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)

Rabeprazole, a new proton pump inhibitor, was studied in patients with acid-peptic-related diseases (duodenal ulcer, gastric ulcer, GERD) in three placebo-controlled, double-blind, randomized clinical trials. Men and women over the age of 18 were enrolled if the presence of an active duodenal or gastric ulcer or erosive or ulcerative esophagitis was confirmed on upper gastrointestinal endoscopy. Patients were randomly allocated to either placebo or rabeprazole 20 mg or 40 mg in the duodenal and gastric ulcer protocols or to placebo or rabeprazole 10 mg, 20 mg, or 40 mg in the GERD protocol. All doses of rabeprazole in all three studies were statistically significantly superior to placebo in healing acid-related lesions. There were no treatment differences between the rabeprazole doses in healing active peptic lesions. The incidence of positive [13C]urea breath test for H. pylori was 53% in patients with duodenal or gastric ulcers. H. pylori status was not effected by treatment with rabeprazole.
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PMID:Rabeprazole in treatment of acid peptic diseases: results of three placebo-controlled dose-response clinical trials in duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease (GERD). The Rabeprazole Study Group. 959 Apr 13

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

An algorithmic approach to evaluation of dyspepsia or abdominal discomfort begins with differentiation between peptic ulcer disease and gastroesophageal reflux disease as well as recognition of alarm signs and symptoms for gastric cancer, which are indications for early endoscopy. In the absence of alarm symptoms, most patients should undergo noninvasive testing for H pylori infection with a serologic, urea breath, or stool antigen test. Factors to consider in selection of appropriate testing include reliability, specificity, sensitivity, cost, and local access and expertise. As a general rule, physicians should choose a test that has the best accuracy for the level of testing expertise available. The basic principle underlying testing for H pylori is that patients should not undergo testing unless the physician is willing to treat on the basis of a positive test result. In patients who receive treatment, confirmation of cure is important for preventing further morbidity and reducing risk of transmission of infection.
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PMID:Recognizing peptic ulcer disease. Keys to clinical and laboratory diagnosis. 1008 37

Clinicians are familiar with the concepts of sensitivity and specificity to describe the accuracy of a diagnostic test. These measures do not always express the probability that a patient has a disease with a given test result as this will vary with the prevalence of the disorder in the population. The likelihood ratio is a more clinically relevant method of reporting accuracy, and the probability of having a disease after a positive or negative test can be calculated. The likelihood ratio can be applied to the clinical problem of dyspepsia management. This suggests that Helicobacter pylori (H. pylori) test and treat will detect and treat most peptic ulcers with only 0.5% of H. pylori-negative patients having peptic ulcer disease. Serology is possibly acceptable in populations with an H. pylori prevalence of approximately 50%. The urea breath tests are more appropriate in more extreme prevalence ranges. Once the prevalence of H. pylori falls below 10%, then the urea breath test becomes inaccurate, and screening and treatment may be less appropriate. The absolute probability of having peptic ulcer disease in a largely H. pylori-negative population will be very small, however, and the appropriateness of performing any investigation in these circumstances is debatable. Finally, likelihood ratios indicate that the clinical diagnosis of gastroesophageal reflux disease (GERD) is not straightforward. Traditionally, it is believed that patients with dominant heartburn are likely to have GERD. Likelihood ratios predict, however, that patients with these symptoms have a little over 50% chance of having GERD as defined by 24-h esophageal pH studies.
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PMID:The usefulness of the likelihood ratio in the diagnosis of dyspepsia and gastroesophageal reflux disease. 1056 1

In-depth meetings of the XIth International Workshop on Gastroduodenal Pathology and Helicobacter pylori led to the presentation and discussion of extensive new data on H. pylori and its diseases. The mode of transmission of H. pylori remains unclear, and it remains unknown why only a small proportion of infected individuals develop duodenal or gastric ulcer disease and even fewer develop gastric cancer. The role of H. pylori eradication in persons with uninvestigated dyspepsia remains controversial. New clinical trials of H. pylori treatment show symptom relief and improvement in the quality of life of persons with functional dyspepsia, especially in those with ulcer-like or reflux-like dyspepsia. Clearly the move is toward symptom-based management of persons with dyspepsia, with fewer endoscopies being needed in the otherwise healthy young dyspeptic patients. It remains controversial whether eradicating H. pylori in duodenal ulcer or functional dyspepsia increases the risk of subsequent development of gastroesophageal reflux disease. The one-week proton pump inhibitor-based triple regimens remain the gold standard of H. pylori therapy, but some of the ranitidine bismuth citrate plus two antibiotic regimens also achieve an 80% H. pylori eradication rate on an intention-to-treat basis. While the urea breath test remains the noninvasive test of choice, interesting new data are available on the use of stool antigen testing to diagnose H. pylori infection. The number of H pylori-associated gastroduodenal diseases grows to include possible liver, vascular, immune and skin conditions.
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PMID:From bench to bedside to bug: an update of clinically relevant advances in the care of persons with Helicobacter pylori- associated diseases. 1075 16

This review focuses on the gastric acid pump as a therapeutic target for the control of acid secretion in peptic ulcer and gastro-oesophageal reflux disease. The mechanism of the proton pump inhibitors is discussed as well as their clinical use. The biology of Helicobacter pylori as a gastric denizen is then discussed, with special regard to its mechanisms of acid resistance. Here the properties of the products of the urease gene clusters, ureA, B and ureI, E, F, G and H are explored in order to explain the unique location of this pathogen. The dominant requirement for acid resistance is the presence of a proton gated urea transporter, UreI, which increases access of gastric juice urea to the intrabacterial urease 300-fold. This enables rapid and continuous buffering of the bacterial periplasm to approximately pH 6.0, allowing acid resistance and growth at acidic pH in the presence of 1 mM urea. A hypothesis for the basis of combination therapy for eradication is also presented.
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PMID:Review article: the control of gastric acid and Helicobacter pylori eradication. 1106 9

Significant progress and new insights have been gained in the 4 years since the first Maastricht Consensus Report, necessitating an update of the original guidelines. To achieve this, the European Helicobacter Pylori Study Group organized a meeting of specialists and experts from around the world, representatives from National Gastroenterology Societies and general practitioners from Europe to establish updated guidelines on the current management of Helicobacter pylori infection. The meeting took place on 21-22 September 2000. A "test and treat" approach is recommended in adult patients under the age of 45 years (the age cut-off may vary locally) presenting in primary care with persistent dyspepsia, having excluded those with predominantly gastro-oesophageal reflux disease symptoms, non-steroidal anti-inflammatory drug users and those with alarm symptoms. Diagnosis of infection should be by urea breath test or stool antigen test. As in the previous guidelines, the eradication of H. pylori is strongly recommended in all patients with peptic ulcer, including those with complications, in those with low-grade gastric mucosa-associated lymphoid tissue lymphoma, in those with atrophic gastritis and following gastric cancer resection. It is also strongly recommended in patients who are first-degree relatives of gastric cancer patients and according to patients' wishes after full consultation. It is advised that H. pylori eradication is considered to be an appropriate option in infected patients with functional dyspepsia, as it leads to long-term symptom improvement in a subset of patients. There was consensus that the eradication of H. pylori is not associated with the development of gastro-oesophageal reflux disease in most cases, and does not exacerbate existing gastro-oesophageal reflux disease. It was agreed that the eradication of H. pylori prior to the use of non-steroidal anti-inflammatory drugs reduces the incidence of peptic ulcer, but does not enhance the healing of gastric or duodenal ulcer in patients receiving antisecretory therapy who continue to take non-steroidal anti-inflammatory drugs. Treatment should be thought of as a package which considers first- and second-line eradication therapies together. First-line therapy should be with triple therapy using a proton pump inhibitor or ranitidine bismuth citrate, combined with clarithromycin and amoxicillin or metronidazole. Second-line therapy should use quadruple therapy with a proton pump inhibitor, bismuth, metronidazole and tetracycline. Where bismuth is not available, second-line therapy should be with proton pump inhibitor-based triple therapy. If second-line quadruple therapy fails in primary care, patients should be referred to a specialist. Subsequent failures should be handled on a case-by-case basis by the specialist. In patients with uncomplicated duodenal ulcer, eradication therapy does not need to be followed by further antisecretory treatment. Successful eradication should always be confirmed by urea breath test or an endoscopy-based test if endoscopy is clinically indicated. Stool antigen test is the alternative if urea breath test is not available.
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PMID:Current concepts in the management of Helicobacter pylori infection--the Maastricht 2-2000 Consensus Report. 1186 Mar 99

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

Previous studies showed that either the urease activity possessed by H. pylori and the bacterial load may influence the results of the [13C] urea breath test. However, the correlation between urease activity and dyspepsia is unclear. The aim of our study was to evaluate whether the urease activity of the gastroduodenal tract may influence the severity of dyspeptic symptoms. In all, 2520 dyspeptic patients (1109 men, 1411 women; mean age 47 +/- 16 years) without gastroesophageal reflux disease, diabetes, vascular disorders, liver and biliary tract diseases, and tumors of the gastrointestinal tract and with a normal appearing abdominal ultrasonography were enrolled. All these patients underwent a [13C] urea breath test and filled out a questionnaire on dyspeptic symptoms. Subjects were divided in five different groups according to delta over baseline (DOB) values (group 1 < 3.5, group 2 = 3.5-6; group 3 = 6.1-11, group 4 = 11.1-23, group 5 > 23.1). The prevalence and intensity of dyspeptic symptoms were compared among groups. In all, 1688 patients (67%, 928 females and 760 males; mean age 48 +/- 15 years) were H. pylori-positive. The chi-squared test and analysis of variance showed increase of frequency and intensity of each dyspeptic symptom according to DOB values. In conclusion, Dyspepsia may parallel gastric urease activity. However, whether higher DOB values are related to higher bacterial load or, alternatively, to the presence of particular H. pylori strains able to produce larger amounts of urease is uncertain.
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PMID:Delta13CO2 excretion and expression of dyspeptic symptoms in patients evaluated for Helicobacter pylori infection by [13C] urea breath test. 1199 14

Treatment recommendations for H. pylori infection are peptic ulcer disease, MALT lymphoma, atrophic gastritis and following gastric cancer resection as well as first degree relatives of gastric cancer patients. Advisable situations are functional dyspepsia, before introduction of NSAID's or intended long-term proton-pump inhibitor treatment. It is thought that eradication therapy is not associated with gastro-esophageal reflux disease and does not enhance NSAID induced peptic ulcer healing. Therapy should be given as a package which considers first and second line eradication therapies together; in uncomplicated duodenal ulcer patients, eradication therapy does not need to be followed by further antisecretory treatment. First line therapy should be with triple therapy using a proton pump inhibitor (PPI), combined with clarithromycin and amoxycilline or metronidazole. Second-line therapy should use a quadruple therapy with a PPI, bismuth, metronidazole and tetracycline. Where bismuth is not available, second line therapy should be with a PPI triple therapy. If second line quadruple therapy fails in primary care, patients should be referred to the specialist and handled on a case by case basis. Successful eradication should always be confirmed by urea breath test (UBT), or endoscopy-based tests if endoscopy is clinically indicated. Stool antigen test is the alternative if UBT is not available. A 'test and treat' approach based on non-invasive testing can be offered to adult patients presenting in primary care with persistent dyspepsia under the age of 45 years (the age cut-off may vary locally), having excluded those with predominantly gastroesophageal reflux disease (GERD) symptoms, NSAID users, and patients with alarm symptoms.
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PMID:[Helicobacter pylori--2002]. 1207 Oct 78


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