In patients with NERD and mild symptoms, both on-demand and daily treatment models of maintenance therapy showed a similar high efficacy, whereas intermittent therapy was significantly less effective. However, general satisfaction of each treatment options was high and non-significantly different between the groups. Due to a pilot character of this study further investigation based on a larger number of patients is necessary to confirm the clinical value of cheaper models of maintenance therapy which could be then recommended as more cost-effective.
The eradication resistance index in subjects showing eradication failure and those showing successful eradication was 9.72 +/- 6.63 and 1.25 +/- 2.31, respectively (p < 0.001). When a cutoff value of 3 was used, the eradication resistance index predicted the response to therapy with a specificity of 93.8%, sensitivity of 81.8%, and accuracy of 92.5%.
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Lansoprazole increased HO-1 mRNA levels in endothelial cells and HO-1 protein levels in macrophages. In addition, lansoprazole-induced ferritin protein levels in both cell systems. Moreover, induction of the antioxidant proteins HO-1 and ferritin by lansoprazole was followed by a decrease in NADPH-mediated ROS formation. The radical scavenging properties of lansoprazole were diminished in the presence of the HO inhibitor, chromium mesoporphyrin IX. Induction of HO-1 gene expression by lansoprazole was not related to oxidative stress or to the activation of the mitogen-activated protein kinase pathway. However, the phosphatidylinositol 3-kinase inhibitor LY294002 showed a concentration-dependent inhibition of HO-1 mRNA and promoter activity.
Extremely effective drugs used in the therapy of diseases etiologically associated with excessive HCl secretion by the gastric mucosa include proton pump blockers. Their obvious advantage, as compared with commonly used drugs, is that they cause a marked drop of HCl production by the gastric mucosa regardless of the type of stimulus, i.e. whether parietal cell receptors are influenced. Their therapeutic action is extremely effective, while side-effects are minimal. The publication gives the basic indications of administration of proton pump blockers, compares their therapeutic efficiency with H2 blockers and draws attention to possible pitfalls of therapy.
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The most frequent symptom was abdominal pain (89.2%). Fifty-four per cent of the subjects had a family history of dyspeptic symptoms. Sixty-six patients (64.7%) exhibited nodularity in the antral mucosa. The sensitivities of the diagnostic tests in histologically proven cases were as follows: urea breath test 100%, rapid urease test 89.2%, serology 71.9%, and culture 54.9%. Metronidazole had the highest frequency of resistance (36.4%) and the rate of clarithromycin resistance was 18.2%. The eradication rate after first-line therapy was 75.5%, and abdominal pain and dyspeptic symptoms were reduced or completely resolved in 75.7% of the successful-eradication cases. The proportion of failed-eradication cases that responded well to quadruple-drug therapy was 93.8%.
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Lansoprazole was superior to gefarnate in reducing the risk of gastric or duodenal ulcer recurrence in patients with a definite history of gastric or duodenal ulcers who required long-term LDA therapy.
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In a placebo-controlled clinical study of peptic ulcer patients with H. pylori infection, patients were randomized to receive lansoprazole, clarithromycin and tinidazole twice-daily, clarithromycin and tinidazole once-daily with lansoprazole or with placebo. Helicobacter pylori status was assessed by culture and antibiotic susceptibility by E-test minimal inhibitory concentration (MIC) in 205 clinical isolates.
prevacid 30 mg
Medial vascular calcification (MVC) is common in patients with chronic kidney disease, obesity, and aging. MVC is an actively regulated process that resembles skeletal mineralization, resulting from chondro-osteogenic transformation of vascular smooth muscle cells (VSMCs). Here, we used mineralizing murine VSMCs to study the expression of PHOSPHO1, a phosphatase that participates in the first step of matrix vesicles-mediated initiation of mineralization during endochondral ossification. Wild-type (WT) VSMCs cultured under calcifying conditions exhibited increased Phospho1 gene expression and Phospho1(-/-) VSMCs failed to mineralize in vitro. Using natural PHOSPHO1 substrates, potent and specific inhibitors of PHOSPHO1 were identified via high-throughput screening and mechanistic analysis and two of these inhibitors, designated MLS-0390838 and MLS-0263839, were selected for further analysis. Their effectiveness in preventing VSMC calcification by targeting PHOSPHO1 function was assessed, alone and in combination with a potent tissue-nonspecific alkaline phosphatase (TNAP) inhibitor MLS-0038949. PHOSPHO1 inhibition by MLS-0263839 in mineralizing WT cells (cultured with added inorganic phosphate) reduced calcification in culture to 41.8% ± 2.0% of control. Combined inhibition of PHOSPHO1 by MLS-0263839 and TNAP by MLS-0038949 significantly reduced calcification to 20.9% ± 0.74% of control. Furthermore, the dual inhibition strategy affected the expression of several mineralization-related enzymes while increasing expression of the smooth muscle cell marker Acta2. We conclude that PHOSPHO1 plays a critical role in VSMC mineralization and that "phosphatase inhibition" may be a useful therapeutic strategy to reduce MVC.
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We studied the influence of lansoprazole on Helicobacter pylori-elicited neutrophil activation, including the oxidative burst and infiltration of gastric mucosa, and confirmed whether radiolabeled lansoprazole is actually detected in gastric neutrophils. The oxidative burst of purified human neutrophils was measured by luminol-dependent chemiluminescence (ChL). [3H]Lansoprazole uptake sites in human gastric mucosa were observed by autoradiography. The magnitude of neutrophil infiltration of gastric mucosa was assessed by tissue myeloperoxidase (MPO) content. ChL assay indicated that oxygen-derived free radical production was increased twofold by adding H. pylori water extract, which was significantly inhibited by lansoprazole (10(-4) M). Gastric biopsy samples were obtained endoscopically from patients with H. pylori-positive gastritis. Autoradiographic examination revealed that the [3H]lansoprazole binding site was present in the cytoplasmic granules of infiltrated neutrophils. Tissue MPO content was significantly decreased after treatment with lansoprazole. These data suggest that lansoprazole binds directly to neutrophils, subsequently inhibiting neutrophil accumulation and release of toxic metabolites.
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Proton pump inhibitors are the most potent drug treatment for gastro-oesophageal reflux disease. Pre-meal dosing maximizes efficacy while sub-optimal dose timing may limit efficacy.
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Lansoprazole 30 mg maintained an intragastric pH > 4 for 10.5 h vs. 9.6 h for lansoprazole 15 mg (P = 0.44). The percentage total time at oesophageal pH < 4 was similar for lansoprazole 30 mg and 15 mg (2.0% vs. 2.3%, P = 0.30). The proportion of patients with complete cure of heartburn and acid regurgitation and the quality of life assessment were similar for lansoprazole 30 mg and 15 mg. Both dosages of lansoprazole were well tolerated and the compliance was 100% in both groups.
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Polymorphism in interleukin-1beta (IL-1beta) is associated with intragastric pH levels in Helicobacter pylori-positive subjects. Intragastric pH levels affect the activity of antibiotics against H. pylori in the stomach. The aim of this study was to investigate whether IL-1beta polymorphism is associated with eradication rates of H. pylori by triple therapy with a proton pump inhibitor (PPI), amoxicillin, and clarithromycin.
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31 (33%) of 93 patients in whom H. pylori was not eradicated had a negative breath test result while receiving lansoprazole. The proportions of patients whose breath test results were positive after completion of lansoprazole therapy were 91% (95% CI, 83% to 96%) at 3 days, 97% (CI, 90% to 99%) at 7 days, and 100% (CI, 96% to 100%) at 14 days.
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The protective effects of the proton pump inhibitor lansoprazole on gastric mucosal damage induced by ethanol-HCl or hemorrhagic shock were investigated in the present study. The morphometric analysis of gastric histological sections revealed that lansoprazole dose-dependently reduced mucosal injury evoked by ethanol-HCl (ED50 = 24.3 micromol/kg) or hemorrhagic shock (ED50 = 38.9 micromol/kg), these effects being associated with marked increments of Alcian blue recovery from gastric bound mucus (ED50 = 31.4 micromol/kg and 27.6 micromol/kg, respectively). In addition, lansoprazole inhibited gastric acid secretion from pylorus-ligated rats (ED50 = 9.8 micromol/kg). Further experiments, performed on rats with ethanol-HCl-induced gastric injury, indicated that the protective effects of lansoprazole were not modified by L-365,260, suramin, N(G)-nitro-L-arginine, or systemic ablation of capsaicin-sensitive sensory nerves, whereas they were partly blocked by indomethacin and fully prevented by N-ethyl-maleimide. In addition, lansoprazole did not modify somatostatin concentrations in gastric mucosa. The present results provide evidence that lansoprazole prevents the necrotic damage of gastric mucosa induced by ethanol-HCl or hemorrhagic shock. According to the rank order of ED50 values, these effects appear to depend mainly on the enhancement of the gastric mucus barrier rather than on the reduction of acid secretion. It is also proposed that an increased production of prostaglandins, as well as an increased availability of sulfhydryl compounds at level of gastric mucosa may account for the gastroprotective effects of lansoprazole.
Three hundred fifty-three patients with an active, nonmalignant gastric ulcer at least 5 mm in diameter confirmed by endoscopy and biopsy and who continued to receive stable doses of NSAIDs.
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Esomeprazole, a new proton pump inhibitor, is the S-isomer of omeprazole and is the first such inhibitor to be developed as a single isomer. Esomeprazole provided better control of intragastric pH than omeprazole, lansoprazole and pantoprazole in trials conducted in patients with gastro-oesophageal reflux disease (GORD) or healthy volunteers (n = 20 to 115). In 2 large randomised, double-blind multicentre trials esomeprazole 20 and/or 40mg for 8 weeks produced higher healing rates of erosive oesophagitis and better symptom control than omeprazole 20 mg in patients with GORD. Esomeprazole 10, 20 or 40mg once daily for 6 months maintained healing versus placebo (p < 0.001) in patients with endoscopically confirmed healed erosive oesophagitis in 2 large randomised, double-blind multicentre trials. Similarly, symptom-driven on-demand use of esomeprazole effectively controlled symptoms of GORD (heartburn) for 6 months in 2 large placebo-controlled trials. Esomeprazole-based triple therapy for 7 days was as effective for eradication of Helicobacter pylori as longer omeprazole-based therapy in 2 randomised double-blind trials including about 450 patients each. Endoscopically confirmed ulcer healing 4 weeks after treatment initiation was reported in about 90% of patients with active duodenal ulcer in both treatment groups. Esomeprazole-based triple therapy for 10 days was more effective than esomeprazole plus clarithromycin for eradication of H. pylori in 233 patients.
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In order to investigate the mechanism by which proton pump inhibitor increases serum pepsinogen levels, we evaluated the effects of ulcer location and IgG antibody against Helicobacter pylori on lansoprazole-induced elevations. Patients with endoscopically proven peptic ulcer received lansoprazole 30 mg/day for 6 or 8 weeks; pepsinogen I and II levels, along with antibody to H. pylori, were measured in fasting blood samples. We found that whether or not antibody to H. pylori was present, pepsinogen I and II levels and the I/II ratio rose significantly in lansoprazole-treated patients. Patients with stomach-body ulcers showed smaller increases in both pepsinogens than did those with ulcers in the gastric angle/antrum or in the duodenum. In conclusion, lansoprazole increases serum levels of both pepsinogens I and II, although a larger increase in pepsinogen I elevates the pepsinogen I/II ratio. The relatively small increases seen in patients with stomach-body ulcers suggest atrophic changes in the gastric mucosa in patients with stomach-body ulcer.
prevacid recommended dosage
Dehydroabietic acid derivatives have been reported to display antisecretory and antipepsin effect in animal models. Some 19 dehydroabietic acid diterpenes were prepared and assessed for gastroprotective activity in the HCl/EtOH-induced gastric lesions in mice as well as for cytotoxicity in human lung fibroblasts (MRC-5) and human epithelial gastric (AGS) cells. At a single oral dose of 100 mg kg(-1), highest gastroprotective effect was provided by dehydroabietanol, its corresponding aldehyde, dehydroabietic acid (DHA) and its methyl ester, N-(m-nitrophenyl)-, N-(o-chlorophenyl)- and N-(p-iodophenyl)abieta-8,11,13-trien-18-amide (compounds 12-14), N-2-aminothiazolyl- and N-benzylabieta-8,11,13-trien-18-amide (compounds 18-19) being as active as lansoprazole at 20 mg kg(-1) and reducing the lesion index by at least 75%. In the compound series including the alcohol, ester, aldehyde, acid and methyl ester at C-18 (compounds 1-9), highest activity was related with the presence of an alcohol, aldehyde, acid or methyl ester at C-18, the activity being strongly reduced after esterification. The cytotoxicity of the compounds 1-9 towards AGS cells and fibroblasts was higher than the values for the amides 10-19. In the compounds 10-19, the best gastroprotective effect was observed for the aromatic amides 12-14 (75-85% inhibition of gastric lesions) bearing a nitro or halogen function in the N-benzoyl moiety. Lowest cytotoxicity was found for the amides, with IC(50) values >1000 microM for fibroblasts and from 200 up to >1000 microM for AGS cells, respectively. The N-2-aminothiazolyl- and N-benzylamide derivatives were also very active as gastroprotectors with higher cytotoxicity against AGS cells.
Seventy patients were surveyed within 1 year following surgery (subchronic phase), of whom 35 (50%) suffered from coughing, as compared to 30 (18%) of 170 whose postoperative time was 1 year or more (p < 0.0001). Presence of lung cancer, mediastinal lymph node resection, and gastroesophageal reflux (GER) symptoms were significant factors in the group of subchronic patients. Of the 20 patients who received empiric therapy, 90% saw their coughing symptoms improve after the course of medication.
prevacid usual dosage
A total of 24 healthy male subjects were enrolled. Co-administration with lansoprazole decreased the mean maximum plasma concentration (C(max)) of bosutinib from 70.2 to 42.9 ng/mL, and the total area under the plasma concentration-time curve (AUC) from 1,940 to 1,470 ng·h/mL. Log-transformed bosutinib pharmacokinetic parameters indicated significant between-treatment differences; the least squares geometric mean ratio for C(max) was 54 % (95 % CI 42-70) and for AUC was 74 % (95 % CI 60-90). Mean apparent total body clearance from plasma after oral administration increased from 237 to 330 L/h, and the median time to reach Cmax increased from 5 to 6 h, although this change may be related to decreased bosutinib absorption when combined with lansoprazole. When co-administered with lansoprazole, bosutinib maintained an acceptable safety profile, which was primarily characterized by diarrhea (33 %), headache (21 %), and nausea (13 %). One subject experienced serious adverse events of diverticulitis, gastritis, and duodenitis after co-administration; however, no participant withdrew because of toxicity.
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Clopidogrel is a widely used antiplatelet agent for the secondary prevention of cardiovascular events in patients with stable coronary heart disease, acute coronary syndromes and ischemic stroke. Even though clopidogrel is safer than aspirin in terms of risk for gastrointestinal (GI) bleeding, the elderly, and patients with a history of prior GI bleeding, with Helicobacter pylori infection or those who are also treated with aspirin, anticoagulants, corticosteroids or nonsteroidal anti-inflammatory drugs are at high risk for GI complications when treated with clopidogrel. Accordingly, proton pump inhibitors are frequently administered in combination with clopidogrel to reduce the risk for GI bleeding. Nevertheless, pharmacodynamic studies suggest that omeprazole might attenuate the antiplatelet effect of clopidogrel. However, in observational studies, this interaction does not appear to translate into increased cardiovascular risk in patients treated with this combination. Moreover, in the only randomized, double-blind study that assessed the cardiovascular implications of combining clopidogrel and omeprazole, patients treated with clopidogrel/omeprazole combination had reduced risk for GI events and similar risk for cardiovascular events than patients treated with clopidogrel and placebo. However, the premature interruption of the study and the lack of power analysis in terms of the cardiovascular endpoint do not allow definite conclusions regarding the cardiovascular safety of clopidogrel/omeprazole combination. Other proton pump inhibitors do not appear to interact with clopidogrel. Nevertheless, given the limitations of existing observational and interventional studies, the decision to administer proton pump inhibitors to patients treated with clopidogrel should be individualized based on the patient's bleeding and cardiovascular risk.
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Using 24-h pH monitoring, we studied the optimal dose and mode of administration of lansoprazole (LAN) injection in healthy adult male volunteers in three tests of antisecretory effect. We followed this with a dose-finding study, using the drug's suppressive effect on increased gastric acid secretion due to surgical stress as the indicator. Finally, we conducted a pilot study to determine the optimal mode of administration and efficacy of the drug in patients with haemorrhage from the upper gastrointestinal tract. Twenty-four-hour intragastric pH monitoring established the order of potency of the different regimens: LAN 30 mg b.d. > LAN 15 mg b.d.; and LAN 30 mg b.d., intravenous drip infusion = LAN 30 mg b.d., bolus injection. Lansoprazole 30 mg b.d. appeared to be slightly more effective than LAN 15 mg b.d. in suppressing increased gastric acid secretion due to post-operative stress and in haemostasis in patients with upper gastrointestinal bleeding. No severe adverse effects were observed in either study.
Seventy-five reports of trials with 104 dual therapy treatment arms were reviewed. H. pylori eradication rates reported with ranitidine bismuth citrate plus clarithromycin range from 70-96% with a pooled observed rate of 85%. With omeprazole plus clarithromycin, reported eradication rates range from 27-90% with the pooled reported rate being 66%. Few data are available with either lansoprazole or ranitidine hydrochloride plus clarithromycin.
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Genotypic clarithromycin resistance was detected in only 11.3% of H. pylori infections in Thailand. Sequential therapy is highly effective in clarithromycin-sensitive but is less effective in clarithromycin-resistant H. pylori. PCR-molecular test could be a useful tool to identify antimicrobial resistance for optimizing an eradication regimen.
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To determine the prevalence of sub-optimal proton pump inhibitor dosing in a community-based gastro-oesophageal reflux disease population.
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The purpose of this study was to elucidate the systemic effects of H. pylori infection by comparing differential counts of leukocytes and platelets in peripheral blood before and after eradication of H. pylori.
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Our results indicate that chemokines produced locally in the esophageal mucosa may be involved in the development and progression of RE.