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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 32 (1960), S. 1489-1494 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 35 (1963), S. 511-515 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Langmuir 11 (1995), S. 3408-3416 
    ISSN: 1520-5827
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Industrial & engineering chemistry 48 (1956), S. 82-85 
    ISSN: 1520-5045
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 9 (1995), S. 0 
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Gastro-oesophageal reflux disease (GERD) is generally considered to be the result of a motility disorder which permits the abnormal and prolonged exposure of the lumen of the oesophagus to the acidic gastric contents.This view is supported by experimental data, intraoesophageal pH measurement, and the dramatic results of symptom relief and healing seen with effective antisecretory treatment.Oesophageal mucosal injury is determined by the pH of the refluxate and duration of acid exposure. Most patients experience meal-stimulated reflux during the day and the more severe cases experience 24-h acid exposure. In contrast to the H2-receptor antagonists (H2RAs), the proton pump inhibitors (PPIs) are more effective at controlling meal-stimulated acid secretion when each is given in standard doses. Therefore, the degree and duration of acid suppression throughout 24 h is greater.Treatments which maintain intra-oesophageal pH 〉 4 for 96% or more of the 24 h normalize acid exposure and are associated with the highest healing rates. Peptic activity is minimized at or above pH 4. The time above pH 4 is significantly longer with the PPIs than with the H2RAs. Thus, the healing-time curves for GERD (grades II-IV) are shifted to the left for the PPIs which heal a significantly greater proportion of patients earlier than the H2RAs or sucralfate.Symptoms in GERD are related to the degree and duration of oesophageal acid exposure. Symptom relief is more rapid and complete with the PPIs than with the H2RAs or other treatments in standard doses.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Aims: To determine the influences of prostaglandin inhibition by indomethacin on 24-h intragastric acidity and plasma gastrin concentration, related to gastric mucosal injury. Methods: A pre- and post-treatment study design was employed in 10 Helicobacter pylori negative healthy male subjects. All subjects underwent upper gastrointestinal endoscopy at least 3 days before and after 7 days dosing with indomethacin 50 mg t.d.s. Mucosal damage was scored according to the Lanza method, and biopsies were taken for H. pylori status and assay of mucosal concentrations of prostaglandin (PG)E2 and leukotriene (LT)B4. Before and on the last day of dosing, intragastric acidity was measured by continuous 24-h pH monitoring, and plasma gastrin levels determined by radioimmunoassay in blood samples collected over the same period. Results: All subjects completed the study and no serious adverse events were reported. The mucosal injury score increased significantly from 0 (0–2) to 3.4 (0–8) (mean and range of values, P 〈 0.05) after dosing with indomethacin. No differences were observed in 24-h mean pH or meal stimulated plasma gastrin concentrations. Mucosal PGE2 and LTB4 were unchanged 8–10 h after the last indomethacin dose. Conclusions: Endogenous prostaglandins do not appear to alter intragastric acidity or gastrin secretion, in contrast to the PGE analogues, whose effects must be more pharmacological than physiological.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 4 (1990), S. 0 
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have investigated the relationship between the suppression of acidity by antisecretory drugs for the treatment of benign gastric ulcer and their corresponding ulcer-healing rates. For a variety of antisecretory drug regimens, there was a significant correlation between suppression of 24-h intragastric acidity and ulcer healing rates after 2, 4 and 8 weeks of treatment. There was a lesser degree of correlation between healing and suppression of nocturnal acidity and the association between suppression of acidity and gastric-ulcer healing rates was less marked than that previously described for duodenal ulcer.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: To compare the effect of lansoprazole, 30 mg once daily, with that of pantoprazole, 40 mg once daily, for the inhibition of gastric acid secretion.〈section xml:id="abs1-2"〉〈title type="main"〉Methods:Two randomized, single-blind, two-way, crossover studies were conducted in 74 healthy male volunteers. Lansoprazole, 30 mg, or pantoprazole, 40 mg, was administered once daily for five consecutive days with at least a 2-week washout period between regimens. Ambulatory 24-h intragastric pH was recorded at baseline and on days 1 and 5 of each crossover treatment period.〈section xml:id="abs1-3"〉〈title type="main"〉Results:On day 1 in both studies, lansoprazole, 30 mg, produced significantly higher mean 24-h intragastric pH values when compared to pantoprazole, 40 mg (3.78 vs. 3.08, P 〈 0.001, and 3.97 vs. 3.20, P 〈 0.001, in the first and second studies, respectively). In both studies, lansoprazole, 30 mg, produced significantly greater proportions of time that the intragastric pH was above 3, 4 and 5 when compared with pantoprazole, 40 mg (P 〈 0.005 in all comparisons). By treatment day 5 in the first study, lansoprazole, 30 mg, continued to produce a higher mean 24-h intragastric pH (4.15 vs. 3.91, P=0.014) and a significantly greater percentage of time that the intragastric pH was above 4 (63% vs. 56%, P=0.017) and 5 (41% vs. 30%, P 〈 0.001) when compared with pantoprazole, 40 mg. In the second study, the effects on intragastric pH were comparable between the two treatment groups. Headache was the most commonly reported adverse experience (nine lansoprazole-treated subjects, seven in the first study and two in the second study; six pantoprazole-treated subjects, five in the first study and one in the second study).〈section xml:id="abs1-4"〉〈title type="main"〉Conclusions:Lansoprazole, 30 mg once daily, produces a faster onset and greater degree of acid inhibition than pantoprazole, 40 mg once daily. The implications for these differences on symptom relief and healing of erosive oesophagitis should be explored.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 14 (2000), S. 0 
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Although the incidence of gastric cancer has declined dramatically in Western countries, the most recent data from the International Agency for Research on Cancer show that it remains the second most common cancer worldwide and caused 628 000 deaths in 1990. The incidence and prevalence of gastric cancer are projected to increase over the next few decades in less developed countries as a result of the increased longevity of H. pylori-infected populations and improved therapies. Gastric carcinogenesis is a multistep and multifactorial process beginning with H. pylori-associated gastritis in most cases. H. pylori infection, together with other environmental factors and individual susceptibility, determine the final risk for the development of gastric cancer. The magnitude of H. pylori infection as a risk factor for gastric cancer in the published H. pylori and gastric cancer epidemiology studies may have been underestimated due to the inclusion of improperly selected controls. Eradication of the infection has been shown to prevent the occurrence of metachronous gastric cancer following endoscopic resection of early gastric cancer in a Japanese study. However, the generalization of this study to other populations is difficult because of the vast differences in the definition of gastric atrophy and early gastric cancer between Japanese and Western pathologists. Until an international consensus on the pathological diagnosis of gastric atrophy and early gastric cancer is reached, interpretation of studies performed in different countries remains difficult. Clinicians rely on the correct pathological diagnosis to guide the management of H. pylori infection-associated gastrointestinal diseases.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 15 (2001), S. 0 
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A double-blind, placebo-controlled study to assess the duration of effect of lansoprazole 30 mg o.m. on intragastric pH, acid secretion, gastrin levels, the potential for rebound acidity, and the relationship between gastric acid and drug pharmacokinetic parameters.〈section xml:id="abs1-2"〉〈title type="main"〉Methods:Sixteen subjects were treated with lansoprazole 30 mg daily or placebo for 14 days, followed by a 7-day post-dosing period and a post-study evaluation on day 28. Ambulatory 24-h pH was recorded and pentagastrin-stimulated acid secretion measured. Plasma kinetics of lansoprazole were determined.〈section xml:id="abs1-3"〉〈title type="main"〉Results:Mean intragastric pH in the lansoprazole group increased significantly (P 〈 0.05) from baseline to day 14 compared to placebo. After cessation of treatment, secretory activity, as measured by intragastric pH, basal acid output and stimulated acid output, returned to baseline in 2 to 4 days without any overshoot, indicating the absence of acid rebound. Lansoprazole’s terminal disposition half-life was 1.11 h. Mean pH and serum gastrin returned to baseline with half-lives of 22 and 19 h, respectively.〈section xml:id="abs1-4"〉〈title type="main"〉Conclusions:Lansoprazole 30 mg daily significantly increases mean intragastric pH without producing acid rebound. Regeneration of acid production depends primarily on de novo synthesis of the acid pump.
    Type of Medium: Electronic Resource
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