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)

From August 1987 through July 1988, we evaluated antral biopsy specimens for Campylobacter pylori (CP) in 212 patients undergoing upper endoscopy. For those patients who had multiple endoscopies, the first endoscopy in which a urease test, histology, and culture were done was used to determine CP status. A patient was regarded as CP-positive if the culture was positive or if both a urease test and the histology were positive. Blacks had an increased CP positivity (61.2%) compared to whites (31.5%). Among non-ulcer patients, CP positivity was 52% in black patients and 18% in white patients. Age and gender were unrelated to CP positivity among controls and those without ulcers. There was increased CP positivity in patients with duodenal ulcers (85%), compared with those without ulcers (37%), and a trend toward increased positivity in those with gastric ulcer (53%) and duodenitis (50%). There was no increased CP positivity in patients with gastroesophageal reflux disease (28%), gastritis (29%), non-ulcer dyspepsia (43%), or the control patients with no gastroduodenal mucosal abnormalities (40%). CP-negative DU patients were older (average 71 yr) than CP-positive DU patients (43 yr), and female DU patients had a lower CP positivity (71%) than males (94%).
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PMID:Prevalence of Campylobacter pylori in patients undergoing upper endoscopy. 272 34

Helicobacter pylori is an important factor in the pathogenesis of chronic gastritis and gastroduodenal ulcer disease. However, the basic causal mechanisms of H pylori colonization on the gastric mucosa are still unclear. The authors evaluated the prevalence of H pylori colonization in 266 children who underwent upper gastrointestinal endoscopy during a 12-month period. The indications for endoscopy were follow-up of esophagitis related to gastroesophageal reflux (n = 17), suspicion of gastroesophageal reflux (n = 51), abdominal pain (n = 28), vomiting (n = 30), follow-up of esophageal atresia (n = 46) and duodenal atresia (n = 28), inflammatory bowel disease (n = 28), and miscellaneous (n = 38). The methods used to detect H pylori colonization were histology and the rapid urease test. H pylori colonization was demonstrated in 31 (11.6%) of the 266 patients. In two patient groups, a high prevalence of colonization was identified. In patients with an operated duodenal atresia, 36% (10 of 28) had H pylori on the gastric mucosa. The organism was demonstrated on the gastric mucosa in 47% (8 of 17) of the patients with gastroesophageal reflux-related esophagitis; five of the eight patients had neurological impairment. In the other patient groups, the prevalence of H pylori infection ranged from 2% to 14%. The present study suggests that, in children, the disturbed esophagogastroduodenal motility, which is commonly associated with gastroesophageal reflux and duodenal atresia, predisposes to H pylori infection.
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PMID:Does disordered upper gastrointestinal motility predispose to Helicobacter pylori colonization of the stomach in children? 807 8

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output > 10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence of Helicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis). Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P < 0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found among Helicobacter pylori-positive compared to Helicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr were Helicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence of Helicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.
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PMID:Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion. 842 Jul 45

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

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

Rabeprazole sodium is a new substituted benzimidazole proton pump inhibitor with several differences compared with existing proton pump inhibitors. In vitro and animal studies have demonstrated that rabeprazole is a more potent inhibitor of H+,K(+)-ATPase and acid secretion than omeprazole, and is a more rapid inhibitor of proton pumps than omeprazole, lansoprazole, or pantoprazole. This probably reflects rabeprazole's faster activation in the parietal cell canaliculus. In human studies, once-daily doses of 5-40 mg of rabeprazole inhibit gastric acid secretion in a dose-dependent fashion. A once-daily dose of 20 mg has consistently achieved profound decreases in 24-h intragastric acidity in single and repeat dosing studies, in healthy volunteers and patients with either peptic ulcer disease or gastro-oesophageal reflux disease. Significantly greater decreases in intragastric acidity are achieved on day 1 of dosing with rabeprazole 20 mg than with omeprazole 20 mg. As with other proton pump inhibitors, rabeprazole has in vitro antibacterial activity against Helicobacter pylori, with greater activity against this organism than either lansoprazole or omeprazole. In addition to inhibiting bacterial urease activity, rabeprazole binds to several molecules on H. pylori. Clinical trials are needed to assess the clinical importance of these findings, as well as to assess whether the potential advantages of rabeprazole result in clinical benefit for patients with acid-related diseases.
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PMID:Review article: the pharmacology of rabeprazole. 1049 23

The transmission of Helicobacter pylori may occur by spread of organisms from gastric juice which has been introduced into the mouth by gastro-oesophageal reflux. The aim of this study was to quantify the load of H. pylori present in gastric juice available for transmission. Gastric antral biopsy and gastric juice samples were collected from 108 adult dyspeptic patients undergoing routine upper gastroscopy and the presence of H. pylori was determined. In all, 54 (50%) of 108 patients gave positive results in the gastric antral biopsy rapid urease test and for H. pylori histology. The gastric juice of 40 (37%) of patients gave positive results for the urease A gene by PCR assay; 34 (31%) of patients were positive by these three tests and H. pylori was cultured from the gastric juice of 13 (38%) of these patients. The median count of H. pylori in gastric juice was 1.75 x 10(1) cfu/ml. Viable organisms in gastric juice may lead to transmission of H. pylori when refluxed or vomited into the mouth.
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PMID:Quantitative culture of Helicobacter pylori from gastric juice: the potential for transmission. 1075 28

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

The precise role of Helicobacter pylori infection in gastroesophageal reflux disease (GERD) is a matter of intense debate. Twenty-four-hour esophageal pH monitoring has a higher accuracy than endoscopy for the diagnosis of GERD, but the correlation between H. pylori infection and esophageal pH-metric parameters has almost never been assessed. Therefore, we evaluated the relationship between the infection and the presence of disturbances not only in endoscopy but also in 24-hour esophageal pH monitoring. One hundred consecutive patients undergoing 24-hour esophageal pH monitoring because of symptoms suggestive of GERD were included in the study. Esophageal manometry was carried out to study the position and the pressure of the lower esophageal sphincter (LES). Prevalence of H. pylori infection was evaluated by histology (hematoxylin and eosin stain) and rapid urease test. The mean age of the patients was 50 +/- 15 years; 50% were men and 56% had an abnormal pH-metry (DeMeester score more than 14.7). The prevalence of H. pylori in patients with abnormal pH-metry was 57% (95% CI, 42-70%) and was 52% (95% CI, 39-64%) in those with normal pH-metry (nonsignificant differences [NS]). In the multivariate analysis, H. pylori infection did not correlate with an abnormal pH-metry (odds ratio, 0.8; 95% CI, 0.4-1.8; NS). The proportion of cases with abnormal pH-metry among infected patients was 54% (95% CI, 41-66%) and was 59% (95% CI, 44-72%) among uninfected patients (NS). Mean values of pH-metric parameters (+/-SD), respectively for H. pylori-positive and -negative patients, were total score (30 +/- 33 vs. 36 +/- 38), number of reflux episodes (7 +/- 7 vs. 11 +/- 11), number of episodes more than 5 minutes (3.7 +/- 5 vs. 3.8 +/- 5), longest reflux episode (2.4 +/- 2 minutes vs. 3.1 +/- 3 minutes), and fraction time (%) with pH less than 4 (total, 6 +/- 7 vs. 6.8 +/- 8; upright, 3.9 +/- 4 vs. 4.5 +/- 5; supine, 7.4 +/- 12 vs. 7.2 +/- 10) (all findings were NS). Endoscopic findings, respectively for H. pylori-positive and -negative, were hiatus hernia (41% vs. 41%), endoscopic esophagitis (Savary-Miller) (54% vs. 46%), and Barrett's esophagus (15% vs. 11%) (all findings were NS). Finally, differences were not demonstrated in the pressure of the lower esophageal sphincter (12 +/- 8 mmHg vs. 14 +/- 12 mmHg) among H. pylori-positive and -negative patients. H. pylori infection is not associated with gastroesophageal reflux disease, as evaluated endoscopically and with 24-hour esophageal pH monitoring.
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PMID:Helicobacter pylori and gastroesophageal reflux disease: lack of influence of infection on twenty-four-hour esophageal pH monitoring and endoscopic findings. 1124 45

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


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