The substituted benzimidazoles omeprazole, lansoprazole, rabeprazole, and pantoprazole were found to have in vitro activity against three different isolates of Plasmodium falciparum: D6 (which is chloroquine and pyrimethamine sensitive), W2 (chloroquine and pyrimethamine resistant), and TM91C235 (multidrug resistant). Lansoprazole and rabeprazole were the most effective against all three isolates, with a 50% inhibitory concentration (IC(50)) range of 7 to 11 microM. Omeprazole showed intermediate activity against D6 and W2 isolates, with IC(50)s of 27 to 28 microM, but had poor activity against TM91C235, with an IC(50) of 76 microM. Pantoprazole was the least effective, with IC(50)s of 73 microM against D6, 53 microM against W2, and 39 microM against TM91C235. A pharmacophore model describing the important features responsible for potent activity of the drugs was developed using computational techniques of semiempirical quantum chemical methods and the three-dimensional QSAR procedure of the CATALYST software. The important features of the pharmacophore, according to the findings based on the CATALYST procedures, are the hydrogen bond acceptor and donor sites at the benzimidine nitrogen atoms and the two aromatic hydrophobic sites in the molecules. AM1 quantum chemical calculations identified the electrostatic potential surface surrounding the sulfoxide atom as crucial for potent activity.
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Infants ages 1 to 11 months, with symptomatic GERD resistant to conservative therapy and/or previous exposure to acid-suppressive medications, were screened. After scoring >16 on a GERD symptom score (Infant Gastroesophageal Reflux Questionnaire-Revised [I-GERQ]), 344 infants were enrolled in a 1- to 3-week open-label (OL) phase and received rabeprazole 10 mg/day. Following caregiver-rated clinical improvement during the OL phase, patients were randomized to placebo, rabeprazole 5 mg, or rabeprazole 10 mg in the ensuing 5-week double-blind (DB) withdrawal phase. Primary endpoints evaluated from DB baseline to the end of the DB withdrawal phase included frequency of regurgitation, weight-for-age z score, and daily and weekly GERD symptom scores.
Proton pump inhibitors should be administered prophylactically early after esophagectomy to relieve and prevent reflux-related symptoms. Candidates for preventive therapy include those less than 64 years of age or older patients who are H. pylori-negative and without chronic atrophic gastritis.
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There was no significant difference among various proton pump inhibitors given through different routes on raising intragastric pH above 6 for 72 h after successful endoscopic hemostasis in bleeding peptic ulcer.
We aimed to evaluate the benefit of 5 days pretreatment with oral PPI before ESD to prevent bleeding.
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The plasma concentration of rabeprazole in patients treated for gastroesophageal reflux disease (GERD) has not been reported, although the concentration in healthy volunteers has been reported previously. Here, CYP2C19 genotype effects of rabeprazole on the area under the plasma concentration-time curve (AUC) and the pH elevation were studied in GERD patients.
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Rabeprazole sodium is a proton pump inhibitor that covalently binds and inactivates the gastric parietal cell proton pump (H+/K+ ATPase). Little has been published about the quantitative determination of this drug. The aim of this research was to develop a new liquid chromatographic method for quantitative determination of rabeprazole in coated tablets. The system consisted of a Hypersil Keystone Betabasic C8 column (250 x 4.6 mm, 5 microm particle size), an isocratic acetonitrile-water (35 + 65) mobile phase at a flow rate of 1.0 mL/min, and a diode array detector set at 282 nm. The following validation parameters were evaluated: linearity, precision, accuracy, specificity, detection and quantitation limits, and robustness. The method showed good linearity in the concentration range of 10-70 microg/mL. The quantitation limit was 2.43 microg/mL, and the detection limit was 0.80 microg/mL. The intra- and interday precision data showed that the method has good reproducibility (relative standard deviation = 1.03). Accuracy and robustness were also evaluated, and the results were satisfactory. The mean recovery was 101.61%. The analysis of a placebo mixture demonstrated the method is also specific.
Eligible patients with persistent infection following one or more conventional clarithromycin-containing triple therapies were enrolled in this open-label trial. Eradication of infection was documented by (14)C-urea breath test a minimum of 4 weeks after therapy and 2 weeks off any acid suppressive therapy. Culture of H. pylori and in vitro susceptibility testing to amoxicillin, clarithromycin, and gatifloxacin was done in cases of failed eradication.
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The endoscopic non-relapse rate for RE was 87.3% for the 104-week period. GERD symptoms improved based on the fact that the mean change from baseline in GERD symptom score after treatment was a negative value. Treatment was safe; and atrophy was found to have developed in virtually no cases. A few new benign fundic gland or hyperplastic polyps developed throughout the study, but no ECL carcinoids were found to have developed. Serum gastrin levels tended to increase up to 24 weeks, but there were no subsequent changes thereafter up to 104 weeks.
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Transforming growth factor-alpha (TGF-alpha), which binds to epidermal growth factor receptors (EGF-R), stimulates esophageal epithelial cell proliferation, enabling rapid repair after mucosal injury. The aim of the present study was to examine epithelial proliferation and dynamics of TGF-alpha and EGF-R gene and protein expression in rat chronic acid reflux esophagitis.
Rabeprazole clearance was lower in CYP2C19 PMs than in EMs (with average values of 10.7 vs. 16.8 l h(-1) in PMs and EMs, respectively), resulting in higher plasma levels in the former group. The values of EC(50) and k(eo) of gastrin response increased with multiple doses of rabeprazole. The k(eo) values were lower in CYP2C19 PMs than in EMs on day 1 (0.012 vs. 0.017 x 10(-4) l min(-1)), and higher than in EMs on day 4 (0.804 vs. 0.169 x 10(-4) l min(-1)) of rabeprazole treatment. The predicted gastrin-time profile showed a higher response in CYP2C19 PMs than in EMs on days 4 and 7. Helicobacter pylori was eradicated in all CYP2C19 PMs except in one patient infected by a resistant strain. In contrast, in CYP2C19 EMs the eradication rates ranged from 58 to 85%.
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Once-daily treatment with rabeprazole 10 mg or 20 mg is effective and well tolerated in preventing relapse of erosive or ulcerative GORD and associated symptoms and maintaining quality of life.
While 74% (17/23) of the controls developed esophageal cancer, animals administered rabeprazole had an incidence of cancer of 29% (5/17) (p < 0.05, Fisher's exact test). Barrett's metaplasia was found on 100% (23/23) of the rats in the placebo group, but there was a protective effect in the rabeprazole group with 65% (11/17) of the rats displaying signs of Barrett's metaplasia (p < 0.05, Fisher's exact test). All of the rats developed proliferative hyperplasia.
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Ten hospitals participated in this study. Esophageal biopsy was performed when the patients had typical EoE symptoms or when endoscopic findings revealed a typical EoE appearance. EEI was defined as the intraepithelial eosinophilic infiltration of ≥15 per HPF. Patients with EEI received rabeprazole for 8 weeks to distinguish EoE from PPI-R EEI.
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The studies presented at the recent American Congress of Gastroenterology in the field of non-variceal upper gastrointestinal bleeding (associated or not to NSAIDs or ASA use) have not been numerous but interesting. The key findings are: a) rabeprazole, the only PPI that had few studies in this field, is effective in the prevention of gastric ulcers; b) famotidine could also be effective in the prevention of complications by AAS; c) the new competitive inhibitors of the acid potassium pump are effective (as much as PPIs) on the recurrence of peptic ulcers by ASA; d) early endoscop (<8 h) in non-variceal upper gastrointestinal bleeding seems to offer no better results than those made in the first 24 h; e) endoscopic therapy in Forrest 1a ulcers does not obliterate the bleeding artery in 30% of cases and is the cause of bleeding recurrence; f) alternative therapies with glue or clotting products are being increasingly used in endoscopic therapy of gastrointestinal bleeding; g) liberal administration of blood in the GI bleeding is associated with poor prognosis; h) lesions of the small intestine are frequent cause of gastrointestinal bleeding when upper endoscopy shows no positive stigmata; and i) capsule endoscopy studies have high performance in gastrointestinal bleeding of obscure origin, if performed early in the first two days after the beginning of the bleeding episode.
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No randomized controlled trial (RCT) has compared all European-licensed standard- and double-dose PPIs for the healing of severe erosive oesophagitis.
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A total of 200 patients with proven Helicobacter pylori infection randomly received 10-day standard sequential therapy (n = 100) or levofloxacin-containing sequential therapy (n = 100). The standard sequential therapy group received rabeprazole and amoxicillin for 5 days, followed by rabeprazole, clarithromycin, and metronidazole for 5 more days. The levofloxacin-containing sequential therapy group was treated with rabeprazole and amoxicillin for 5 days, followed by rabeprazole, levofloxacin, and metronidazole for 5 more days.
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A rapid, simple and sensitive reversed-phase high-performance liquid chromatographic-tandem mass/mass spectrometry (HPLC/MS/MS) method has been developed for the measurement of rabeprazole (CAS 117976-89-3) concentrations in human plasma and its use in bioavailability studies has been evaluated. The method was linear in the concentration range of 0.05-2.5 microg/ml. The lower limit of quantification (LLOQ) was 0.05 microg/ml in 1 ml plasma sample. The intra- and inter-day relative standard deviation across three validation runs over the entire concentration range was less than 8.2% and 7.53%, respectively. This method was successfully applied for the evaluation of pharmacokinetic profiles of rabeprazole tablet in 18 healthy volunteers. The main pharmacokinetic parameters obtained were: AUC(0-t) 1415.88 +/- 505.46 and 1457.44 +/- 524.40 ng x h/ml, AUC(0-infinity) 1439.10 +/- 507.47 and 1479.81 +/- 527.83 ng h/ml, C(max) 678.24 +/- 278.93 and 657.83 +/- 250.86 ng/ml, t1/2 1.48 +/- 0.19 and 1.38 +/- 0.24 h, t(max) 3.8 +/- 0.8 and 3.7 +/- 0.5 h for the test and reference formulations, respectively. No statistical differences were observed for C(max) and the area under the plasma concentration time curve for rabeprazole. 90% confidence limits calculated for C(max) and AUC from zero to infinity (AUC(0-infinity)) of rabeprazole were included in the bioequivalence range (0.8-1.25 for AUC).
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Patients with recurrent angina-like chest pain and normal coronary angiogram were recruited. The frequency and severity of chest pain were recorded. All patients underwent esophagogastroduodenoscopy and 48-h Bravo ambulatory pH monitoring before receiving rabeprazole 20 mg bd for 2 weeks.
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Investigated FD was diagnosed using the Rome III criteria. Subjects who did not respond to 1 week of single-blind placebo treatment in a run-in period were randomly assigned to 8 weeks of double-blind treatment with rabeprazole 10 mg, 20 mg, 40 mg or placebo, once daily. Dyspeptic symptoms were assessed by a dyspepsia symptom questionnaire (7-point Likert scale) and symptom diary.
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Extended pH recording improves the detection of abnormal acid reflux and increases the number of recorded symptoms and acid reflux events. Combined off and on PPI therapy pH testing enhances the interpretation of pH monitoring and symptom-reflux correlations, which can be helpful in the management of patients with PPI-unresponsive gastroesophageal acid reflux symptoms.
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A total of 116 patients with proven H. pylori infection received 10-day sequential therapy (20 mg rabeprazole and 1 g amoxicillin, twice daily for the first 5 days, followed by 20 mg rabeprazole, 500 mg clarithromycin, and 500 mg metronidazole, twice daily for the remaining 5 days); 130 patients received 7-day triple therapy (20 mg rabeprazole, 500 mg clarithromycin, and 1 g amoxicillin, twice daily for 7 days). Eradication was evaluated by the (13) C-urea breath test, 4 weeks after the completion of treatment. Compliance and adverse events were assessed.
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Acute interstitial nephritis is an uncommon but important cause of acute renal failure. Proton pump inhibitors are now thought to be the most common class of drugs implicated in drug-induced acute interstitial nephritis. This is the first reported case of rabeprazole-induced acute interstitial nephritis.
To perform a systematic review of the efficacy of rabeprazole-based therapies in Helicobacter pylori eradication, and to conduct a meta-analysis comparing the efficacy of rabeprazole and other proton pump inhibitors when co-prescribed with antibiotics.
Artificial ulcers remain a major complication after Endoscopic submucosal dissection (ESD). The development of more effective treatment regimen for this ulcer is required than the use of proton pump inhibitor (PPI) alone.
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To compare the acid-inhibitory effects of esomeprazole 40 mg and rabeprazole 20 mg in relation to CYP2C19 genotype and pharmacokinetics.
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CLE can be objective, accurate, and real time in investigating gap density. Teprenone and rabeprazole can prevent indomethacin-induced intestinal lesions and protect the epithelial barrier by intervening in the tumor necrosis factor-α pathway. Gap density was expected to be an indicator of evaluating intestinal inflammation and drug efficacy.