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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 25 (1983), S. 347-351 
    ISSN: 1432-1041
    Keywords: ranitidine ; chronic renal failure ; pharmacokinetics ; duodenal ulceration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The pharmacokinetic behaviour of a single oral 150 mg ranitidine dose was studied in six patients with severe chronic renal failure (CRF) (creatinine clearance 2–18 ml/min) and compared to that in ten patients with duodenal ulceration but normal renal function (N) (creatinine clearance 69–125 ml/min). Although the maximum concentrations (Cmax) were significantly higher in CRF group when compared to N group (p〈0.025) there was no difference in the time taken to reach Cmax (t max). The area under the curve (AUC) was also significantly larger in the CRF group (p〈0.001) than in the N group. Within the CRF group there was a large variation in Cmax (CV = 38%) and AUC (46%) which may reflect variable bioavailability of ranitidine. The terminal elimination rate constant (β) was significantly smaller (p〈0.001) in CRF group when compared with N group resulting in a median t1/2 for the CRF group of 7.3 h, 2.4 times that of N group. The recovery of unchanged ranitidine in the urine was significantly less in CRF group (p〈0.001) despite a great interindividual variation in both groups. A significant linear relationship betweenβ and creatinine clearance was shown (r=0.81p〈0.001). The results indicate that ranitidine elimination is appreciably reduced in renal failure. It is tentatively suggested that the standard 150 mg dose should be halved while keeping the dose interval unchanged at twelve hours in patients with severe renal failure (creatinine clearance less than 30 ml/min).
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1041
    Keywords: ranitidine ; duodenal ulceration ; pharmacokinetics ; non-responders ; therapeutic response ; bioavailability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The pharmacokinetics of orally administered ranitidine were studied in 17 male patients with chronic duodenal ulceration. The patients were divided into 2 groups, 10 responders and 7 nonresponders, on the basis of their endoscopic response to ranitidine treatment. The 10 responders were studied both after a single 150 mg dose (SD) and after multiple dosing (MD) with ranitidine 150 mg twice daily for 4 weeks. The area under the curve (AUC) and maximum concentration (Cmax) were significantly higher (p〈0.01 andp〈0.05, respectively) after MD than after SD, but the half-life (t1/2) and minimum concentration (Cmin) 12 h postdosing did not differ. The non-responders were studied after MD only and their pharmacokinetic characteristics were compared with those of responders. No differences between the 2 groups were found. However, 2 non-responders had particularly low plasma ranitidine levels and high acid output. Such patients may need larger doses of ranitidine for adequate suppression of gastric acid. Five patients (4 responders and 1 non-responder) received ranitidine 20 mg i.v. The drug followed a two-compartment model, with mean values for t1/2β, volume of distribution steady-state and total plasma clearance of 80 min, 701 and 680 ml/min, respectively. The oral bioavailability of ranitidine in these 5 patients showed wide variation (27–76%; mean 51%).
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 6 (1992), S. 0 
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effect of Helicobacter pylori lipopolysaccharide on guinea pig gastric mucosal pepsinogen secretion has been examined using an Ussing chamber technique. Luminal addition of H. pylori lipopolysaccharide resulted in a fifty-fold stimulation of pepsinogen secretion compared to a twelve-fold increase with E. coil lipopolysaccharide. Electron microscopy showed marked degranulation of zymogen granules but no evidence of chief cell disruption.
    Type of Medium: Electronic Resource
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  • 4
    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: The effect of duodenal ulcer healing on the acid secretory responses to modified sham feeding and maximal pentagastrin stimulation has been studied in 17 patients treated successfully with ranitidine (n= 9) and sucralfate (n= 8). Parietal cell sensitivity was calculated as the ratio of the modified sham feeding response to the peak pentagastrin response, expressed as a percentage. Ulcer healing after sucralfate therapy resulted in significant falls in modified sham feeding stimulated acid output (P 〈 0.02), from 9.4 (1.8–17.0) (median + range) to 3.7 (0.2–9.4) mmol/h; in peak acid output (P 〈 0.05) from 42.8 (23.0–61.4) to 27.7 (7.2–51.0)mmol/h; and in the parietal cell sensitivity (P 〈 0.05) from 19.2 (4.4–42.6) to 14.3 (2.8–19.7)%. No significant falls in any of these parameters were noted following ulcer healing with ranitidine. Duodenal ulcer healing with sucralfate results in decreased acid secretory responses to vagal and pentagastrin stimulation.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background. Helicobacter pylori lipopolysaccharide (LPS) affects pepsinogen release by a nontoxic mechanism. We hypothesized that this effect was characteristic of the organism and related to the clinical status of the strain.Materials and methods. LPS was isolated from 11 H. pylori strains whose pathogenic profile was known and four other nongastric bacteria. The effects of luminal LPS on guinea pig gastric mucosal pepsinogen release was evaluated using the Ussing chamber technique. CCK-8 (10−9M) was used as a positive control.Results. H. pylori LPS dose-dependently stimulated pepsinogen release with a maximal stimulation at 250 µg/ml (~4500%; p 〈 .001 vs. control). LPS from other Helicobacter or Campylobacter species had no effect on pepsinogen release. ANOVA demonstrated significant differences in the efficacies of pepsinogen release between the 11 clinical H. pylori strains (p 〈 .0001) despite the fact that they were all cagA+ and 90% had the cytotoxic vacA subtype s1. Physical and chemical disruption of the LPS suggested that both the structure and the carbohydrate composition of this molecule may play a critical role in pepsinogen release. Polymyxin B partly (p 〈 .03) inhibited and dephosphorylation completely inhibited (p = .0002) LPS-stimulated pepsinogen release.Conclusion. Pepsinogen release is an innate property of all cagA+H. pylori LPS. The structure of the molecule and composition of side-chains are important in this response which appears to be partially lipid A driven.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Proton pump inhibitor based combination therapy is one standard strategy for Helicobacter pylori eradication.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To compare the eradication and duodenal ulcer healing efficacy of two 2-week, single dose, lansoprazole based combination therapies.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:Healthy adult patients with endoscopically confirmed, H. pylori associated duodenal ulcer disease (3 mm 〉 ulcer 〈 20 mm) were eligible for the study. All patients received a 14 day course of lansoprazole 30 mg o.m., and were randomized to receive either 7 or 14 days of amoxycillin 1 g b.d. and clarithromycin 500 mg b.d. Patients were endoscoped at entry and 14–17 days later. Symptomatic, unhealed patients received a further 14 days of therapy with lansoprazole 30 mg o.m. Eradication was confirmed a minimum of 28 days after cessation of all therapy by urease reaction and histological assessment of gastric body and antral biopsies (three biopsies each site).〈section xml:id="abs1-4"〉〈title type="main"〉Results:Sixty-two patients were randomized to a treatment arm, of which 58 could be included in an intention-to-treat and key-point-available analysis. H. pylori eradication rates were identical, at 93% (95% CI: 73–98% (1 week), 78–99% (2 week)). In the combined group, all but 13 ulcers were healed at 2 weeks; six required further therapy because of symptoms, while six of the seven asymptomatic patients went on to heal.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusion:An eradication regimen, based on a 2-week course of single dose lansoprazole with 1 week of antibiotic co-therapy, is effective in eradicating H. pylori, while the 2 weeks of acid suppression is usually effective in duodenal ulcer healing.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    World journal of surgery 5 (1981), S. 348-350 
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 5 (1960), S. 1-23 
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary and conclusions The augmented histamine test, the Ewald test meal, and the Diagnex tests have been compared in a series of 130 patients. The results indicate that although the results of these tests follow the same trend in a group of patients, no one test can be used to predict satisfactorily the results of the other two tests in the majority of individual patients. Although the Ewald test is as informative as the augmented histamine test in supporting a clinical diagnosis of duodenal ulcer, the latter shows most clearly the wide variations in the degree of hypersecretion in different patients with duodenal ulcer and is the most reliable test for establishing the presence of achlorhydria. The augmented histamine test is virtually free of any serious side effects and, furthermore, provides a reliable index of the parietal-cell mass. The augmented histamine test would thus appear to be of particular value as a guide to the nature and extent of surgery necessary for the satisfactory reduction of acid secretion in patients with peptic ulcer. Our findings support the claims made by previous workers regarding the value of the Diagnex test in the screening of large numbers of patients for achlorhydria or marked hypochlorhydria. Apart from its usefulness as an initial screening test in cancer detection programs, the test has a limited place in excluding a diagnosis of pericious anemia or duodenal ulcer.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1573-2568
    Keywords: antisecretory drugs ; duodenal ulcer ; gastric ulcer ; gastroesophageal reflux disease ; intragastric acidity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract 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.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1573-2568
    Keywords: MUCOSAL TURNOVER ; PEPTIC ULCER DISEASE ; GROWTH FACTORS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In order to investigate whether chronic duodenalulcer disease is a consequence of disturbed mucosalturnover and growth factor expression, we studied 16patients with duodenal ulcers before, during, and after endoscopic healing with lansoprazole orsucralfate. Before treatment, gastric fundal and antralmucosal protein turnover rates were higher in patientsthan controls, without parallel increases in growth factors. Both forms of therapy producedsimilar changes, with overall increases in duodenalmucosal turnover and transforming growth factor-α(TGF-α) and epidermal growth factor receptor (EGF-r) levels. Measurements after healingshowed persistent elevations of mucosal turnover in theantrum and duodenum and depressions of basic fibroblastgrowth factor (bFGF) in gastric fundal and duodenal mucosa. We conclude that mucosal turnover isabnormally high in patients with chronic duodenal ulcerdisease and is not easily explained by growth factorchanges. The failure of lansoprazole and sucralfate to normalize rates, despite endoscopic healing,may explain the high ulcer relapse rates innon-HP-eradicated patients.
    Type of Medium: Electronic Resource
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