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After a first clinical study showing a high prevalence of gastrointestinal tract diseases in brachycephalic dogs presented for upper respiratory syndrome, a prospective study was performed to determine the influence of medical treatment for gastrointestinal tract disorders associated with upper respiratory syndrome surgery.
Twenty-eight evaluable patients were included in the analysis. In patients treated with erlotinib and esomeprazole with cola, the mean AUC0-12h increased 39% (range, -12% to 136%; P = .004), whereas in patients not treated with the PPI, the mean AUC0-12h was only slightly higher (9%; range, -10% to +30%; P = .03) after erlotinib intake with cola.
Clopidogrel is a pro-drug and its intestinal absorption is limited by the P-glycoprotein encoded by the ABCB1 gene. It is metabolized hepatically by cytochrome P450 enzymes encoded by CYP genes to produce an active metabolite that antagonizes the P2Y12 platelet receptor. Some patients exhibit poor clopidogrel responsiveness due to polymorphisms, resulting in thrombotic events. The aim of this study was to determine the relationship between poor clopidogrel responsiveness and the ABCB1, CYP and P2RY12 gene polymorphisms among patients undergoing percutaneous coronary intervention (PCI).
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A high proportion of our patients with metronidazole resistant strains of H. pylori failed eradication therapy when a nitroimidazole containing regime was used. It may not be appropriate to use a nitroimidazole containing without prior knowledge of the antibiotic sensitivity pattern of the H. pylori isolate.
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Before treatment, 88% (132/150) of the study cases had H. pylori found in antrum and 3.3% (5/150) of cases presented with bacteria only in cardia. After treatment, 38 cases had failure of dual therapy. The detection rates of H. pylori by biopsies without cardia decreased after the dual therapy (by antrum only: 88% to 60.5%, p < 0.05; antrum and body: 96.7% to 81.6%, p < 0.05). In contrast, the incidence of patients with only cardia involvement by H. pylori significantly increased from 3.3% (5/150) before to 18.4% (7/38) after treatment (p < 0.01). Among the 7 patients with H. pylori only in cardia after dual therapy, 3 cases had recurrent dyspepsia during follow-up because of no further anti-H. pylori therapy. Two of these 3 cases disclosed diffuse bacterial involvement in antrum and body besides cardia; the last case later had a positive result of urea breath test.
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Immune thrombocytopenic purpura (ITP) is the condition caused by increased platelet destruction and or decreased platelet production. Previous studies have demonstrated the association and efficacy of Helicobacter pylori (H. pylori) eradication therapy in patients with chronic ITP. Data in Thai patients, however, are limited. A prospective cross-sectional analytic study was conducted in adult patients with chronic ITP to determine the prevalence and clinical predictive factors of H. pylori infection and evaluate the efficacy of H. pylori eradication therapy. H. pylori-infected patients received eradication therapy (omeprazole 40 mg/day, clarithromycin 1000 mg/day, amoxicillin 2000 mg/day) for 2 weeks. The platelet counts at baseline and monthly for 6 months after the end of treatment were evaluated. Of the 25 patients, 9 patients (36%) had H.pylori infection. H. pylori infection is higher among women than men. There were two clinical factors included 1) relapsed ITP 2) response after the first-line treatment statistically proven to be associated with H. pylori infection with an odds ratio and p value of 7.7, p = 0.035 and ND (not determined due to small sample size), p < 0.001. Nearly 80% of infected patients had the platelet count response after eradication therapy with the median time to response of 4 months. The prevalence of H. pylori infection is modest in Thai adult patients with chronic ITP. A history of relapsed ITP and high quality of response after first-line treatment indicated H. pylori infection. Therefore, the urea breath test should be recommended in patients who have a relapsed ITP condition with a history of good response after first-line therapy.
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Eligible patients were randomized to receive SST (500 microg/h+250 microg bolus), or PAN (8 mg/h+80 mg bolus) or PLA (normal saline) i.v., for 24 h. All patients underwent gastric pH monitoring during the infusion of the trial drugs.
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Patients with grade I-IV symptomatic reflux oesophagitis were randomized to double-blind omeprazole 20 mg once morning, lansoprazole 30 mg o.m. or pantoprazole 40 mg o.m. Patient satisfaction and symptoms were evaluated after 4 and 8 weeks. Patients not satisfied after 8 weeks were treated for another 4 weeks with omeprazole 40 mg MUPS (open). Successful treatment was followed by 3 months' maintenance treatment with omeprazole MUPS 20 mg (patients satisfied after 4 or 8 weeks) or omeprazole MUPS 40 mg (patients satisfied after 12 weeks).
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Gastroesophageal reflux is implicated in some cases of laryngitis. There are no established predictors of response to acid suppression therapy in suspected reflux laryngitis.
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The objective of this study was to test whether the apparent synergy found in vitro between ranitidine bismuth citrate (RBC) and clarithromycin also exists in vivo against resistant strains.
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MEDLINE (1966-May 2005) and the Cochrane Library databases were searched using the key words proton pump inhibitor, acid suppression, peptic ulcer disease, gastrointestinal bleeding, stress ulcer prophylaxis, critical care, safety, and cost-effectiveness. Bibliographies of cited references were reviewed, and a manual search of abstracts from recent gastroenterology, critical care, and surgery scientific meetings was completed.
Aim of this overview was to evaluate the main clinical trials with lansoprazole published from 1997 to 1999 in English-language journals, regarding gastroesophageal reflux disease, peptic ulcer, NSAID-induced ulcer, and ZES. Results of clinical trials for therapy and prevention of lesions/symptoms have been evaluated separately. In direct comparisons, lansoprazole alone (not combined with antibiotics) proves to be equieffective to other PPI and more effective than H2-RA in both therapy and prevention of GERD, peptic ulcer (a part from anti-Hp regimens) and NSAID-induced ulcer. Among Hp-eradicating regimens in patients with peptic ulcer or functional dyspepsia, lansoprazole-based triple therapy is equal in efficacy to other PPI-based or RBC-based triple therapies and, in any case, significantly better than dual therapies. The in vitro anti-Hp activity of lansoprazole, more marked than with other PPI, does not seem to effort clinical advantages. Safety of lansoprazole is largely satisfactory and no different from other PPI and H2-RA.
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Two well-controlled trials were carried out to investigate the effectiveness of intravenous proton pump inhibitors (PPIs) to reduce peptic ulcer rebleeding after successful hemostasis. The results demonstrated that the PPI reduced the rate of rebleeding significantly. The recent availability of the first intravenous PPI formulation in the United States, intravenous pantoprazole, represents an alternative to intravenous histamine-2 receptor antagonists. The results of 16 randomized, controlled trials involving a total of >3,800 patients (1,892 receiving PPIs and 1,911 controls) suggest that bolus administration plus continuous infusion of PPIs is a more effective pharmacotherapy than bolus infusion alone in decreasing both rebleeding and the need for surgery. Optimal effect is achieved with an intravenous 80-mg bolus, followed by continuous infusion of 8 mg/hr for 3 days, after which therapy may be continued with an oral PPI. Intermittent bolus administration yielded a minimal benefit. A difference in mortality rates has not yet been demonstrated.
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We studied 12 patients (7 men and 5 women, ages 22-68 yr) with Du larger than 5 mm in diameter with a positive CLOtest (Delta West Ltd., Australia). Omeprazole, 20 mg bid, was given for 8 weeks to each patient, patients were endoscoped at the end of this period to check for healing of DU, and repeat biopsies were obtained from the gastric antrum for histological analysis, CLOtest, and culture.
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A pragmatic approach dictates an explicit risk-benefit assessment prior to co-prescription to maximize cardiac benefit and minimize the risk of gastrointestinal bleeding.
Sixty-three patients were enrolled and 41 patients completed the study [mean age 52 ± 12 years, 42% (17/41) men, 56% (23/41) Caucasian and 34% (14/41) African American]. Overall, there was no significant decrease in the total number of distal impedance episodes with esomeprazole compared with placebo (mean change 6.1 ± 22, P = 0.100). When analysed separately by GERD status, among GERD-positive patients, there was a significant decrease in distal impedance episodes while on esomeprazole compared with placebo (mean change -16 ± 22, P = 0.023), but not in GERD-negative patients (mean change -0.35 ± 20, P = 0.872).
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The most common causes of chronic cough in nonsmokers of all ages are postnasal drip syndrome, asthma, and GERD. However, persistent cough without bronchospasm or other pulmonary involvement may occur as a drug adverse effect. According to the US omeprazole package insert, cough is observed as an adverse reaction in 1.1% of patients, although this has not been mentioned in international drug information sources or medical literature. A MEDLINE search (1966-June 2003) using the terms cough, drug related, adverse effects, and omeprazole failed to find any data. In our patient, there was a temporal relationship between cough and medication use, suggesting a causal relationship. An objective causality assessment revealed that the adverse drug reaction was probable. The mechanism is unclear.
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Acidification of the urine is mediated by vectorial H+ transport from cells at a number of sites in the kidney. A proton ATPase has been described that appears to mediate a significant proportion of this H+ transport. In particular, in proximal tubule and collecting duct, there is evidence both for the presence of transporter protein and for H+ transport with features that have been identified with it. This review highlights some of the unresolved questions regarding this transporter, specifically, its distribution and relationship to the vacuolar pump present in endocytotic vesicles, how physiologic control is asserted, and its role in pathophysiology. The review discusses in greater detail the issue of whether the vacuolar H+ ATPase is responsible for all of the urinary acidification and concludes that it probably is not. Specifically, compelling evidence for acidification at sites in the kidney that appear to lack this transporter is presented. In addition, the evidence for the presence in the kidney of a gastric-type H(+)-K+ ATPase is also reviewed. The evidence appears to be strong for a K(+)-stimulated ATPase that is sensitive to omeprazole and SCH 28080, the prototypical H(+)-K+ ATPase inhibitors; however, uncertainties remain because of problems of transport inhibition specificity and discordant results of molecular biologic studies.
In CLASS, patients with OA/RA who were aged ≥ 18 years and required continuous NSAID treatment were included; patients who were Helicobacter pylori positive and/or using aspirin were not excluded. In contrast, in the CONDOR trial, comparing celecoxib alone to diclofenac sustained release (plus omeprazole), patients were aged ≥ 60 years or ≥ 18 years with a history of gastroduodenal ulcer and were H. pylori negative; aspirin or other anti-platelet users were excluded. To make a parallel post hoc analysis we limited our study to 6 months and the populations to only the non-aspirin users in CLASS and those patients receiving either celecoxib or diclofenac. A decrease in haemoglobin of ≥ 2 g/dL defined the primary end point.
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By protocol analysis the ulcer healing rates of the groups A1, A2, B1, B2, C1, and C2 were 93.3% (42/45), 92.7% (38/41); 89.2% (33/37), 94.9% (37/39); 88.4% (38/43), and 93.0% (40/43) respectively without a significant difference between any 2 groups (all P > 0.05); and the Hp eradication rates of the groups A1, A2, B1, B2, C1, and C2 were 86.7% (39/45), 90.2% (37/41); 89.2% (33/37), 92.3% (36/39); 67.4% (29/43), and 86.0% (37/43) respectively. The Hp eradication rate of OAM for 1-week group was significantly lower than the OAC(250)/OAC(250) for 1-week groups (all P < 0.05), and the Hp eradication rate of OAM for 1-week group was significantly lower than that of the OAM for 2-weeks group (P < 0.05). The 6-month follow-up showed an ulcer recurrence rate of 41.2% (7/17) for the patients without successful Hp eradication and an ulcer recurrence rate of 0% (0/130) for the patients with successful Hp eradication (P < 0.001). One-year follow-up showed an ulcer recurrence rate of 58.9% (10/17) for the patients without successful Hp eradication and an ulcer recurrence rate of 2.3% (3/130) for the patients with successful Hp eradication (P < 0.001).
The one-day quadruple therapy is less effective than the one-week regimen in curing H pylori infection in Chinese patients.
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A total of 704 patients in the UK, the Republic of Ireland, Germany, France, Italy and Spain were randomised to 1 of the 3 treatment groups.
Nocturnal gastric acid breakthrough, defined as intragastric pH < 4 for more than 1 h in the overnight period, is observed in up to 70% of normal subjects on proton pump inhibitors taken twice daily. The frequency of this breakthrough in patients with gastro-oesophageal reflux and accompanying oesophageal reflux during this period has not been studied.
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Systematic review of CENTRAL, EMBASE and MEDLINE for RCTs in patients with erosive oesophagitis (completed October 2008). Endoscopically verified healing rates at 4 and 8 weeks were extracted and re-calculated if not analysed by intention-to-treat. A mixed treatment comparison was used to combine direct treatment comparisons with indirect trial evidence while maintaining randomization. Odds ratios (OR) are reported compared to omeprazole 20 mg.
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Patients with H. pylori positive active peptic ulcer disease were randomly assigned to receive lansoprazole 30 mg o.d., amoxycillin 1 g b.d. and ornidazole 500 mg b.d. (LAO) or lansoprazole 30 mg o.d., amoxycillin 1 g b.d. and clarithromycin 500 mg b.d. (LAC) for 2 weeks. Pre-treatment resistance to ornidazole and clarithromycin was assessed by Epsilometer (E-) test. Four weeks after completion of treatment, patients underwent a 13C urea breath test to assess H. pylori status.
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A decision analysis model that represents treatment pathways for patients with UGIB was constructed and structuralized by 30-day outcomes. Direct costs of medical treatment, diagnostic and therapeutic endoscopy, endoscopic re-treatment, surgery, and hospitalization were analyzed.
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Thirty-three studies (11 prospective studies) comprising 619 patients with symptomatic esophageal eosinophilia (188 children and 431 adults) were included. PPI therapy led to a clinical response in 60.8% (95% confidence interval, 48.38%-72.2%; I(2) = 80.2) and histologic remission in 50.5% (95% confidence interval, 42.2%-58.7%; I(2) = 67.5) of patients. No differences were observed regarding the study population (children vs adults), the type of publication, or its quality. PPIs were nonsignificantly more effective in prospective studies (52.6% vs 39.1%) administered twice daily compared with once daily (55.9% vs 49.7%), and with pathologic pH monitoring (65.4% vs 49.3%). A significant publication bias in favor of studies reporting histologic responses to PPIs was observed.
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RG has no relevant potential to cause CYP enzyme- or P-gp-related interactions. Clinical trial registration number (ClinicalTrials.gov): NCT02056743.