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At least 541 records · Page 30Linked to original sources
PubMed1999

Pantoprazole versus omeprazole: influence on meal-stimulated gastric acid secretion.

AIMS: To determine the influence of recommended therapeutic doses of pantoprazole and omeprazole on meal-stimulated acid secretion. METHODS: In this double-blind, placebo-controlled, three-period crossover study, 12 healthy male volunteers received 40 mg pantoprazole od, 20 mg omeprazole od or placebo at 08:00 h for 5 days in a randomized order. Meal-stimulated acid secretion was determined by means of a homogenized test meal, and intragastric titration on day 1, 4-6 h, 8-10 h, 16-18 h, and 24-26 h, and on days 3 and 5, 4-6 h after oral drug administration. RESULTS: On day 1 (4-6 h after oral drug administration), meal-stimulated acid secretion was decreased by 36% and 24% after administration of 40 mg pantoprazole or 20 mg omeprazole, respectively. After 3 and 5 days of dosing, the decreases were 88% and 85% with 40 mg pantoprazole, and 70% and 74% with 20 mg omeprazole. At all measuring points during the 5-day dosing periods, 40 mg pantoprazole proved superior to 20 mg omeprazole in inhibiting meal-stimulated gastric acid secretion. The differences were statistically significant for pantoprazole on day 1, 24-26 h after oral drug administration and on day 3 (P = 0.0425 and P = 0.0244, respectively). On day 1, only pantoprazole was significantly better than placebo (P = 0.0210, 4-6 h after dosing; P = 0.0093, 8-10 h after dosing and P = 0.0068, 16-18 h after dosing). CONCLUSION: Pantoprazole 40 mg is significantly more effective than omeprazole 20 mg in inhibiting meal-stimulated acid secretion. In addition, pantoprazole exhibits a more rapid onset of action.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2004

The influence of rapid food intake on postprandial reflux: studies in healthy volunteers.

BACKGROUND: The postprandial increase of gastroesophageal reflux (GER) results largely from an increase in the rate of transient lower esophageal sphincter relaxations (TLESRs). Gastric distension is believed to be the most important contributing factor. The aim of this study was to determine the impact of rapid food intake on GER in healthy volunteers using combined multichannel intraluminal impedance and pH (MII-pH) testing to record both acid and nonacid reflux. Our hypothesis was that rapid food intake overstresses the gastric pressure-volume response and contributes to increased postprandial GER. METHODS: Twenty healthy volunteers were included in the study. On two separate days the participants were asked to eat the same standard meal within 5 or 30 min in random order. Acid and nonacid reflux episodes were recorded over a 2-h postprandial period. RESULTS: Intake of a standard meal within 5 min was associated with more reflux episodes (median = 14) than an intake within 30 min (median = 10, p= 0.021). The increase was confined to the first postprandial hour and was caused predominantly by an increase of nonacid reflux. During the entire 2-h postprandial period, 469 reflux episodes were noted in the 40 studies. During the first postprandial hour 45% (135/303) of reflux events were nonacid as opposed to 22% (37/166) noted during the second hour (p < 0.0001). CONCLUSION: Since rapid food intake produces more GER in healthy volunteers, studies in GERD patients are warranted to evaluate if eating slowly may represent another "life-style modification" aimed at reducing GER.

Adult↗
PubMed1992

Therapeutic effects of oral rebamipide and in combination with cimetidine on experimental gastritis in rats.

The present study evaluated the therapeutic effects of rebamipide alone and in combination with cimetidine on experimental gastritis established by the administration of 5 mM sodium taurocholate (TCA) for 6 months in rats. Morphological and biochemical analyses were performed to determine the effects of rebamipide, administered alone or in combination with cimetidine, on chronic, atrophic and erosive gastritis. Rebamipide and cimetidine were administered to rats as a dietary admixture for 4 weeks after withdrawal of TCA. Rebamipide dose-dependently reduced the total length of the erosion, normalized the mucosal thickness and increased the number of parietal and total cells, and tended to reduce interstitial infiltration of inflammatory cells and proliferation of collagenous fibers. Moreover, histochemical and biochemical studies also showed rebamipide to be effective. Rebamipide increased the PAS-positive mucus and normalized the reduced gastric mucosal SOD activity. The therapeutic effect of rebamipide on the experimental gastritis was enhanced by the combined use of cimetidine. These results suggest that rebamipide has a therapeutic effect on chronic atrophic erosive gastritis induced by TCA, and that the mechanism of the therapeutic effect is partially due to the increase in PAS-positive mucus and gastric mucosal SOD activity. Furthermore, the enhanced effect of the combination therapy of rebamipide with cimetidine was considered to be due to the actions of both cimetidine and rebamipide.

Administration, Oral↗
PubMed1993

Problems with the interpretation of gastric pH measurement.

The present study examines some of the assumptions underlying the use of intragastric pH-metry for assessing the degree of therapeutic gastric inhibition. Three separate studies were performed to determine the relationship between pH and titratable hydrogen ion concentration in gastric juice and to assess the relationship between the concentration of acid and the rate of gastric secretion. The concentration of acid derived from pH measurements tended to be lower than the titrated hydrogen ion concentration. The difference between the two readings--the "buffered" hydrogen ion concentration--was increased by the presence of food and was reduced during gastric secretory inhibition with ranitidine. The titrated hydrogen ion concentration reflected more accurately the amount of hydrochloric acid added to a container in vitro than pH measurement. However, in vivo even the measurement of titratable acidity was poorly correlated with the volume of secreted gastric juice so that measurement of gastric acid concentration does not permit inferences about the rate of gastric secretion. The results of the present study indicate that measurement of intragastric pH is unsatisfactory for assessing gastric secretion, particularly in response to a food stimulus, so that measurement of gastric acidity alone does not reflect the rate, or changes in the rate, of gastric acid secretion.

Artifacts↗
PubMed1989

Pathophysiology of gastroesophageal reflux.

The factors controlling competence of the gastroesophageal junction have been carefully analyzed over the last decade. Although the presence of an anatomic sphincter guarding the lower esophagus has not been confirmed in humans, a manometrically defined high-pressure zone is present in the lower esophagus. The magnitude of sphincter pressure correlates well with the incidence of pathologic gastroesophageal reflux. Another important determinant of cardial competence is the length of intra-abdominal esophagus. The interaction of length and pressure in maintaining competence is demonstrated by several clinical and experimental studies. Twenty percent of refluxors have normal components of cardial competence. Several physical factors, namely components of Laplace's law, may govern control of reflux especially after antireflux repairs. The occurrence of esophagitis as a complication of gastroesophageal reflux is determined by the ability of the esophageal body to rid itself of an acid load as well as by factors that delay gastric emptying.

Animals↗
PubMed1976

Altered serum gastrin levels in achlorhydric states.

Hypergastrinemia occurs in achlorhydric states if the antrum is not diseased, and evidence has been presented that suggests that antral gastritis diminishes gastrin levels in achlorhydric patients. There is a dramatic gastrin response to calcium challenge in patients with pernicious anemia. Only minimal response was observed in patients with atrophic gastritis. Unlike the response observed in the Zollinger-Ellison syndrome, secretin challenge suppresses gastrin in achlorhydric states. These findings add a new dimension to the utility of serum gastrin determinations.

Achlorhydria↗
PubMed1986

Clinical relevance of gastroduodenal dysfunction in reflux esophagitis.

This review critically evaluates the gastroduodenal factors that may play a clinically relevant role in the pathogenesis of reflux esophagitis. The gastroesophageal pressure gradient is of obvious importance, but the role of gastric contraction/relaxation is poorly understood. The intragastric volume, as well as the factors that influence it, could theoretically play a role in gastroesophageal reflux (GER). For example, suppression of gastric emptying and gastric motility would be expected to increase GER, and treatment with gastrokinetic agents appears to provide symptomatic improvement. However, only a fraction of patients with GER have delayed gastric emptying, and there is no correlation between either subjective epigastric fullness or esophagitis on one hand and gastric emptying on the other hand. Gastric acid and pepsin, and possibly the hypersecretion of acid, play a pivotal role in reflux esophagitis, as demonstrated by the efficacy of the treatment with histamine H2 antagonists and antacids. Other important factors in experimental esophagitis are duodenogastric reflux, the presence of bile acids in the gastric contents, as well as trypsin if the pH is alkaline. It is suggested that these important findings may lead to novel therapeutic approaches of reflux esophagitis.

Animals↗
PubMed1988

Effects of a synthetic prostanoid, rosaprostol, on the changes of gastric acidity and digestive disorders induced by NSAID.

In 24 subjects without upper gastrointestinal lesions, gastric pH was measured from 30 min before until 90 min after the administration of diclofenac sodium (50 mg), piroxicam (20 mg), or 500 mg acetylsalicylic acid. In all these cases a drop of gastric pH was recorded, which started with all the drugs 15 min after their administration and lasted throughout the recording. Pre-treatment with rosaprostol (2 g given 30 min before the start of the trial) prevented the drop in pH. Twenty subjects with chronic joint diseases were divided into two groups in a cross-over double-blind randomized experimental design. One group received piroxicam (20 mg) + rosaprostol (2 g) daily; the other group was treated with piroxicam 20 mg + placebo. The patients were clinically reviewed every week in a month and questioned about their symptoms. Statistical analysis demonstrated that patients with articular diseases treated with NSAIDs + rosaprostol exhibited a frequency and severity of symptoms lower than those recorded in subjects receiving NSAIDs + placebo. Rosaprostol was found to be capable of antagonizing the variations of gastric acid output induced by the oral administration of NSAIDs, and to prevent and treat the occurrence of digestive disorders when given in combination with NSAIDs. These effects result from the action of rosaprostol on the mucosal barrier, and this cytoprotective action is confirmed by the present study with continuous measurements of gastric pH.

Adult↗
PubMed1979

[Treatment of duodenal ulcer with Tagamet (cimetidine)].

The results from the treatment of 25 patients with duodenal ulcer with 1 g tagamet daily (3x200 mg after meal and 400 mg in the evening before going to bed) in the course of 20 days, are reported. The subjective complaints of the patients disappeared in 87--100 per cent (in 2/3 of the patients even in the first three days after the initiation of the treatment) and the ulcer in 44 per cent. The immediate results obtained are statistically more significant as compared with the control group (only on diet), but the differences are not significant as regards the groups treated only with oxyferoscorbon and only with Caved-S. Tagamet treatment leads to a decrease of the basic indices of gastric secretion and does not change the content of N-acetylneuroamine acid in the gastric juice. The venous administration of tagamet inhibits the gastric acid production stimulated by pentagastrin. Tagamet treatment does not change the biochemical laboratory indices, the inflammatory and structural changes in the gastric-duodenal mucosa and induces no adverse effects and complications.

Adolescent↗