Seven patients (18.4%) suffered from esophagitis, six of these patients were H. pylori-negative. The H. pylori-infected patients received triple therapy for one week, in case of esophogitis Omeprazole 20 mg BID was prescribed. Six weeks later a follow-up endoscopy was performed. The eradication rate was 12/14 (85.7%), in all patients with reflux the esophagitis was cured. The laryngitis was clinically and endoscopically unchanged in ten of the twelve (83.3%) patients after successful treatment for H. pylori; in the remaining two patients as well as in the two H. pylori-positive patients the laryngitis was improved. In six out of the seven patients with esophagitis the laryngitis had healed completely and was improved in the remaining patient. It may be concluded that there is no evidence for the existence of H. pylori-associated laryngitis, suggesting that acid reflux is the underlying etiology.
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PMID:[Is chronic laryngitis associated with Helicobacter pylori? Results of a prospective study]. 965 3

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

Two problems can be identified as possible long term negative consequences of HP eradication: diminished efficacy of acid-lowering drugs, and an accelerated development of GERD. It was shown that omeprazole produces a greater decrease in gastric acidity in subjects with H. pylori infection than in those who are H. pylori negative, and that omeprazole produces a smaller decrease in gastric acidity after cure of H. pylori. This effect persisted for at least one year after HP eradication. It is not limited to omeprazole, but can also be seen with the H2 receptor antagonist ranitidine. At least one proven mechanism involved in this phenomenon is the disappearance of the alkalinizing effect of ammonia, generated from urea by HP's urease, after eradication of the bacteria; other mechanisms may also be involved. HP eradication may therefore potentially hamper acid inhibitory treatment. It is unknown to what extent this is clinically relevant. Although one study did not observe a relation between H. pylori status and efficacy of omeprazole maintenance therapy for GERD, it cannot be excluded that some patients may need more potent or higher doses of acid-lowering medication after HP eradication. Three studies suggest that duodenal ulcer patients who were successfully treated with H. pylori eradication therapy, may be at increased risk to develop GERD. Labenz's study finds that the incidence of GERD may be double 3 years after eradication. The life-table analysis suggested that cure of the infection was associated with an increased risk of reflux oesophagitis during the first year after treatment, whereas later the incidence of reflux oesophagitis was similar in both groups. Patients who developed reflux oesophagitis after the cure had a more severe body gastritis before cure, gained weight more frequently after cure, and were predominantly men. There are no data on the fate of the oesophagus after HP eradication in patients with reflux oesophagitis. The data thus strongly suggest that there is a risk for developing reflux oesophagitis after HP eradication in patients with duodenal ulcer. It is unknown whether HP eradication in patients without duodenal ulcer also increases the risk for developing reflux oesophagitis.
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PMID:Adverse events of HP eradication: long-term negative consequences of HP eradication. 979 71

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


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