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In this study, we evaluated the effect of proton pump inhibitors (PPIs) on in vitro antimicrobial activity of tigecycline against several species of clinical pathogens. Clinical non-duplicate isolates of Acinetobacter baumannii, Staphylococcus aureus, Enterococcus faecalis and three species of Enterobacteriaceae (Escherichia coli, Klebsiella pneumonia and Enterobacter cloacae) were collected from a tertiary hospital and their MICs of tigecycline alone and in combination with PPIs (omeprazole, lansoprazole and pantoprazole) were determined. With one randomly selected isolate of each bacterial species, an in vitro time-kill study was performed for the confirmation of the effect of PPIs on tigecycline activity. The MIC changes after PPIs addition correlated with the PPIs concentrations in the test media. Compared with tigecycline alone, the addition of 5 mg/L PPIs could increase the MICs of tigecycline by 0 to 2-fold and the addition of 50 mg/L PPIs could increase the MICs of tigecycline by 4 to >128-fold. The time-kill study confirmed that the addition of PPIs could affect the in vitro activity of tigecycline. Even at low concentration (5 mg/L) of omeprazole and pantoprazole, antagonistic effect could be observed in E. cloacae and E. faecalis strains. We conclude that In vitro activity of tigecycline can be influenced by the presence of PPIs in a concentration-dependent manner.
H pylori eradication (intention to treat) was 104/121 (86.0%) with LAC, 87/131 (66.4%) with LAM, 103/118 (87.3%) with LCM, and 94/126 (74.6%) with OAM. There was a significant difference (p < 0.001) in the proportion of patients in whom eradication was successful between LAC and LCM when compared with LAM, but no significant difference (p = 0.15) between LAM and OAM. Metronidazole resistance before treatment was identified as a significant prognostic factor with regard to eradication of H pylori. The regimens which contained metronidazole were significantly less effective than those without metronidazole in the presence of pretreatment resistant H pylori. There was no difference among the treatment groups with regard to the incidence and severity of adverse events reported.
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During the 12-month period, 11/20 patients (52.4%) taking lansoprazole 15 mg daily suffered recurrence of symptoms, compared to 4/20 patients (20%) treated with lansoprazole 15 mg and rebamipide 300 mg daily (P < 0.05). Rebamipide was detected in the esophageal mucosa 90-180 min after oral administration. IL-8 mRNA expression in the esophageal mucosa of patients with rebamipide was significantly decreased compared with that of patients without rebamipide.
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Many of the drugs currently used in medical practice are racemates. The enantiomers of a racemic drug differ in pharmacodynamics and/or pharmacokinetics, thus in some cases it is preferable to develop pure enantiomers by racemic switch. In a recent study by Pai et al, dexrabeprazole [R(+)-rabeprazole] (10 mg) was found to be more effective than rabeprazole (20 mg) in the treatment of gastroesophageal reflux disease. We read with great interest in this study and discussed whether such racemic switch would be applicable to other proton-pump inhibitors (PPIs). A literature review indicates that stereoselective pharmacokinetics, rather than stereoselective pharmacological activity, is the main cause of differences in clinical efficacy between pure enantiomer and racemic PPI. Racemic switches of PPI provide the therapeutic advantages such as reducing metabolic load on the body, simplifying pharmacokinetics, providing benefit to the non-responders to standard dose of racemate, more homogenous response to treatment and better efficacy with equal safety. Further studies in quantitative structure-activity relationships (QSARs) are needed to address the fact that the preferred enantiomer of PPI is not always in the same absolute configuration, i.e. S-form is for omeprazole, pantoprazole and tenatoprazole whereas R-form is for lansoprazole and rabeprazole.
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It is possible to combine the components of bismuth-based triple therapy into a single capsule. Based on the results it can be assumed that the capsule releases its content in the stomach. When combined with lansoprazole it reaches high cure rates, especially in metronidazole sensitive strains. This new approach simplifies bismuth-based anti-Helicobacter therapy.
prevacid 40 mg
Peptic ulcer disease in children is rare. Therefore, the diagnosis can be missed until complications such as perforation or hemorrhage occur. Few reports have investigated the procedures and outcomes of children who have undergone operations for perforated duodenal ulcers. We report our experience with the modified Graham technique for perforated duodenal ulcers in nine children and review the literature. Methods : The records of patients operated on for a perforated duodenal ulcer in the last 8 years in two pediatric surgery centers were evaluated retrospectively. Patient demographics, symptoms, time to admission to hospital, operative findings, and postoperative clinical course were evaluated. Results : Nine children (mean age 13.2 years, range 6-170 years) were included. All patients were admitted in the first six hours after their abdominal pain started. In three patients, there was free air on plain x-rays, while the x-rays were normal in six. All perforations were located on the anterior surface of the first part of the duodenum and repaired with primary suturing and Graham patch omentoplasty. The recovery was uneventful in all patients. In five patients, urea breath tests were performed postoperatively for Helicobacter Pylori, and the results were positive. All patients underwent triple therapy with lansoprazole, amoxicillin, and clarithromycin. The mean follow-up time was 58 (range 3-94) months. Conclusions : Peptic ulcer perforation should be suspected in children who have acute abdominal pain and peritoneal signs, especially when their suffering is intense. The simple patch repair and postoperative triple therapy for Helicobacter Pylori are safe and satisfactory for treating peptic ulcer perforation in children.
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Forty-four patients (male to female ratio, 27 : 17; mean age, 53 years; 55% with oesophagitis) with gastro-oesophageal reflux disease were randomized to receive lansoprazole 30 mg or 15 mg once daily for 4 weeks. Measurement of the 24-h oesophageal and intragastric pH, gastro-oesophageal reflux disease symptoms and quality of life was performed at baseline and during the last week of each dosing period.
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It has been documented that sucralfate, a basic aluminum salt, enhances the efficacies of antibiotics against Helicobacter pylori, resulting in eradication rates comparable to those associated with the use of proton pump inhibitors. However, its mechanism of action remains unclear. The aim of the present study was to investigate sucralfate's ability to complement antibiotic treatment of H. pylori infection in vivo. Four weeks following induced H. pylori infection, clarithromycin (CAM) and amoxicillin (AMPC) were administered orally to C57BL/6 mice for 5 days, both with and without sucralfate or lansoprazole. When sucralfate was concurrently given with CAM and AMPC at the maximum noninhibitory doses for the treatment of H. pylori infection, the bacterial clearance rates were comparable to those achieved by treatment with lansoprazole plus those antibiotics. The results of pharmacokinetic studies showed that lansoprazole delayed gastric clearance and accelerated the absorption of CAM, whereas sucralfate suppressed both gastric clearance and absorption. AMPC was undetectable in all samples. Scanning electron microscopy with a microscope to which a energy dispersive spectrometer was attached revealed that aluminum-containing aggregated substances coated the mucosa surrounding H. pylori in mice receiving sucralfate plus antibiotics, whereas the gastric surface and pits where H. pylori had attached were clearly visible in mice receiving lansoprazole plus antibiotics. The addition of sucralfate to the antibiotic suspension resulted in a more viscous mixture that bound to the H. pylori-infected mucosa and that inhibited the loss of CAM bioavailability in the acidic environment. Sucralfate delays gastric clearance of CAM and physically captures H. pylori through the creation of an adherent mucus, which leads to bacterial clearance.
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Patients with 2 - 6 cm of Barrett's esophagus with histology demonstrating LGD on their last two sequential endoscopies over the previous 2 years and confirmed by two pathologists were enrolled in this prospective, single-center trial. Circumferential ablation was carried out at baseline and at 4 months (if residual Barrett's esophagus present). Endoscopy with 4-quadrant biopsies every 1 cm was performed at 1, 3, 6, 12, and 24 months. After 1 year, focal ablation was applied to any visible Barrett's esophagus or irregularity of the squamocolumnar junction. Patients received lansoprazole 30 mg bid. Complete responses for dysplasia (CR-dysplasia) and intestinal metaplasia (CR-IM) at 2-year follow-up, with complete response defined as "all biopsies negative for dysplasia or intestinal metaplasia" were the main outcomes.
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To assess the risk of reflux oesophagitis in patients with functional dyspepsia after treatment for H. pylori infection.
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Helicobacter pylori (HP) eradication therapy is a useful treatment for idiopathic thrombocytopenic purpura (ITP). Some investigators have also reported the effects of proton pump inhibitor (PPI) monotherapy on ITP. We performed a randomized study of HP eradication therapy and PPI monotherapy on ITP. Four of nine patients achieved complete remission (CR), two of nine achieved partial remission (PR) in HP eradication therapy, three of eight achieved CR, and two of eight achieved PR in PPI monotherapy. No significant differences were observed in the CR + PR of these patients between HP eradication therapy and PPI monotherapy. As for cost comparisons, HP eradication therapy is cheaper than PPI monotherapy, but it is less effective.
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With these cut-off values, the sensitivity, specificity, and validity for determination of eradication of H. pylori-on the basis of culture, histology, the rapid urease test, and a polymerase chain reaction method-were 100.0%, 93.1%, and 96.2%, respectively. These cut-off values could be applied to both gastric ulcer and duodenal ulcer.
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It is helpful in clinical practice to predict the effects of eradication therapy on Helicobacter pylori.
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The efficacy of levofloxacin triple therapy has fallen below 80% in the second-line treatment of Helicobacter pylori (H. pylori). We aimed to assess whether the levofloxacin sequential therapy is more effective than levofloxacin triple therapy in the second-line treatment.
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Children were divided into two groups based upon age: group 1 included children aged 6-8 years and group 2 included children aged 9-11 years. Within each group an equal number of male and female subjects were recruited. Within each of the four strata defined by group and sex, an equal number of subjects were randomised to taste the strawberry-flavoured lansoprazole 15mg orally disintegrating tablet or the ranitidine 75mg/5mL peppermint-flavoured syrup samples in position 1. In group 1, the lansoprazole 15mg delayed-release orally disintegrating tablet was dispersed in 5mL of water, while in group 2, children gently rolled the tablet on the tongue until dissolution, before swallowing the particles. Children given the dose of lansoprazole dispersed in water (group 1) and the ranitidine dose (groups 1 and 2) were to taste it, swish it in their mouth for up to 10 seconds, and then swallow it. Children were given ambient temperature water and unsalted crackers to cleanse the palate during a 10-minute break between tastings.
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In two standardized, randomized crossover studies, Helicobacter pylori negative healthy volunteers (study A: 19 males, 5 females; study B: 13 males, 10 females) received esomeprazole 40 mg and either lansoprazole 30 mg (study A) or rabeprazole 20 mg (study B) orally once daily in the morning for 5 days. Continuous 24-hour intragastric pH recording was performed on day 5.
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Fifty-five medical charts were reviewed at the beginning and end of 1 month.
Forty consecutive patients with LPR documented by double-probe pH monitoring were evaluated prospectively. Symptom response to therapy with proton pump inhibitors was assessed at 2, 4, and 6 months of treatment with a self-administered reflux symptom index (RSI). In addition, transnasal fiberoptic laryngoscopy (TFL) was performed and a reflux finding score (RFS) was determined for each patient at each visit.
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The results of studies of the effects of effervescent ranitidine tablets on intragastric pH and on the relief of heartburn are reviewed.
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The aims of this study were to investigate the clinical plasma pharmacokinetic properties of lansoprazole and its metabolites in healthy Chinese male volunteers, and to assess the influences of CYP2C19 on the pharmacokinetics of lansoprazole.
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To evaluate the role of antibiotic susceptibility for the treatment outcome of proton pump inhibitor-dependent and independent Helicobacter pylori eradication regimens.
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Combination therapy based on proton pump inhibitor and two antibiotics is superior to bismuth-based therapy for one week. Gastric-mucosal culture testing for sensitivity of H. pylori to antibiotics is probably unnecessary before the initiation of therapy for patients with eradication failure.
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A strict correlation between Helicobacter pylori eradication and an increase in platelet count has previously been reported in patients with chronic idiopathic thrombocytopenic purpura (ITP). To clarify the pathogenesis of H. pylori-induced ITP and the factors predicting the platelet response to H. pylori eradication therapy, we evaluated the markers of atrophic gastritis in ITP patients.