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

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.
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PMID:Helicobacter pylori and gastroesophageal reflux disease: the bug may not be all bad. 1052 Aug 76

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

Gastro-oesophageal reflux (GOR) is a common phenomenon in infants, which may occur with or without accompanying symptoms. Although most infants presenting with regurgitation have a normal physical examination, it is now recognized that infants may also present with a wide variety of symptoms. Oesophagitis is associated with increased oesophageal acid exposure. The determination of cause and effect is difficult, as there are many aspects of reflux disease where cause and effect relationships are cyclic. Reflux disease is present when there is an imbalance between a number of factors that can contribute to a decrease, as well as an increase, of GOR. Oesophageal pH monitoring with a semi-disposable monocrysant antimony pH catheter with three sensors is very good at documenting oesophageal acidification and gastric buffering and, therefore, quantifies acid reflux frequency and duration. However, the interpretation of the data is complex as they are influenced by numerous factors, such as position, activity (sleep, crying), feeding (frequency and composition) or medication. The duration of buffering of gastric acidity during pH monitoring might, in the future, appear to be a relevant factor in the interpretation of oesophageal pH data.
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PMID:Gastro-oesophageal reflux in infancy. 1002 72

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 esophagus is lined by a moist stratified squamous epithelium. In humans, this epithelium, as evidenced by the Bernstein test, has considerable capacity to resist damage even upon direct contact of high concentrations of luminal acid. This intrinsic property of the epithelium to defend itself against luminal acid is called "tissue resistance." Tissue resistance is comprised of a number of important structures and functions, the individual functions of which are described in this review. Moreover, when luminal acidity is sufficiently noxious, tissue resistance can be overcome, leading to heartburn and ultimately cell necrosis. Herein are described the mechanisms by which acid overcomes the epithelial defense to produce these typical signs and symptoms of gastroesophageal reflux disease.
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PMID:Mechanisms of reflux-induced epithelial injuries in the esophagus. 1071 61

Until relatively recently, gastroesophageal reflux disease (GERD) was thought to be a relatively trivial problem, and pharmaceutical companies initially had remarkably little interest in clinical trials for GERD. Over the last ten years, GERD therapy has become the subject of intense interest, since reflux disease is now recognized as a major market for antisecretory and prokinetic drugs. Even low-technology antacids are now known to effectively neutralize esophageal acid prevent acid reflux for up to 90 minutes. Esophageal pH profiling is known to be an excellent surrogate for clinical efficacy of GERD drugs, particularly in erosive esophagitis. Years ago, famotidine normalized esophageal mucosal exposure to pH < 4.0 only when administered in doses of 40 mg twice a day. Subsequent studies confirmed that multiple daily dosing of histamine-2 receptor antagonists (H2RAs) was mandatory for GERD treatment, with clear dose-response relationships for each agent. Proton pump inhibitors (PPIs) have each been carefully assessed in terms esophageal and gastric pH profiles. Omeprazole has a particularly flat dose response curve, making it difficult to differentiate pH or clinical effects of 20 vs. 40 mg doses. Improved rapidity of onset and/or enhanced potency is demonstrable in pH data obtained with lansoprazole, rabeprazole and pantoprazole. Such differences will translate to improved clinical efficacy, based on the meta-analyses of Richard Hunt and his group in Canada that correlate pH effects and symptom relief/healing. PPI's have dependably surpassed H2RAs and prokinetic drugs in management of the more severe grades of esophagitis. Helicobacter pylori has a peculiar relationship to GERD. There has been some concern that PPIs given to patients with H. pylori might accelerate development of severe atrophic gastritis. It is also now known that eradication of H. pylori may increase symptomatic GERD (possibly as a result of increased gastric acid secretion once the bacteria have been eliminated). New data confirm nocturnal breakthrough of acid secretion and esophageal acid exposure in three-fourths of patients on omeprazole 20 mg twice daily. This nocturnal acidity can be controlled more effectively with a nighttime dose of an H2RA than with a third dose of omeprazole. Control of acid secretion and improved gastric and esophageal pH profiles are goals of modern GERD therapy, and the product that most cost effectively normalizes esophageal acid exposure will have a substantial advantage in the ever-growing GERD marketplace.
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PMID:Drugs, bugs, and esophageal pH profiles. 1078 May 78

Gastroesophageal reflux symptoms are common and occur in all of us from time to time. In others, reflux may be associated with ulcerative esophagitis. The symptoms may be aggravated by large meals, coffee, smoking and position. Physiological and pathological reflux can be separated by the frequency and duration of the exposure of the lower esophagus to acid. Pathological reflux results in symptoms and also esophagitis and ulceration in some patients. Although gastroesophageal reflux disease (GERD) is considered to result from a disorder of motility in the esophagus, gastric acid and peptic activity are deemed pivotal to the initiation and continuation of the esophageal damage and the development of symptoms. Acid exposure in the esophagus is normally less than 4 percent of the 24 hours with a pH below 4. An increase over 4 percent of the time with a pH less than 4 is considered pathological. Hence, antisecretory drugs have become the principle approach to the treatment of reflux symptoms and esophagitis since they reduce the acidity, of gastric juice and the activity of pepsin. Importantly, they also reduce the volume of gastric juice available for reflux into the esophagus. There is a clear relationship between the degree and duration of acid suppression and the relief of heartburn and healing of esophagitis. Pharmacodynamic studies with different dose regimens of the H2-receptor antagonists and the proton pump inhibitors show a difference in the degree and duration of the antisecretory effect, and this correlates closely with the results of clinical trials with respect to the healing of esophagitis and the relief of symptoms. Proton pump inhibitors achieve healing rates by week four, which are not achieved by H2-receptor antagonists even after 12 weeks of treatment. The advantage of proton pump inhibitors over H2-receptor antagonists is due to the greater degree, longer duration of effect and more complete inhibition of acid secretion that maintains intragastric pH above 4 for a maximal duration. Although there is no significant difference between proton pump inhibitors with respect to healing of esophagitis, symptom relief occurs earlier with lansoprazole than omeprazole, and this is probably due to the greater oral bioavailability and faster onset of action of lansoprazole when compared to omeprazole.
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PMID:pH, healing rate, and symptom relief in patients with GERD. 1078 May 80

Gastroesophageal reflux (GER) in infants becomes gastroesophageal reflux disease (GERD) through association with distinct clinical symptoms. Monitoring of pH is considered the standard diagnostic tool through which episodes of acidity can be detected. Apparently, however, the major amount of GER occurs in the physiologic esophageal pH range, which is concealed to pHmetry. Intraluminal impedance is a new method for pH-independent detection of esophageal bolus movement. Long-term measurements and combination with other diagnostic methods, e.g., pHmetry or polygraphic recordings, are possible. Intraluminal impedance has proved especially useful in diagnosing GER and GERD in infants. It may develop into the ideal technique for this group of patients.
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PMID:Intraluminal impedance: an ideal technique for evaluation of pediatric gastroesophageal reflux disease. 1095 39

Gastroesophageal reflux disease (GERD) affects more than one third of the population. It is generally a chronic condition and has the potential to be serious. Some patients with GERD experience persistent daytime or nighttime heartburn and some sustain severe damage, including ulceration, stricture, and Barrett's esophagus, which can predispose to development of adenocarcinoma. Extraesophageal manifestations of GERD can include otolaryngologic, respiratory, and cardiac problems. Severe GERD responds best to agents that suppress gastric acid secretion. Of these, proton pump inhibitors (PPIs) provide the most effective control of gastric acidity and are, therefore, the medical treatment of choice. In fact, nonresponse to a PPI should raise the suspicion that the diagnosis is not GERD. Proton pump inhibitors are quickly becoming the treatment of choice for GERD, especially for severe or refractory cases. For patients whose GERD is refractory even to PPIs or who are unwilling to face years of PPI therapy, antireflux surgery remains an option.
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PMID:Management of severe gastroesophageal reflux disease. 1115 63

Proton pump inhibitors (PPIs) are the most effective antisecretory drugs available for controlling gastric acid acidity and volume. They are the drugs of choice in the treatment of moderate-to-severe gastroesophageal reflux disease, hypersecretory disorders, and peptic ulcers. Currently in the United States, they are only available in an oral formulation. However, pantoprazole will soon be available in an intravenous formulation and will extend the power of PPIs to inpatient hospital settings. Intravenous pantoprazole has been shown to be effective and safe in clinical trials. Intravenous pantoprazole is indicated for the treatment of patients who require PPI therapy but who are unable to take oral medication. Intravenous pantoprazole has been shown to maintain acid suppression in patients switched from oral PPIs, so no change in dosage is required when switching from one formulation to the other. Potential hospital-based uses for intravenous PPI therapy include perioperative use as prophylaxis for acid aspiration syndrome during induction of anesthesia, prophylaxis for stress-related mucosal disease, and management of gastrointestinal bleeding from stress or acid peptic disease.
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PMID:Switching between intravenous and oral pantoprazole. 1115 64


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