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The expression of CD11b and CD18 on neutrophils and neutrophil-dependent adhesion to endothelial cells elicited by HPE were inhibited by lansoprazole and omeprazole at clinical relevant doses, and the expression of ICAM-1 and VCAM-1 on endothelial cells and endothelial-dependent neutrophil adherence induced by IL-1beta were also inhibited by lansoprazole and omeprazole at similar doses. Famotidine and ranitidine had no effect on neutrophil-endothelial cell interactions.
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Two hundred eighty patients with duodenal ulcer entered in to the study from 30 centers. They were randomized in a double-blind manner into four groups with 80 patients entered into each active treatment group and 40 patients into the placebo group. Endoscopy was performed at 2- and 4-wk intervals to assess healing. Symptom relief was recorded, serum gastrin levels were measured, and gastric mucosal biopsies were obtained to evaluate for the presence of acute and chronic inflammation, the presence of neoplasia, and the extent of gastric endocrine growth at the time of endoscopy.
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Lansoprazole (AG 1749/CG 4801) is an inhibitor of gastric acid secretion by blocking H+,K(+)-ATPase. In this 2:1 randomized, double-blind, multicentre trial lansoprazole 30 mg am was compared to 40 mg famotidine nocte in 264 out-patients suffering from uncomplicated duodenal ulcer. After 2 weeks of treatment ulcer healing was confirmed endoscopically in a significantly higher proportion (P = 0.027) of patients treated with lansoprazole (94/174 = 54.0%) compared to patients receiving famotidine (35/90 = 38.9%). Cumulative healing rates after 4 weeks were 91.4% for the lansoprazole group and 83.3% for the famotidine group (P = 0.065). Pain relief and decrease of concomitant antacid consumption during treatment were comparable in both groups. Both compounds were well tolerated. Rates of recurrent duodenal ulcer in the 6 months after trial treatment were 45/158 (28.5%) after lansoprazole, and 18/69 (26.1%) after famotidine.
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Venous blood was collected from normal subjects and peripheral blood mononuclear cells (PBMCs) were isolated using centrifugation techniques over a Ficoll-Hypaque density gradient. PBMCs were added to 12-well culture plates in four groups of media: a) control; b) control plus lansoprazole (25 microg/mL); c) control plus omeprazole (0.35 microg/mL); and d) control plus ranitidine (50 microg/mL). PBMCs were exposed to the drug for 96 hrs, with addition of phytohemagglutinin (2.5 microg/ mL) for the last 48 hrs, and 3H-thymidine (1 microCi) during the final 6 hrs. PBMCs were filtered onto glass-fiber filter paper and the radioactivity was determined by scintillation counting. Since radioactivity is measured only in those cells undergoing DNA synthesis or cell division, results are expressed as quantification of 3H-thymidine uptake. Median disintegrations per min (DPM)/number of PBMCs per well+/-SEM are reported: control 68.3+/-37.8; ranitidine 38.4 +/-94.2; lansoprazole 14.6+/-84.4; and omeprazole 15.1+/-48.9. There was a significant difference between lansoprazole vs. ranitidine (p< .01), and omeprazole vs. ranitidine (p< .05), and no significant difference between lansoprazole and omeprazole.
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Measurement of the pH and 8-isoprostane level of exhaled breath condensate may be useful to evaluate the influence of GERD on asthma, as well as to determine the timing of intermittent PPI therapy.
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Summary In patients with gastro-oesophageal reflux disease, the pH of refluxed gastric contents has a direct bearing on disease severity and oesophageal damage. A pH of 4 has been defined as a threshold below which refluxed gastric contents become injurious to the oesophagus. Studies in patients with erosive oesophagitis have shown that the 8-week healing rates produced by acid suppressive therapy are related to the duration of time over a 24-h period that the intragastric pH > 4. The most effective agents, providing more hours with gastric pH > 4 and higher healing rates in erosive oesophagitis patients, are the proton pump inhibitors. The intragastric pH is often used to gauge the efficacy of acid suppressive therapies. There are several factors, however, that may affect the clinical relevance of such data, and these should be taken into account when comparing the effectiveness of different therapies. Firstly, because of inter-individual variation, studies comparing therapies should be of a crossover design, so that responses to therapy are measured in the same individuals. Secondly, the Helicobacter pylori status of the individual should be known, as H. pylori infection has been shown to increase intragastric pH readings when examining the effect of acid suppressive therapy. Other factors, such as positioning of the pH electrode and the duration of previous therapy, also need to be standardized when using intragastric pH to assess the efficacy of different therapies. Crossover studies comparing standard doses of different proton pump inhibitors have shown that esomeprazole 40 mg produces a significantly greater amount of time at intragastric pH > 4 on day 5 of treatment than standard doses of other proton pump inhibitors. The correlation between greater efficacy in acid suppression and clinical benefit is supported by the findings that esomeprazole 40 mg is the only proton pump inhibitor to provide greater 8-week healing rates in patients with erosive oesophagitis than both omeprazole and lansoprazole. These data all suggest strongly that intragastric pH monitoring is an effective surrogate marker and a relevant predictor of outcome in gastro-oesophageal reflux disease.
All 78 strains showed MICs of faropenem that were equal to or less than 0.2 microg/mL. The eradication rates according to intention-to-treat analyses were 46.5% with the 7-day therapy (n = 43) and 62.5% with the 14-day therapy (n = 32). No special measures were required to treat the adverse events observed in approximately one-third of the patients.
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The primary endpoint was the development of gastric or duodenal ulcers. The cumulative incidence of gastric or duodenal ulcers on days 91, 181, and 361 from the start of the study was calculated by the Kaplan-Meier method as 1.5, 2.1, and 3.7%, respectively, in the lansoprazole group versus 15.2, 24.0, and 31.7%, respectively, in the gefarnate group. The risk of ulcer development was significantly (log-rank test, P < 0.001) lower in the lansoprazole group than in the gefarnate group, with the hazard ratio being 0.099 (95% confidence interval [CI] 0.042-0.230).