bluuebunny/crossref_metadata_2025_split huggingface dataset:
Continuous treatment with omeprazole 20 mg daily for up to 6 years in Barrett’s oesophagus
Authors: Cooper B. T. , Neumann C. S. , Cox M. A. , Iqbal T. H. 
Published: March 2003

Background:Because of the malignant potential of Barrett’s oesophagus, an aim of treatment is to cause the columnar epithelium to regress. A logical approach is to decrease acid reflux which is an important aetiological factor in Barrett’s oesophagus. Treatment with omeprazole 20–80 mg over 1–3 years has yielded conflicting but largely disappointing results.Aim:To determine if treatment of Barrett’s oesophagus with omeprazole 20 mg daily for up to 6 years can cause regression of the Barrett’s epithelium.Patients and Methods:Forty‐seven patients with Barrett’s oesophagus were treated in an open prospective study. Nine patients were treated for 2 years, 12 for 3 years, 10 for 4 years, eight for 5 years and eight for 6 years. Patients were endoscoped at 1–2‐year intervals and endoscoped at the end of the treatment period.Results:No significant shortening of the length of the Barrett’s segment was seen during any treatment period, although omeprazole controlled reflux symptoms and was well tolerated. Macroscopic squamous islands appeared in 55% of patients, mostly in the first 2–3 years although in five patients they appeared later in treatment.Conclusion:Treatment of Barrett’s oesophagus with omeprazole 20 mg daily for periods of up to 6 years did not cause regression in the length of the Barrett’s segment, but it did lead in over half of the patients to partial re‐epithelialization in the form of squamous islands.
H2‐antagonist maintenance therapy versus Helicobacter pylori eradication in patients with chronic duodenal ulcer disease: a prospective study
Authors: Prach A. T. , Malek M. , Tavakoli M. , Hopwood D. , Senior B. W. , Murray F. E. 
Published: March 2003

Background:Few outcome studies directly compare Helicobacter pylori eradication therapy with maintenance H2‐antagonist therapy in duodenal ulcer disease.Aim:To examine prospectively the efficacy of H. pylori eradication therapy with ranitidine maintenance therapy over 1 year in patients with confirmed chronic duodenal ulcer.Methods:One hundred and nineteen patients with active H. pylori infection were randomized to receive ranitidine, 150 mg/day initially (58 patients), or omeprazole, 40 mg/day, amoxycillin 2 g/day and metronidazole 1.2 g/day for 14 days, or omeprazole 40 mg/day and clarithromycin 1.5 g/day, for 14 days (if penicillin‐allergic). Symptoms were assessed using the Gastro‐intestinal System Rating Scale (GSRS) and SF36 quality of life index.Results: 13C urea breath testing confirmed overall treatment success in 100% of patients (58/58) per protocol and 95.1% (58/61) on an intention‐to‐treat basis. At 4 and 12 months there were no differences in any GSRS symptoms between treatment groups. SF36 analysis showed a perceived health improvement at 4 and 12 months in patients who received H. pylori eradication. However, despite successful H. pylori eradication, one‐fifth of patients still required antisecretory therapy.Conclusion:Following successful H. pylori eradication, chronic duodenal ulcer patients were at least as well symptomatically as when taking maintenance ranitidine. They perceived that their health had improved, but a subgroup was still acid‐suppression dependent.
Double‐blind, placebo‐controlled comparison of rabeprazole 20 mg vs. omeprazole 20 mg in the treatment of erosive or ulcerative gastro‐oesophageal reflux disease
Authors: DEKKERS  , BEKER  , THJODLEIFSSON  , GABRYELEWICZ  , BELL  , HUMPHRIES  
Published: March 2003

Background:Rabeprazole sodium is the most recent member of a class of substituted benzimidazole molecules known as proton pump inhibitors. Other proton pump inhibitors have been shown to be effective in healing oesophagitis.Methods:In this randomised, double‐blind, multicentre study, conducted at 27 European sites, the efficacy and safety of rabeprazole and omeprazole were compared in patients with erosive or ulcerative gastro‐oesophageal reflux disease (GERD).100 patients received rabeprazole 20 mg, and 102 patients omeprazole 20 mg once daily for 4 or 8 weeks, with healing monitored by endoscopy.Results:Overall GERD healing rates observed and evaluated at weeks 4 and 8 were equivalent. Four‐week healing rates for rabeprazole and omeprazole were 81%–81% and 92%–94% for 8‐week healing. Rabeprazole‐treated patients had similar relief of the frequency and intensity of heartburn to those treated with omeprazole. Both drugs were well tolerated over the 8‐week treatment period. Mean changes in fasting serum gastrin were comparable. No significant differences in laboratory parameters were seen. Biopsies for argyrophil ECL cell histology at the end‐point revealed a similar distributions of hyperplasia grades to those at baseline in both groups. Biopsies of body and antral mucosa for other parameters were similar between treatments for Helicobacter pylori colonization, presence or degree of inflammation, atrophy or intestinal metaplasia at the end‐point.Conclusion:In this study, GERD healing rates following rabeprazole 20 mg once daily were equivalent to those obtained with omeprazole 20 mg once daily. Both treatments resulted in a comparable relief of the frequency and intensity of heartburn associated with this disease, and both were well tolerated.
Bedtime ranitidine does not eliminate the need for a second daily dose of omeprazole to suppress nocturnal gastric pH
Authors: KHOURY  , KATZ  , HAMMOD  , CASTELL  
Published: March 2003

Background: We have previously shown that 70% of patients experience nocturnal gastric acid breakthrough (defined as pH < 4 for more than 60 min between 22.00 and 06.00 hours) on twice a day (b.d.) proton pump inhibitor. Adding 150 or 300 mg of ranitidine at bedtime is more effective than additional omeprazole at bedtime in control of night‐time acid breakthrough.Aim: To assess whether omeprazole 20 mg AM plus ranitidine 150 mg HS would be as effective as omeprazole 20 mg before breakfast and dinner (b.d. AC) in intragastric pH control, particularly during the overnight period.Methods: Twenty healthy volunteers (11 males, 9 females, mean age 32.7 years) were treated with omeprazole (OME) 20 mg b.d. AC and placebo HS or omeprazole 20 mg AM and placebo before dinner plus ranitidine (RAN) 150 mg HS for 7 days, in a randomized, double‐blind, crossover design, with a 1 week washout between study periods. On day 8 subjects were monitored for 24 h with a single channel pH probe placed in the stomach 10 cm below the proximal border of the LES. Percentage time pH < 4 for total, upright and recumbent positions were compared between the two regimens using Wilcoxon matched pairs testing.Results: Expressed in median values of percentage time pH < 4: upright time intragastric pH < 4 on OME 20 mg b.d. AC was 18.9 compared to 29.7 on OME AM + RAN HS (P = 0.003). Recumbent time pH < 4 on OME 20 mg b.d. AC was 23.45 compared to 44.75 on OME AM + RAN HS (P = 0.02).Conclusion: Bedtime ranitidine does not eliminate the need for an evening dose of omeprazole to control intragastric pH in patients requiring more than a single daily dose of omeprazole.
The effect of antibiotic resistance on the outcome of three 1‐week triple therapies against Helicobacter pylori
Authors: PILOTTO  , LEANDRO  , FRANCESCHI  , RASSU  , BOZZOLA  , FURLAN  , DI MARIO  , VALERIO  
Published: March 2003

Background: Resistance of Helicobacter pylori to antibiotics may be a major reason for treatment failure.Aim: To evaluate the effect of primary H. pylori resistance to antibiotics on the cure rates of three anti‐H. pylori 1‐week triple therapies.Methods: One hundred and sixteen consecutive patients diagnosed H. pylori‐positive by gastric histology, rapid urease test and culture were enrolled. Activity of tested antibiotics was determined by means of the E‐test. Patients were treated for 7 days with: (i) pantoprazole 40 mg o.d. plus amoxycillin 1 g b.d. and metronidazole 250 mg q.d.s. (PAM); (ii) pantoprazole 40 mg o.d. plus clarithromycin 250 mg b.d. and metronidazole 250 mg q.d.s. (PCM); or (iii) pantoprazole 40 mg o.d. plus amoxycillin 1 g b.d. and clarithromycin 250 mg b.d. (PAC). Two months after completion of therapy, endoscopy and gastric biopsies were repeated.Results: Primary resistance rates to metronidazole, clarithromycin and amoxycillin were 17.2, 6.9 and 0%, respectively. Overall H. pylori cure rates expressed as intention‐to‐treat and per protocol analyses were, respectively, 79% and 86% with PAM, 82% and 89% with PCM, and 85% and 85% with PAC. Significantly lower cure rates were observed in metronidazole‐resistant patients treated with PAM (56% vs. 96%, P = 0.01) or PCM (50% vs. 97%, P = 0.01). A trend towards lower H. pylori cure rates was observed in clarithromycin‐resistant patients treated with PCM (67% vs. 91%, P = 0.74) or PAC (50% vs. 87%, P = 0.68).Conclusion: Primary resistance to metronidazole influences the H. pylori cure rate of anti‐H. pylori proton pump inhibitor‐based triple therapies which include this antibiotic. A similar trend exists for primary clarithromycin resistance.
The GU‐MACH study: the effect of 1‐week omeprazole triple therapy on Helicobacter pylori infection in patients with gastric ulcer
Authors: Malfertheiner P. , Bayerdörffer E. , Diete U. , Gil J. , Lind T. , Misiuna P. , O'Morain C. , Sipponen P. , Spiller R. C. , Stasiewicz J. , Treichel H.‐C. , Ujszászy L. , Unge P. , Veldhuyzen van Zanten S. J. O. , Zeijlon L. 
Published: March 2003

Aims: To study the efficacy of omeprazole triple therapy in the eradication of Helicobacter pylori in patients with active gastric ulcer, and to assess healing and relapse of gastric ulcer.Methods: A double‐blind, randomized study was carried out in 18 centres in Germany, Hungary and Poland. Patients (n = 160) with gastric ulcer and a positive H. pylori screening test were randomized to a 7‐day twice daily treatment with omeprazole 20 mg, clarithromycin 500 mg and amoxycillin 1000 mg (OAC) or omeprazole 20 mg, clarithromycin 250 mg and metronidazole 400 mg (OMC), or with omeprazole 20 mg once daily (O). After completion of this 1‐week treatment, patients were treated with omeprazole until healing (maximum 12 weeks), and followed for 6 months. H. pylori was assessed by urea breath test (UBT) and histology.Results: Eradication rates ITT were OAC 79% (95% CI: 65–90%), OMC 86% (95% CI: 73–94%) and O 4% (95% CI: 0–14%). Eradication rates PP were OAC 83% (95% CI: 68–93%), OMC 93% (95% CI: 80–98%) and O 3% (95% CI: 0–13%). Gastric ulcer relapses occurred in 5, 0 and 11 patients in the groups, respectively.Conclusions: The results from the study demonstrate that OMC and OAC 1‐week regimens are safe and effective for eradication of H. pylori in gastric ulcer patients, and that ulcer relapse is infrequent after successful eradication.
Review article: cardiac adverse effects of gastrointestinal prokinetics
Authors: Tonini  , De Ponti  , Di Nucci  , Crema  
Published: March 2003

Gastrointestinal prokinetics, such as metoclopramide, cisapride and levosulpiride, are widely used for the management of functional gut disorders. Recently, several studies have shown that cisapride (a partial 5‐HT4 receptor agonist) can induce dose‐dependent cardiac adverse effects, including lengthening of the electrocardiographic QT interval, syncopal episodes and ventricular dysrhythmias.Until recently, it was not clear whether these effects were dependent on 5‐HT4 receptor activation or related to peculiar characteristics in the molecular structure of single agents within the benzamide class. Experimental evidence now favours the second hypothesis: cisapride possesses Class III antiarrhythmic properties and prolongs the action potential duration through blockade of distinct voltage‐dependent K+ channels, thus delaying cardiac repolarization and prolonging the QT interval.Patients at risk of cardiac adverse effects are children, subjects with idiopathic, congenital or acquired long QT syndrome and, in particular, those receiving concomitant medication with Class III antiarrhythmic agents, some H1‐receptor antagonists (e.g. terfenadine), or drugs such as azole antifungals (e.g. ketoconazole, itraconazole, miconazole and fluconazole) and macrolide antibacterials (e.g. erythromycin, clarithrod‐mycin and troleandomycin), which can inhibit cisapride metabolism by interfering with the CYP3A4 isoenzyme.
Non‐steroidal anti‐inflammatory drugs, Helicobacter pylori and bleeding gastric ulcer
Authors: Ng  , Fock  , Khor  , Teo  , Sim  , Tan  , Machin  
Published: March 2003

Background: Helicobacter pylori infection and NSAID usage are considered to be independent risk factors for gastric ulcer (GU). Whether they interact to influence the risk of bleeding in GU is unclear.Aim:To determine the prevalence of H. pylori infection and NSAID ingestion in a group of patients with GU and determine their roles in bleeding and non‐bleeding GU.Methods and results:From January 1993 to June 1996, a total of 217 GU patients (150 male, 67 female, median age 61 years, range 26–94) were eligible for the study. Eighty‐five per cent were H. pylori‐positive and 15% were H. pylori‐negative. NSAID usage within 4 weeks prior to endoscopy was present in 30%, more in the H. pylori‐negative than H. pylori‐positive patients (59% vs. 25% P = 0.0002). Aspirin was most commonly used (43%). One hundred patients bled from GU (69 male, 31 female, mean age 67 years, range 26–94) and 117 did not (81 male, 36 female, mean age 57 years, range 28–86). Univariate logistic regression showed that advanced age (≥ 65 years) and NSAID usage carried an increased risk of bleeding GU (odds ratio 3.4 and 6.8, respectively) while H. pylori infection alone was not associated with additional risk (OR = 0.8). However, when three variables were considered jointly in a multiple logistic regression, the OR associated with H. pylori infection increased to 2.4, suggesting that in the presence of NSAIDs and advanced age, H. pylori also increases the risk of bleeding GU, indicating an interaction between the variables.Conclusion:NSAID usage and advanced age are risk factors for bleeding GU, whereas H. pylori infection by itself is not. In the presence of NSAIDs and advanced age, an increased risk of bleeding GU with H. pylori is observed, indicating the possibility of an interaction between these factors.
A double‐blind, randomized, placebo‐controlled dose‐ranging study to evaluate the efficacy of alosetron in the treatment of irritable bowel syndrome
Authors: Bardhan  , Bodemar  , Geldof  , Schütz  , Heath  , Mills  , Jacques  
Published: March 2003

Background:Irritable bowel syndrome is a common gastrointestinal disorder characterized by abdominal pain and discomfort and altered bowel habit. Antagonism at the 5‐HT3 receptor may be of benefit in the treatment of irritable bowel syndrome.Aims:To evaluate the effect of 12 weeks of treatment with alosetron, a 5‐HT3 receptor antagonist at doses of 0.1 mg b.d., 0.5 mg b.d. and 2 mg b.d. in irritable bowel syndrome patients.Methods:A double‐blind, placebo‐controlled, parallel‐group study with a 2‐week screening and a 12‐week treatment period was conducted. A total of 462 patients (335 female) recorded details of the severity of their abdominal pain, and bowel function daily on a diary card throughout the study. At monthly clinic visits patients recorded the severity of their abdominal pain/discomfort and diarrhoea on a visual analogue scale.Results:In the total population and in the female subpopulation (but not in males) alosetron 2 mg b.d. significantly increased the proportion of pain‐free days and decreased the visual analogue scale score for diarrhoea compared with placebo. Alosetron at doses of 0.5 mg b.d. and 2 mg b.d. led to a significant hardening of stool, and a reduction in stool frequency in the total population.Conclusion:Alosetron at a dose of 2 mg b.d. is an effective treatment for female patients with irritable bowel syndrome.
Bismuth‐based quadruple therapy for Helicobacter pylori— a single triple capsule plus lansoprazole
Authors: De Boer  , Van Etten  , Van De Wouw  , Schneeberger  , Van Oijen  , Jansen  
Published: March 2003

Background:Recently a new ‘all in one’ single capsule with the three components of bismuth‐based triple therapy became available in trials for treating Helicobacter pylori.Aim:To investigate the efficacy and tolerability of this new capsule when combined with lansoprazole.Methods:A total of 66 consecutive infected patients from a single centre received two single triple capsules four times daily and lansoprazole 30 mg b.d. for 7 days. Each capsule contained 60 mg of bismuth subcitrate, 125 mg of tetracycline and 125 mg of metronidazole. Endoscopy with biopsies for CLO‐test, histology and culture from antrum and corpus was performed before and at least 5 weeks after treatment.Results:The per protocol cure rate was 56/64 (88%, 95% CI: 79–95%); by intention‐to‐treat 56/65 (86%, 95% CI: 78–95%). The per protocol cure rate in metronidazole sensitive strains was 40/43 (93%, 95% CI: 85–100%); in resistant strains 5/9 (56%, 95% CI: 23–88%). There was one drop‐out due to adverse events.Conclusions: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.
Review article: recognition and treatment of eating disorders in primary and secondary care
Authors: Robinson  
Published: March 2003

Eating disorders are serious illnesses affecting 1–2% of young women. Patients may present to any doctor, sometimes atypically (e.g. unexplained weight loss, food allergy, infertility, diarrhoea), delaying diagnosis and leading to needless investigation. The cardinal signs are weight loss, amenorrhoea, bingeing with vomiting and other compensatory behaviours, and disturbances in body image with an exaggeration of the importance of slimness. When other causes have been excluded, useful investigations are serum potassium, bone mineral density scanning and pelvic ultrasound. In emaciated patients multiple systems may fail with pancytopaenia, neuromyopathy and heart failure. Clinical assessment of muscle power is used to monitor physical risk.Treatment may involve individual, group or family sessions, using cognitive‐behavioural, psychodynamic and family approaches. More severe or intractable illness is treated with day care, with in‐patient care in a medical or specialist psychiatric unit reserved for the most severely ill patients. Antidepressants have a place in the treatment of bulimia nervosa unresponsive to psychological approaches, and when severe depressive symptoms develop. The children of people with eating disorders may have an increased risk of difficulties. Support for the patient and family, and effective liaison between professionals, are essential in the treatment of severe eating disorders.
Ridogrel, a dual thromboxane synthase inhibitor and receptor antagonist: anti‐inflammatory profile in inflammatory bowel disease
Authors: Carty  , Macey  , Mccartney  , Rampton  
Published: March 2003

Background:Thromboxanes, prostaglandins, reactive oxygen metabolites and pro‐inflammatory cytokines are produced in excess in inflammatory bowel disease. Preliminary reports suggest that ridogrel, a thromboxane synthesis inhibitor and receptor blocker, may have therapeutic benefits in ulcerative colitis.Aims:To investigate the anti‐inflammatory profile of ridogrel.Methods:The effects of ridogrel on the production of eicosanoids, reactive oxygen metabolites and cytokines by cultured inflamed colorectal mucosal biopsies were made using ELISA and chemiluminescence, reactive oxygen metabolite generation in a cell‐free system, and platelet activation using flow cytometry. The effects of oral ridogrel on mucosal release of eicosanoids in two patients with active ulcerative colitis were assessed using rectal dialysis.Results:Ridogrel significantly reduced the release of thromboxane B2, but not prostaglandin E2 or tumour necrosis factor‐α, from biopsies (P < 0.01 for 10 μM ridogrel). Ridogrel showed no direct antioxidant activity but significantly reduced reactive oxygen metabolite production from cultured biopsies (P < 0.01 for 10 μM ridogrel). Platelet activation in vitro was inhibited by ridogrel (P ≤ 0.05 for ≥ 10 μM ridogrel). Mean rectal mucosal thromboxane B2 release was reduced to 86% of pre‐treatment levels in two patients treated with oral ridogrel.Conclusions:Its inhibition of mucosal production of thromboxane B2, reactive oxygen metabolites, and of platelet activation, suggests that ridogrel could have a therapeutic role in inflammatory bowel disease.
Regulation of nitric oxide production in cultured human T84 intestinal epithelial cells by nuclear factor‐κB‐dependent induction of inducible nitric oxide synthase after exposure to bacterial endotoxin
Authors: Lähde  , Korhonen  , Moilanen  
Published: March 2003

Background:Intestinal epithelium is consistently in contact with lipopolysaccharide (LPS) produced by intraluminal microbes. LPS induces nitric oxide production in many rodent cells, but in human cells it is very differently regulated.Aim:To test the hypothesis that exposure to LPS up‐regulates nitric oxide synthesis in human intestinal epithelium.Methods and results:LPS induced nitric oxide synthesis in T84 cells in a time‐ and dose‐dependent manner whereas detectable amounts of peroxynitrite were not produced. A novel selective inducible nitric oxide synthase (iNOS) inhibitor 1400 W potently inhibited LPS‐induced nitric oxide synthesis in T84 cells while dexamethasone was relatively ineffective. Nitric oxide production was sensitive to cycloheximide, indicating that it was dependent on de novo protein synthesis. Nuclear factor‐κB (NF‐κB) inhibitor pyrrolidinedithiocarbamate abolished iNOS and nitric oxide production. Nitric oxide synthesis was also suppressed by genistein (tyrosine kinase inhibitor) and PD 98059 (p44/42 MAP kinase inhibitor) but enhanced by SB 203580 (p38 MAP kinase inhibitor).Conclusions:Intestinal epithelial cells express iNOS and produce nitric oxide in a nuclear factor‐κB‐dependent manner when exposed to LPS. The process is regulated by tyrosine kinases, and p44/42 and p38 MAP kinases. Because nitric oxide acts as an antimicrobial agent and immune modulator, these findings are implicated in the regulation of gut mucosal immunity.
Helicobacter pylori infection influences nocturnal gastric acid breakthrough
Authors: Katsube T. , Adachi K. , Kawamura A. , Amano K. , Uchida Y. , Watanabe M. , Kinoshita Y. 
Published: March 2003

Background:Nocturnal gastric acid breakthrough is defined as night‐time periods when gastrin pH falls below 4.0 for greater than 1h during administration of a proton pump inhibitor. This phenomenon is a serious problem for patients who require strict control of their gastric acid secretions.Aim:To investigate the prevalence of nocturnal gastric acid breakthrough in Japanese subjects during administration of rabeprazole, and to clarify the relationship between Helicobacter pylori infection and nocturnal gastric acid breakthrough.Methods:Thirty‐one normal male volunteers were examined by ambulatory 24 h gastric pH monitoring four times: without medication, after a morning or an evening dose of 20 mg rabeprazole, and after administration of an H2‐receptor antagonist at bedtime, in addition to the morning dose of rabeprazole. H. pylori infection was determined by the 13C‐urea breath test and an assay for serum anti‐H. pylori antibody.Result:Nocturnal gastric acid breakthrough was observed in 12 patients (39%) after the morning dose of 20 mg rabeprazole. In all cases, nocturnal gastric acid breakthrough was inhibited completely by administration of the H2‐receptor antagonist at bedtime. Only one patient with nocturnal gastric acid breakthrough had H. pylori infection.Conclusion:The absence of H. pylori infection appears to be closely related to the occurrence of nocturnal gastric acid breakthrough during dosing with a proton pump inhibitor.