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

Antacids have served us well for over a century. In terms of peptic ulcer disease, the attitude in the late 1950s to 1970s that antacids should be taken only on demand was unjustified and erroneous. 13 recent endoscopic controlled studies have confirmed the efficacy of antacids in the healing of duodenal ulcer, achieving about 75% healing in 4 weeks. The efficacy of antacids in promoting gastric ulcer healing has been less well studied and the results are controversial. The most appropriate and economical antacid regimens for the treatment of duodenal ulcer disease should include tablets or liquid that have acid neutralising capacity of 400 mmol/day given at least an hour after meals. As a long term therapy, antacids appear to work, but need be taken in multiple daily doses, a regimen which is unlikely to meet with long term patient compliance. Patients with gastro-oesophageal reflux disorders or pregnancy-related reflux have also benefited from the usage of antacids ad libitum. Early previous studies have clearly demonstrated the efficacy of antacids in reducing gastro-oesophageal reflux and healing of reflux oesophagitis. The acidity of the gastric contents is the major determining factor in the outcome of the aspiration pneumonitis occurring during delivery. The prophylactic use of antacids during delivery has helped to reduce the severity of this complication. Similarly, the prophylactic administration of antacid aiming to maintain gastric pH between 3.5 to 7.0 has resulted in significant reduction of bleeding due to stress associated ulcers and/or erosive haemorrhagic gastritis in critically ill patients. Antacid therapy, however, is controversial in the management of nonulcer dyspepsia or nonsteroidal anti-inflammatory drug related upper gastrointestinal mucosal damage. Undoubtedly, antacids have major roles to play in the treatment of gastric acid related disorders. They have clear advantages and disadvantages when compared with the antisecretory agents. New proton pump inhibitors in particular have certainly superseded antacids and even the H2-receptor antagonists in many respects. However, the long term safety record of antacids remains unsurpassed by any of the new antisecretory agents.
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PMID:Antacids. Indications and limitations. 751 3

Successful omeprazole therapy in patients with symptomatic gastroesophageal reflux (GER) refractory to treatment with H2-receptor antagonists has often been reported. In contrast, successful treatment of GER by H2-receptor antagonists in patients resistant to the acid-suppressing effects of omeprazole is rarely reported. We describe two patients who demonstrated therapeutic responses to high dose H2-receptor antagonists after high dose omeprazole failed to suppress gastric acidity and GER.
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PMID:Control of gastric acid with high dose H2-receptor antagonists after omeprazole failure: report of two cases. 757 13

Until recently, suppression of gastric acid secretion in patients with peptic ulcer was empirical and of unproven value. Anticholinergic drugs had only modest inhibitory effects on acid secretion, many side effects, and uncertain efficacy. Controlled trials using antacids demonstrated the value of reducing gastric acidity for healing duodenal ulcer. The discovery of histamine-2 (H2) receptor antagonists in the 1970s and the introduction of H+,K(+)-ATPase inhibitors in the 1980s made reduction of acid secretion the first-choice modality for healing and preventing recurrences of duodenal and gastric ulcers. The demonstration in the late 1980s and early 1990s that Helicobacter pylori (Hp) was a major risk factor for duodenal and gastric ulcer recurrences suggested that peptic ulcer could be cured by eradicating this organism from the stomach. However, antibiotic eradication of Hp can be difficult, often requiring simultaneous administration of a drug that suppresses acid secretion. Therefore, H2 and proton pump inhibitors continue to play a role in the management of duodenal and gastric ulcers associated with Hp and also play a primary role in the therapy of other acid-related disorders, such as gastroesophageal reflux diseases, stress ulcers, ulcers associated with nonsteroidal anti-inflammatory drugs, and gastrinoma (Zollinger-Ellison syndrome) and other acid hypersecretory states.
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PMID:Suppression of acid secretion in peptic ulcer disease. 767 7

Gastric acid is of central importance in the pathogenesis of duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease. Pharmacological reduction of acid secretion is, therefore, the mainstay of current treatment, but the optimal degree of acid suppression remains incompletely understood. This paper considers the ideal ways of assessing and reporting the pharmacological effectiveness of acid-inhibiting drugs and relating such data to clinical efficacy. Twenty-four-hour intragastric pH measurements are widely used for this purpose, although this technique cannot measure secretion quantitatively. Data on suppression of 24-hr intragastric acidity for groups of subjects have been successfully correlated with healing rates for duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease. Three primary determinants of healing have been derived from antisecretory data. These are the degree of suppression of acidity, the duration of suppression of acidity, and the duration of treatment. The order of importance of these determinants varies depending on the disease. Data on 24-hr intragastric acidity should be accompanied whenever possible by data on 24-hr plasma gastrin levels, as the relationship between suppression of acidity and a rise in gastrin varies widely between individuals. It is not possible to predict the plasma gastrin level from the intragastric pH or any other measurement of intragastric acidity. Comparative data sets in groups of subjects may provide useful information. Proton pump inhibitors produce a greater and longer-lasting degree of suppression of acidity than conventional doses of H2-receptor antagonists. For this reason, they are more effective in healing duodenal ulcer and gastric ulcer. However, in view of the importance of duration of treatment, healing rates with the H2-receptor antagonists approach those obtained with proton pump inhibitors if treatment is continued for a longer time. In gastroesophageal reflux disease in particular, although the optimal degree of acid suppression is not yet defined, the consistently superior performance of proton pump inhibitors demonstrates that increased suppression of acidity is clinically beneficial.
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PMID:Optimizing acid suppression for treatment of acid-related diseases. 785 82

The effect of ranitidine and cisapride on acid reflux and oesophageal motility was investigated in 18 patients with endoscopically verified erosive reflux oesophagitis. Each patient was treated with placebo, ranitidine (150 mg twice daily), and ranitidine (150 mg twice daily) plus cisapride (20 mg twice daily) in a double blind, double dummy, within subject, three way cross over design. Oesophageal acidity and motility were monitored under ambulatory conditions for 24 hours on the fourth day of treatment, after a wash out period of 10 days during which patients received only antacids for relief of symptoms. Acid reflux was monitored by a pH electrode located 5 cm above the lower oesophageal sphincter. Intraoesophageal pressure was simultaneously recorded from four transducers placed 20, 15, 10, and 5 cm above the lower oesophageal sphincter. Upright reflux was three times higher than supine reflux (median (range) 13.3 (3.7-35.0)% v 3.7 (0-37.6)% of the time with pH < 4.0, p < 0.01, n = 18). Compared with placebo, ranitidine decreased total reflux (from 10.0 (3.2-32.6)% to 6.4 (1.2-22.9)%, p < 0.01), upright reflux (p < 0.05), supine reflux (p < 0.001), and postprandial reflux (p < 0.01), but did not affect oesophageal motility. The combination of ranitidine with cisapride further diminished the acid reflux found with ranitidine--that is, cisapride led to an additional reduction of total reflux (from 6.4 (1.2-22.9)% to 3.7 (1.0-12.7)%, p < 0.01), supine reflux (p < 0.05), and postprandial reflux (p < 0.05). Cisapride also reduced both the number (p<0.01) and duration (p<0.05) of reflux episodes and significantly increased amplitude, duration, and propagation velocity of oesophageal contractions (p<0.05) but did not affect the number of contractions. The findings show that the 30% reduction of oesophageal acid exposure achieved by a conventional dose of ranitidine (150 mg twice daily) can be improved to more than 60% by combination with cisapride (20 mg twice daily). The cisapride induced increase in oesophageal contractile force and propagation velocity seems to enhance the clearance of gastro-oesophageal reflux. Combination of a histamine H2 receptor antagonist with a prokinetic agent may therefore provide an alternative treatment for reflux oesophagitis.
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PMID:Effects of ranitidine and cisapride on acid reflux and oesophageal motility in patients with reflux oesophagitis: a 24 hour ambulatory combined pH and manometry study. 817 47

Bicarbonate-calcic water Ferrarelle has been administered both in the fasting state and during meals to patients suffering from gastro-esophageal reflux disease submitted to computerized pHmetry. Marked and lasting increase of esophageal and gastric pH was observed with significant differences from the effect of tap water. In addition, patients reported improvement of heart burn and acidity after the administration of the bicarbonate-calcic water. The alkalizing effect of the mineral water employed is therefore fully confirmed.
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PMID:[Alkalizing activity of a calcium-bicarbonate-containing water, evaluated for pH, in patients with gastroesophageal reflux]. 822 43

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

The effect of postprandial administration of a new formulation of almagate (1.5 g, po) or an association of alginate + antacid (2.4 g, po) on gastric alkalinization and gastroesophageal reflux were assessed in a randomized, single-blind, cross-over study in 21 patients with gastroesophageal reflux disease. Continuous intragastric and esophageal acidity was evaluated by postprandial intraluminal pHmetry. When comparing both preparations, the new formulation of almagate significantly improved all pHmetric variables (number of reflux episodes (3 vs 6, p = 0.029), time of esophageal exposition to pH < 4.0 (1vs 9 minutes, p = 0.009), duration of longest reflux episode (1 vs 3 minutes, p = 0.036), reflux index (1 vs 2, p = 0.047), and intragastric time with pH greater than 4.0 (108 vs 46 minutes, p = 0.003). This results suggest that the new formulation of almagate could be effective in the treatment of gastroesophageal reflux disease, since acidity profile of patients treated with it have been shown an intragastric long-lasting alkalinization wave.
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PMID:[The effect of a new formulation of almagate on gastroesophageal reflux in esophagitis patients. A randomized, single-blind and cross-over study]. 849 50

Gastroesophageal reflux is a common disease. Its chronic course, even if mild, is sometimes complicated by erosive oesophagitis. Drug therapy acts against gastric acidity and motility disorders. Treatment of gastroesophageal reflux disease has three aims: improvement of symptoms and quality of life, healing erosive lesions and prevention of symptomatic and endoscopic relapses. Non-drug measures are always useful, even if their efficacy is not well established. Initial therapy of a symptomatic reflux or mild oesophagitis is most of the time effective (antacids, prokinetics, H2 receptor antagonists). Proton-pump inhibitors are also effective in healing and preventing severe oesophagitis. Questions about long-term treatment adverse events with powerful acid inhibitors, such as hypergastrinemia and the risk of gastric carcinoid tumours seem to be resolved. Studies are requested to define the optimal long-term maintenance treatment with cisapride, H2 receptor antagonists or proton-pump inhibitors at low doses in prevention of symptomatic and mild oesophagitis relapses.
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PMID:[Therapeutic principles in gastroesophageal reflux]. 857 Sep 62

Lower oesophageal pH was monitored in 240 anaesthetised dogs. The incidence of gastro-oesophageal reflux was 16.3 per cent and most of the reflux episodes occurred shortly after the induction of anaesthesia. The refluxate was nearly always acid (pH < 4.0), but in 10.3 per cent of the cases it was alkaline (pH > 7.5); gastric contents of pH below 2.5 were refluxed on 19 occasions (7.9 per cent). Regurgitation occurred in only one dog. Prolonging preoperative fasting was associated with an increased incidence of reflux and increased gastric acidity. Premedication with diazepam was associated with fewer reflux episodes than premedication with atropine and propionylpromazine.
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PMID:Gastro-oesophageal reflux during anaesthesia in the dog: the effect of preoperative fasting and premedication. 857 60


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