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)

Evidence-based medicine combines clinical expertise and the best available evidence from systematic research to aid decision making in patient care. Levels of evidence can be graded from I to V, with level I, the strongest, coming from large randomized controlled trials (RCTs). When a definitive RCT has not been performed, or is impracticable or inappropriate, lesser grades of evidence are used. There is level I evidence supporting the treatment of Helicobacter pylori infection in patients with duodenal or gastric ulcers. Prospective RCTs have shown that cure of the infection is associated with ultimate cure of the ulcer diathesis. Therefore, this is a "grade A" recommendation for treatment. In nonulcer dyspepsia, numerous RCTs have yielded conflicting results regarding the benefits of treatment. Although there are methodological problems with many reported studies, there is some evidence (level II at best) to support treatment--a grade B recommendation. In early gastric cancer and gastric mucosa-associated lymphoid tissue lymphoma, the best available evidence supporting treatment of H. pylori infection is of low quality, i.e., levels III and V. Although these carry only grade C treatment recommendations, treatment is safe and carries at least some evidence of efficacy. It is therefore indicated based on the current best available evidence. No evidence exists to support treating the infection in patients receiving long-term proton pump inhibitors for gastroesophageal reflux disease or in patients with any of the nongastrointestinal conditions that have been tentatively linked to H. pylori.
 ...
PMID:For what conditions is there evidence-based justification for treatment of Helicobacter pylori infection? 939 70

Several problems are associated with gastric resection, including the dumping syndrome, reflux esophagitis, and malabsorption. A better understanding of the pathophysiological changes will shed light on new and improved therapy. Serum levels of seven circulating gastrointestinal hormones following a standardized solid meal and a brief score of symptoms were evaluated in 10 patients after partial distal gastrectomy and 12 patients after total gastrectomy, both groups reconstructed by Billroth II anastomosis, and 9 age-matched healthy controls. Patients underwent resection for gastric cancer and were studied 45 +/- 10 months after surgery. At the time of study, the patients had adapted well to surgery and no longer exhibited the severe symptoms of dumping seen immediately post-operatively. In contrast, the total gastrectomy patients exhibited the symptoms of reflux esophagitis. The gastrointestinal hormone changes could be divided into three patterns; obtunded responses (gastrin, PP), normal release (motilin, GIP) and increased secretion (CCK, neurotensin, PYY). In these, the early reaction of neurotensin correlated with the scores of late dumping syndrome and reflux esophagitis. In the literature, many gastrointestinal hormones have been shown to respond as an enhancement rather than adaptation. In other gastrointestinal hormones, secretin belonged to the obtunded type and enteroglucagon were classified in the increased type. However, pathophysiological significance of these hormonal changes remained uncertain. The late adaptive changes in gastrointestinal hormone secretion may help to compensate for loss of gastric motor function which accompanies gastric resection. On the other hand, these hormonal changes may exacerbate the esophageal reflux following gastrectomy.
 ...
PMID:Gastrointestinal hormone in dumping syndrome and reflux esophagitis after gastric surgery. 940 15

To assess the pharmacophysiological significance of the enteric nervous system and the responses of the human lower esophageal sphincter (LES) to motilin and cisapride, the mechanical responses of esophageal tissues from six patients with esophageal cancer and seven patients with gastric cancer were investigated. Circular muscle reactions were recorded to evaluate the in vitro esophageal responses to electrical field stimulation (EFS), motilin, and cisapride, evoking the adrenergic and cholinergic nerves before and after treatment with various autonomic nerve blockers. The findings of this study revealed that: cholinergic nerves are mainly involved in the regulation of enteric nerves in the steady state, while non-adrenergic non-cholinergic (NANC) inhibitory nerves also exist; motilin may act both via nerves and also directly on the LES smooth muscle; and cisapride releases acetylcholine from the end of the postganglionic fiber of the cholinergic nerve in human LES thereby inducing contraction of the LES. These results suggest that cholinergic and NANC inhibitory nerves play an important role in human LES, and that motilin and cisapride is clinically useful for improving the impaired LES of patients with gastroesophageal reflux.
 ...
PMID:The role of motilin and cisapride in the enteric nervous system of the lower esophageal sphincter in humans. 941 48

Dyspepsia, defined as "pain or discomfort centered in the upper abdomen" is reported by one in four adults in Western societies. The most important causes are non-ulcer (functional) dyspepsia, peptic ulcer, gastroesophageal reflux, and, rarely, gastric cancer. Persons with heartburn alone are not considered to have dyspepsia. The division of dyspepsia into symptom-based subgroups (ulcer-like, dysmotility-like, reflux-like, and unspecified dyspepsia) has proven to be of doubtful value for the clinician, as it has a low predictive value for identifying the causes of dyspepsia. Upper endoscopy remains the "gold standard" test; ultrasound and blood tests have a low yield. The role of Helicobacter pylori in peptic ulcer disease is well known, but the clinical role of the infection in non-ulcer dyspepsia remains very controversial. In uninvestigated dyspeptic patients who are H. pylori infected based on a non-invasive test, empiric anti-H. pylori therapy is a reasonable and probably cost-effective option. In documented non-ulcer dyspepsia, prokinetics are superior to placebo while antisecretory therapy is of less certain efficacy.
 ...
PMID:Dyspepsia: current understanding and management. 950 76

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.
 ...
PMID:Should Helicobacter pylori be eradicated before starting long-term proton pump inhibitors? 951 35

Dyspepsia is most optimally defined as pain or discomfort centred in the upper abdomen. The symptom complex may be caused by peptic ulcer disease, gastro-oesophageal reflux, or gastric cancer but is most often due to functional (or non-ulcer) dyspepsia. While upper endoscopy is the method of choice to determine the underlying cause of dyspepsia, it is expensive. A more pragmatic approach is needed in the Asia Pacific region where health services are limited. A detailed treatment algorithm is given for managing patients presenting with new-onset dyspepsia and documented functional dyspepsia after endoscopy, and evidence to support this approach is reviewed. Prompt endoscopy is recommended for patients with alarm features. In patients without alarm features, treatment for 2-4 weeks with an empirical anti-secretory or prokinetic agent, followed by investigation using non-invasive Helicobacter pylori testing and treatment for patients who do not respond or relapse, is recommended. Trials of management strategies are now needed to establish the efficacy and cost-effectiveness of the approaches recommended.
 ...
PMID:Management guidelines for uninvestigated and functional dyspepsia in the Asia-Pacific region: First Asian Pacific Working Party on Functional Dyspepsia. 964 Dec 95

Incidence of adenocarcinomas of the esophagus and gastric cardia has risen dramatically over the past 2 decades in the U. S., for reasons that are not yet clear. A number of common medications (e.g., calcium channel blockers, tricyclic antidepressants, and certain asthma medications) promote gastroesophageal reflux by relaxing the lower esophageal sphincter (LES). Reflux is thought to increase cancer risk by promoting cellular proliferation, and by exposing the esophageal epithelium to potentially genotoxic gastric and intestinal contents. Recent studies have suggested that calcium channel blockers may also increase cancer risk by inhibiting apoptosis. Using personal interview data from a multicenter, population-based case-control study conducted between 1993 and 1995 in three areas of the U. S., we evaluated whether the use of LES-relaxing drugs was associated with increased risk of adenocarcinomas of the esophagus and gastric cardia. Cases of esophageal adenocarcinoma (n = 293) and gastric cardia adenocarcinoma (n = 261) were compared with general population controls (n = 695). Information on additional case groups of esophageal squamous cell carcinoma (n = 221) and noncardia gastric cancer (n = 368) were also available for comparison. Overall, 27.4% of controls had used one or more of these drugs for at least 6 months, compared with 30.2% of esophageal adenocarcinoma and 23.8% of gastric cardia adenocarcinoma cases. The adjusted odds ratios (ORs) for ever use were 1.0 [95% confidence interval (CI) = 0.7-1.5] and 0.8 (95% CI = 0.5-1.1), respectively. There was little evidence of increasing risk with increasing duration of use of all LES-relaxing drugs together. We found an increased risk of esophageal adenocarcinoma among persons reporting use of asthma drugs containing theophylline (OR = 2.5; 95% CI = 1.1-5.6) or beta agonists (OR = 1.7; 95% CI = 0.8-3.8). Risks were higher among long-term users (>5 years) of these drugs (OR = 3.1; 95% CI = 0.9-10.3 and OR = 2.3; 95% CI = 0.8-7.0, respectively). In contrast, there was no evidence that the use of calcium channel blockers or other specific groups of drugs increased the risk of any of the cancers studied. These results provide reassuring evidence that the increases in incidence of adenocarcinomas of the esophagus and gastric cardia are not likely to be related to the use of LES-relaxing drugs as a group, or calcium channel blockers in particular, but they do suggest that persons treated for long-standing asthma may be at increased risk of esophageal adenocarcinoma.
 ...
PMID:Risk of esophageal and gastric adenocarcinomas in relation to use of calcium channel blockers, asthma drugs, and other medications that promote gastroesophageal reflux. 975 82

Peptic ulcer disease and gastric cancer of the antrum and body have been declining in the 20th century. In contrast, a new group of diseases are increasingly rapidly in Western countries: gastroesophageal reflux disease, Barrett's esophagus, and adenocarcinoma of the distal esophagus. Recent studies suggest this phenomenon may be related to the simultaneous fall in the prevalence of Helicobacter pylori (H. pylori) colonization, especially by the virulent cagA + strains. H. pylori infection with the cagA+ strain is potentially protective against the spectrum of gastroesophageal reflux disease because it lowers intragastric acidity as the result of a pangastritis, frequently with multifocal gastric atrophy and possibly increased intragastric ammonia production. Assuming that some types of H. pylori strains are protective, our entire approach to the worldwide elimination of this organism, sometimes indiscriminately, will need critical reevaluation.
 ...
PMID:Helicobacter pylori and gastroesophageal reflux disease: the bug may not be all bad. 1052 Aug 76

Helicobacter pylori gastritis (i.e. H. pylori infection and complications) is a focus of tremendous research activity today. Besides peptic ulcer disease, a large number of reports suggest that other diseases are associated with H. pylori. The International Agency for Research on Cancer sponsored by the World Health organization classified the bacterium as a group I carcinogen in 1994. Population-based studies of H. pylori and gastric cancer in 1991 showed an increased odds ratio, of 3-6, in infected patients, and a calculation of odds ratios in different age groups showed a markedly increased odds ratio, to about 20, in younger ages. Studies of non-ulcer dyspepsia and the effect of cure of H. pylori show either none, small, or significant symptom relief, suggesting a positive effect in a subgroup of non-ulcer dyspepsia patients. Mucosa-associated lymphoid tissue-lymphoma caused by H. pylori could be eradicated, at least in its mild forms. Barrett's ulcer is a possible H. pylori-associated disease as well as gastroesophageal reflux disease. Normal feedback in the acid regulation system is changed in infected patients, which may facilitate an increased gastroesophageal acidic reflux. Gastropathy and/or peptic ulcer due to use of nonsteroidal antiinflammatory drugs is probably aggravated by the infection. The infectious disease H. pylori gastritis is associated with a large number of complications, some of which are serious. There are no data showing any advantages of the infection. Giving anti-H. pylori therapy to infected patients should be regarded as essential.
 ...
PMID:Are there more clinically important complications of Helicobacter pylori infection than peptic ulcer disease? A review of current literature. 984 18

Helicobacter pylori (H. pylori) is the most common cause of peptic ulcers, and is considered as carcinogenic with respect to gastric cancer and MALT lymphoma. The role of H. pylori in other gastroduodenal diseases like atrophic gastritis and functional dyspepsia has been investigated in hundreds of works, but little is done about what role H. pylori may play in non gastric diseases. Gastro-esophageal reflux disease does not seem to be related to H. pylori but Barrett's esophagus might be. Inflammatory bowel diseases tend to be reverse correlated with H. pylori. In coronary heart disease some studies have shown a connection, others not. Diabetes is not likely to be H. pylori-associated and nor do liver diseases with exception for cirrhosis, where a correlation is possible. Respiratory diseases are little examined but bronchiectasis might have a correlation with H. pylori. A small series of children, who had died in sudden infant death, showed a high rate of H. pylori infection.
 ...
PMID:Non-gastric effects of H. pylori infection: a literature review with respect to non gastric diseases which might be associated with H. pylori infection. 1002 62


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