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 relationship between Helicobacter pylori (H. pylori) infection and gastroesophageal reflux disease (GERD) is not well known yet, and has some controversial issues. There is indirect epidemiological evident, not yet proven, that H. pylori may have a protective role against GERD. Hypochlorhydria caused by gastritis located mainly at corpus would be the principal physiopathological protector mechanism against GERD. Even knowing that more studies are needed, the risk of developing GERD after the H. pylori eradication seems to be increased in some groups of patients. In the presence of the microorganism, the efficacy of acid suppression therapy may decrease, and its long-term use could favour the progression to corpus atrophic gastritis. Specialized intestinal metaplasia in an endoscopically normal-appearing cardia may precede adenocarcinoma, and its prevention would vary, depending on its controversial origin, secondary to carditis, H. pylori or GERD.
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PMID:[Gastroesophageal reflux and Helicobacter pylori]. 1089 71

This article reviews the following gastrointestinal infections: esophagitis, gastritis, duodenitis including duodenal ulcers, and enteritis (gastroenteritis). The epidemiology, risk factors, microbiology and pathogenesis, diagnosis, treatment, morbidity/mortality, and prevention are discussed in relation to the most important pathogens. The symptoms and pathogenesis of esophagitis caused by Candida albicans and herpes simplex are contrasted with the symptoms of esophagitis caused by Helicobacter pylori and gastroesophageal reflux disease (GERD). The incidence of gastritis and gastric and duodenal ulcers caused by H. pylori is discussed. The treatment regimens of H. pylori infection recommended by the CDC are presented. Endoscopic findings in esophagitis, gastritis, and duodenal ulcers are presented and discussed. The difference in symptoms caused by viral agents (Norwalk virus), bacterial agents (enterotoxigenic E. coli), and parasites (Giardia lamblia and Cryptosporidium parvum) are compared and contrasted. The symptoms of infections of the terminal small bowel caused by Salmonella and Campylobacter jejuni and the symptoms of pure colonic infection, dysentery, caused by Shigella and enteroinvasive E. coli and Entamoeba histolytica are discussed. The treatment regimens for enteritis are presented.
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PMID:Infectious diseases of gastrointestinal tract in adolescents. 1091 24

The 1998 Guidelines of the American College of Gastroenterology recommend that diagnostic testing for Helicobacter pylori infection should only be performed if treatment is intended, and that testing for H. pylori is not indicated in patients on long-term treatment with a proton pump inhibitor (PPI) for gastro-oesophageal reflux disease (GORD). Moreover, a recent evidence-based workshop evaluating major clinical strategies for the management of GORD reported, with an 'A' category (maximum of evidence), that eradication of H. pylori does not heal or prevent relapse of GORD. In detail, it seems that H. pylori infection per se has no effect on the pathogenic mechanisms determining either reflux or its complications. The relationship between H. pylori and oesophagitis is mediated by the effect of H. pylori on gastric acid secretion; in particular, by the proximal extension of gastritis and related impairment of gastric secretory function. In general, if the corpus is infected, the amount of acid available for reflux is less and the probability of excessive oesophageal acid exposure leading to oesophagitis reduced. However, the clinical relevance of corpus H. pylori infection as a biological antisecretory agent (and of H. pylori eradication) seems small or absent, at least in the long run. Conversely, the previous claim of an increased risk of atrophic gastritis in H. pylori-infected patients treated long term with PPI drugs appears not to be confirmed by subsequent studies. In conclusion, H. pylori infection may, in some circumstances, be moderately favourable and, in other circumstances, it may be neutral, with respect to the management of GORD.
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PMID:Should we eradicate Helicobacter pylori in patients with recurrent gastro-oesophageal reflux disease? 1092 92

The relationship between gastro-oesophageal reflux disease (GERD) and Helicobacter pylori is unclear. Recent data indicate that H. pylori probably exerts a protective effect against GERD. In recent years, the interaction between H. pylori, proton pump inhibitors and GERD has been widely studied. Currently available proton pump inhibitors produce significantly higher intragastric pH in H. pylori-positive patients than in those who are H. pylori negative, and this phenomenon may be clinically relevant. The mechanisms responsible for this difference in efficacy are not fully understood, although there are two major theories. Ammonia, produced by H. pylori, is able to neutralize gastric acid, and thus apparently increase the effect of acid suppressive agents (the 'ammonia theory'). The other theory is that decrease in acid output is due to the development of corpus gastritis during treatment with a proton pump inhibitor (the 'gastritis theory'). Treatment strategies to overcome this lowered sensitivity to acid suppression are to increase the frequency/dose of a proton pump inhibitor or to add an H2-receptor antagonist in the evening-but both have pharmaco-economic implications. An agent that could provide adequate pH control regardless of H. pylori status would be highly beneficial in the treatment of GERD, and may also lower treatment costs.
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PMID:Review article: the clinical influence of Helicobacter pylori in effective acid suppression-implications for the treatment of gastro-oesophageal reflux disease. 1093 Aug 91

The aim of the study was to evaluate the incidence and the etiology of Mallory-Weiss syndrome in children. The study population comprised 2720 children aged 5 months to 18 years who had undergone upper gastrointestinal endoscopy. Mallory-Weiss syndrome was diagnosed in eight (0.3%) of the examined children. Endoscopic examination in five of them revealed linear mucosal tears, mostly above and in one case also below the gastroesophageal junction. In three children a linear scar in the lower portion of the esophagus was seen. No signs of active bleeding were revealed in any of the cases. In four children, Mallory-Weiss syndrome was accompanied by gastritis and duodenitis; two of these children had Helicobacter pylori infection. The concomitant diseases were H. pylori-positive duodenal ulcer (1), bronchial asthma and gastroesophageal reflux disease (1), carbon monoxide poisoning (1). In one case Mallory-Weiss syndrome was diagnosed in early pregnancy. Mallory-Weiss syndrome should be considered, along with others, as a cause of acute upper gastrointestinal bleeding in children. There is a great variety of etiologic factors in Mallory-Weiss syndrome in children.
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PMID:Mallory-Weiss syndrome in children. 1094 65

From 1992-1995 in Victoria Hospital Republic of Seychelles 1037 patients undergone esophago-gastro-duodenoscopic examination. Ulcer was find in 26% patients, gastritis in 23.5%, gastroesophageal reflux in 15.9%, upper gastro-intestinal bleeding in 13.5%., carcinoma of the esophagus in 6%, gastric ulcer in 2.8%, hiatus hernia in 3%, esophageal varices in 2.1%, gastric carcinoma in 2.1% and 0.3% with polyps.
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PMID:[Endoscopy of the esophagus, stomach and duodenum at Victoria Hospital--Seychelles]. 1095 16

The latest accessible data indicate, that Helicobacter pylori (H.p.) infection, particularly by cagA-positive strains, protects against the development of gastroesophageal reflux disease (GERD) and its complications. Various epidemiological, pathophysiological and clinical studies demonstrate this protective effect, which is dependent on the extent of H.p. induced gastritis. Severe corpus gastritis may cause a profound reduction of acid secretion. In regard to acute or chronic PPI therapy of GERD the biological antisecretory effect of H.p. is of minor benefit. Development of atrophic gastritis in patients with GERD treated chronically with PPI is still uncertain. On account of the protective effect of H.p. against GERD, it is prudent to reserve H.p. eradication for the well-established indications.
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PMID:[Helicobacter pylori and gastroesophageal reflux disease]. 1098 81

Concerning the relationship between Helicobacter pylori infection and gastro-oesophageal reflux disease (GORD), the debate is ongoing whether the infection confers protection, is harmful or whether both entities are independent. Epidemiological evidence is given for an increased prevalence of GORD and a decreased prevalence of H. pylori infection in the western world. The assumpton derived from it is that H. pylori protects from GORD. Pathophysiological aspects need to consider the type and expression of gastritis which is associated with varying changes of gastric function. Depending on the type of gastritis, acid secretion may either increase or decrease and thereby impact on acid exposure of the oesophagus. Other changes related to the role of H. pylori in pathophysiology of GORD are still hypothetical. Clinical data are controversial whether or not GORD increases after H. pylori eradication. Prospective studies including characterization of strains and gastric physiology will clarify this issue. An accelerated induction of gastric mucosal atrophy in patients on long-term proton pump inhibitors is reported in most available studies. An increase of inflammatory activity in fundic and corpus mucosa is a consistent phenomenon. Therefore, in the authors' opinion, eradication appears advisable.
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PMID:Helicobacter pylori infection and gastro-oesophageal reflux disease: coincidence or association? 1100 6

H. pylori infection is associated with various gastroduodenal diseases such as gastritis, peptic ulcer, gastric cancer, gastric MALT lymphoma. H. pylori infection is suggested that it plays a role as protective factor not promoting factor for reflux esophagitis and GERD. Epidemiological studies showed lower prevalence of H. pylori infection in reflux esophagitis and Barrett's esophagus comparing the control. Increased occurrence of reflux esophagitis after curing of H. pylori infection was reported. However, the relationship between H. pylori infection and reflux esophagitis has not been actually made clear. Also the mechanism of reflux esophagitis occurrence after H. pylori eradication is not obscure.
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PMID:[Helicobacter pylori infection and eradication]. 1100 6

Sucralfate is a cytoprotective drug widely used in clinical practice to prevent or treat several gastrointestinal diseases such as gastro-esophageal reflux, gastritis, peptic ulcer, stress ulcer and dyspepsia. Sucralfate is a safe and well tolerated drug, as demonstrated by the quite complete lack of side effects and it is, for this reason, one of the most important therapeutic choices in the management of acid related diseases during pregnancy. Moreover, sucralfate has recently been shown to be useful in non-acid related gastrointestinal disease as well. In fact, sucralfate has also been administered topically in patients with radiation-induced mucosal procto-sigmoiditis or ulcerative colitis with surprising results. The drug is actually able to form a physical barrier between epithelium and damaging agents (-bile salts, drugs, refluxate...). Moreover, sucralfate increases the local levels of fibroblast growth factors and induces a rise in the mucosal concentration of prostaglandins which are considered important factors in mucosal healing. The aim of this paper is to describe the current and probably forthcoming uses of sucralfate in the field of gastrointestinal disorders. Moreover, we investigate the role of sucralfate as a reliable means to prevent the occurrence of reflux-like symptoms after Helicobacter pylori eradication and in the management of Helicobacter pylori negative patients affected by non-ulcer dyspepsia.
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PMID:Role of sucralfate in gastrointestinal diseases. 1101 6


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