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Data on Asian patients who present with reflux symptoms to their primary care physicians are limited.
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Proton pump inhibitors (PPIs) decrease the rate of rebleeding following endoscopic hemostatic therapy in patients with bleeding peptic ulcers. This study compares the efficacy of oral omeprazole vs intravenous pantoprazole in decrease of rebleeding of peptic ulcer patients.
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H. pylori infection in gerbils, associated with regenerative hyperplasia of glandular structure, results in the suppression of gastric secretion, overexpression of COX-2, and enhancement in apoptosis and impairment of both, gastric blood flow and gastrin-somatostatin link that were reversed by anti-H. pylori triple therapy and attenuated by probiotics.
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Regarding hospital antiulcer drugs, this ICF strategy was associated with more rational prescribing and usage, and an important saving of resources.
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Barrett's esophagus--intestinal metaplasia within the tubular esophagus - is a premalignant histologic lesion and a marker of cancer risk. Strategies to prevent Barrett's-related esophageal cancer have focused on reversal of Barrett's using pharmacological or surgical antireflux therapies and endoscopically-induced injury. Currently, however, there is little compelling evidence to support the reversal of Barrett's through pharmacological or surgical therapy, and endoscopic reversal of Barrett's has not yet been validated. Chemoprevention using intensive acid suppression and/or inhibition of cyclooxygenase-2 (COX-2) with nonsteroidal anti-inflammatory drugs remains a biologically plausible strategy that is supported by a rapidly growing body of scientific evidence. Data suggest that a combination of acid suppression with COX-2 inhibition might be the most effective chemopreventive strategy. Whether this approach is effective awaits the results of well-designed outcomes studies.
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We show here that concomitant omeprazole use is associated with an increased inflammatory reaction. Drug interactions may reduce the anti-inflammatory effect of clopidogrel. This mechanism maybe responsible for an increased risk of non-fatal, cardiovascular events, following stent placement.
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Healthy subjects (n = 160; ages 20 to 53 years; homozygous CYP2C19 extensive metabolizer genotype; no nicotine for 6 weeks, prescription drugs for 4 weeks, over-the-counter drugs for 2 weeks, and no caffeine or alcohol for 72 h; confined; restricted diet) received clopidogrel 75 mg/day for 9 days, at which time clopidogrel pharmacokinetic and pharmacodynamic endpoints were measured.
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Crossover 12-h oesophageal pH monitoring during Aflurax/placebo treatment. Maintenance treatment for up to 6 months with two tablets of Aflurax 1200 mg or placebo four times daily.
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Current guidelines recommend use of a proton pump inhibitor (PPI) to decrease the risk of gastrointestinal bleeding in patients taking clopidogrel (Plavix) with aspirin. A recent issue of The Medical Letter considered whether omeprazole (Prilosec, and others) or other PPIs could interfere with the antiplatelet effect of clopidogrel. The conclusion was that patients taking both drugs should probably continue to do so until more data became available. Several new publications require reconsideration of that recommendation.
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From April 2001 to January 2002, a total of 58 H. pylori-infected patients were randomly assigned to 1 of 2 regimens for 1 week: cetraxate plus clarithromycin and amoxicillin (CCA group) or pantoprazole plus clarithromycin and amoxicillin (PCA group). Follow-up endoscopy was performed at 8 weeks after the end of treatment to assess the treatment response.
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This was a randomized, open-label study enrolling 279 patients with erosive esophagitis A or B (Los Angeles classification) and typical gastroesophageal reflux disease symptoms. Patients who showed complete endoscopic and symptomatic healing after 8 weeks of proton pump inhibitor treatment were randomly allocated to maintenance treatment with omeprazole 10 mg once daily or rabeprazole 10 mg once daily for 42 weeks. The primary efficacy endpoint was the proportion of patients with symptomatic remission at 42 weeks.
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Gastric metaplasia changed to the complete type after the eradication of Helicobacter pylori, which persisted for a long period.
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EVG exposures were 40%-50% lower upon simultaneous dosing of EVG/r and antacids, probably due to local complexation with cations in gastrointestinal tract, and were unaffected with ≥2 hours staggered dosing. No relevant drug interactions were observed between EVG/co and famotidine or between EVG/r or EVG/co and omeprazole, indicating the absence of a broader pH effect on boosted EVG PK. In all studies, study treatments were well tolerated, with adverse events being generally mild to moderate in severity and primarily gastrointestinal disorders.
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Prospective study conducted on PPI-REE patients. Upon complete remission on high-dose PPI therapy (omeprazole 40 mg b.d. for 8 weeks), PPI doses were tapered followed by an endoscopic procedure after each dose reduction. The primary outcomes were sustained clinical and histological remission (<15 eos/HPF) after decreasing PPI doses.
To determine the number of times patients have brand and generic products substituted under Australia's Pharmaceutical Benefits Scheme (PBS) brand substitution policy.
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Short-term follow up.
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We undertook the present study to clarify the alteration of localization of basic fibroblast growth factor (bFGF), endothelial cells, and myofibroblasts in the healing of ethanol-induced gastric mucosal damage by the combined administration of lansoprazole and sofalcone. Wistar strain male rats were used. Ethanol 50% was given through orogastric intubation. Thirty minutes later, an aqueous solution of lansoprazole, sofalcone, a combination of lansoprazole and sofalcone, or physiologic saline was given orally. The stomach was removed and the localization of bFGF, myofibroblast, and endothelial cells was examined using monoclonal antibodies. Some rats were pretreated with indomethacin to rule out the effect of endogenous prostaglandin. The combined administration of lansoprazole and sofalcone brought about increased concentrations and immunoreactive areas of bFGF and a greater number of endothelial cells, compared with the ethanol-alone treatment. The number of myofibroblasts increased more significantly in the group treated with a combination of agents than in that treated with ethanol alone, ethanol plus sofalcone, or ethanol plus lansoprazole. Indomethacin pretreatment partly abolished the effects of single and combined administration of these agents. In conclusion, the mixed administration of lansoprazole and sofalcone accelerated the microvascular and connective tissue regeneration during the healing of ethanol-induced gastric mucosal damage.
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Ablation of Barrett's epithelium and suppression of acid secretion facilitated squamous re-epithelialization. A progenitor cell within the metaplastic tissue has the potential to differentiate normally.
Specialized intestinal metaplasia of the gastroesophageal junction was observed in 20% and in 17.2% of the patients in Groups A and B, respectively. Eradication rates were similar in subgroups A1 (84%) and B1 (83%). In Group A there was a significant improvement in GERD (P = 0.003) and IBS symptoms (P < 0.0001) as well as esophagitis (P = 0.029), when compared with Group B.
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Evaluating potential adverse effects of complex chemical mixtures in the environment is challenging. One way to address that challenge is through more integrated analysis of chemical monitoring and biological effects data. In the present study, water samples from five locations near two municipal wastewater treatment plants in the St. Croix River basin, on the border of MN and WI, USA, were analyzed for 127 organic contaminants. Known chemical-gene interactions were used to develop site-specific knowledge assembly models (KAMs) and formulate hypotheses concerning possible biological effects associated with chemicals detected in water samples from each location. Additionally, hepatic gene expression data were collected for fathead minnows (Pimephales promelas) exposed in situ, for 12 d, at each location. Expression data from oligonucleotide microarrays were analyzed to identify functional annotation terms enriched among the differentially-expressed probes. The general nature of many of the terms made hypothesis formulation on the basis of the transcriptome-level response alone difficult. However, integrated analysis of the transcriptome data in the context of the site-specific KAMs allowed for evaluation of the likelihood of specific chemicals contributing to observed biological responses. Thirteen chemicals (atrazine, carbamazepine, metformin, thiabendazole, diazepam, cholesterol, p-cresol, phenytoin, omeprazole, ethyromycin, 17β-estradiol, cimetidine, and estrone), for which there was statistically significant concordance between occurrence at a site and expected biological response as represented in the KAM, were identified. While not definitive, the approach provides a line of evidence for evaluating potential cause-effect relationships between components of a complex mixture of contaminants and biological effects data, which can inform subsequent monitoring and investigation.
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Specific-pathogen-free BALB/c mice were infected with H. felis. Colonization was assessed in longitudinal sections of gastric tissue from animals untreated or treated with omeprazole or ranitidine.
The combination of three marker substrates in a single 30-min incubation, in addition to a rapid, sensitive LC-MS/MS method, resulted in an efficient and robust method for assessing cytochrome P450 induction as compared to the conventional methodology.
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The recrudescence rate of the EBMT was 1.7% and of the MEA group 3.3% (p = 0.67). The annual reinfection rate of H. pylori of EBMT was found to be 4.45% and the MEA group 6.46%. Univariate analysis (Log-rank test) showed no association with any clinical risk factor for reinfection.
Enantiomers possess different pharmacokinetic and pharmacodynamic properties and this may not only influence the therapeutic effect of a drug but also its toxicological effects. In the present work we investigated the potential enantioselective endocrine disrupting effects of omeprazole (OME) and its two enantiomers on the human steroidogenesis using the H295R cell line. Differences in production of 16 steroid hormones were analyzed using LC-MS/MS. Additionally, to evaluate the differences in binding modes of these enantiomers, docking and molecular dynamics (MD) simulations of S-omeprazole (S-OME) and R-omeprazole (R-OME) in CYP17A1, CYP19A1 and CYP21A2 were carried out. Exposing H295R cells to OME and its enantiomers resulted in an increase of progesterone (PRO) and 17α-hydroxy-progesterone (OH-PRO) levels. At the same time, a decrease in the corticosteroid and androgen synthesis was observed, indicating inhibition of CYP21A2 and CYP17A1. In both cases, the effect of R-OME was smaller compared to that of the S-OME and a certain degree of enantioselectivity of CYP17A1 and CYP21A2 was suggested. Docking indicated that the N-containing rings of OME possibly could interact with the iron atom of the heme for S-OME in CYP17A1 and S- and R-OME in CYP21A2. However, density functional theory calculations suggest that the direct N-Fe interaction is weak. The study demonstrates enantioselective differences in the endocrine disrupting potential of chiral drugs such as omeprazole. These findings may have potential implications for drug safety and drug design.
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Ligation of the pancreatic duct in pigs leads to severe maldigestion and malabsorption of crude nutrients. Supplementation with 24 capsules of Creon (Solvay Pharmaceuticals GmbH, Hannover, Germany) per meal led to an increased digestibility of crude nutrients. With regard to optimization of the treatment of EPI no essential improvements can be achieved by adding omeprazol or lecithin to the diet. In pancreatic duct-ligated pigs the isolated addition of omeprazol led to an increase of the pre-caecal digestibility of crude fat and organic matter. With additional enzyme substitution, the application of omeprazol did not result in an improved fat digestibility. Isolated addition of lecithin to the diet resulted in a reduced total digestibility of crude fat. Offering the diet twice a day and using a higher frequency of enzyme applications (four or six instead of only two applications) had no effects on the digestibilty of crude fat or organic matter. According to the observations in pancreatic duct-ligated pigs, the addition of missing enzymes to the diet led to the best treatment results in EPI. Administration of omeprazol or a higher feeding frequency as well as the application of enzymes in small proportion of the whole meal or dosages given consecutively over the day showed no advantages. Furthermore, the present study suggests that the addition of lecithin cannot be recommended in EPI, when given diets with butter as the predominant fat source as in human dietetics.
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Barrett's oesophagus patients may continue to have abnormal oesophageal acid exposure on proton pump inhibitor therapy. The effect of factors such as Barrett's oesophagus length, hiatal hernia size and Helicobacter pylori infection on intra-oesophageal pH in Barrett's oesophagus patients has not been adequately studied.
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To assess the relationship between symptom subgroups and the effect of management strategies on primary care patients with dyspepsia.
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253 patients dispensed PPIs from the hospital pharmacy over five consecutive weeks (11 January to 15 February 1999).
Recently, some authors have examined the possibility of an interaction between proton pump inhibitors (especially omeprazole) and clopidogrel. Pharmacodynamically, this interaction is proven and leads to a reduction in anti-aggregation activity. Nevertheless, the clinical implications are not fully clarified. We are all waiting for a randomised prospective study assessing specifically this issue. Meanwhile, caution is recommended when prescribing PPI in patients taking clopidogrel.