bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ranitidine bismuth citrate (RBC) based triple therapy for 7 days is more effective than RBC plus clarithromycin for 14 days in dyspeptic patients with Helicobacter pylori infection
Authors: Cestari  
Published: March 2003

Background:Ranitidine bismuth citrate (RBC) in co‐prescription with clarithromycin for 2 weeks has been shown to be effective for the eradication of Helicobacter pylori. Moreover, several studies have reported good H. pylori eradication rates with RBC plus two antibiotics for 1 week.Aim:To compare the H. pylori eradication rates and safety of two different RBC co‐prescription regimens.Methods:Patients undergoing endoscopy for upper gastrointestinal symptoms were randomized to open treatment with either RBC 400 mg b.d. plus clarithromycin 250 mg b.d. and tinidazole 500 mg b.d. for 1 week (RbcCT) or RBC 400 mg b.d. plus clarithromycin 500 mg b.d. (RbcC) for 2 weeks. H. pylori infection was detected by CLO‐test on antral biopsy and confirmed by histology on antral and corpus biopsies and by 13C‐urea breath test (UBT). A further UBT was performed at least 4 weeks after the end of treatment to assess the H. pylori eradication. H. pylori eradication was calculated for an intention‐to‐treat (ITT) population (all H. pylori‐positive patients who received at least one treatment dose) and for an all‐patients‐treated (APT) population (patients of the ITT population assessed for H. pylori at least 4 weeks after the end of treatment).ResultsTwo hundred and ninety‐five patients (142 males, 153 females, mean age 48 years) were recruited to the study. Of these, 239 had H. pylori infection confirmed by all three tests required by the protocol. The two treatment groups were similar with respect to all the demographic data. H. pylori ITT eradication rates were 85% (104/123) for RbcCT and 67% (78/116) for RbcC. APT eradication rates were 92% (104/113) for RbcCT and 76% (78/103) for RbcC. A significant statistical difference was found between the two treatments, irrespective of the population analysis (P = 0.001). Adverse events occurred in 7% of patients on RbcCT and in 13% on RbcC. No serious adverse events were reported.Conclusions:The 1‐week treatment with RBC plus clarithromycin and tinidazole yielded higher eradication rates than the 2‐week treatment with RBC plus clarithomycin. Both treatments were well tolerated.
Effects of two anticholinergic drugs, trospium chloride and biperiden, on motility and evoked potentials of the oesophagus
Authors: Pehl  , Wendl  , Kaess  , Pfeiffer  
Published: March 2003

Background:Anticholinergic drugs are known to impair the motor function of the oesophagus but their effects on the oesophageal afferent pathways are unknown.Aim:To determine the effects of a peripherally‐acting (trospium chloride) and a centrally‐acting (biperiden) anticholinergic drug on the motility and the evoked potentials of the oesophagus.Methods:Nine healthy volunteers were randomized to receive 1.2 mg trospium chloride (TC), 5 mg biperiden (BIP) or saline i.v. Primary peristalsis was elicited by swallowing a 5 mL water bolus and secondary peristalsis by insufflation of 20 mL air, 10 times each. Oesophageal potentials were evoked by electrical stimulation in the distal and proximal oesophagus (30 stimulations at 0.4 Hz, two runs).Results:Both anticholinergic drugs reduced by a similiar amount the contraction amplitudes (TC 17 mmHg, BIP 25 mmHg, saline 67 mmHg; P < 0.01) and the rate of secondary contractions (TC 60%, BIP 70%, saline 95%; P < 0.01). In contrast, only biperiden prolonged the latencies of the evoked potentials (N1 peak, distal oesophagus: BIP 191 ms, TC 102 ms, saline 101 ms; P < 0.01; P1 peak: BIP 322 ms, TC 161 ms, saline 144 ms; P < 0.01).Conclusions:Both anticholinergic drugs depress oesophageal motility, but only the centrally‐acting anticholinergic drug biperiden modifies the oesophageal evoked potentials, suggesting a central cholinergic transmission of the oesophageal afferent pathways.
Prospective study of the risk of Clostridium difficile diarrhoea in elderly patients following treatment with cefotaxime or piperacillin–tazobactam
Authors: Settle  , Wilcox  , Fawley  , Corrado  , Hawkey  
Published: March 2003

BackgroundRates of Clostridium difficile diarrhoea have recently been rising, with the elderly being at highest risk.AimTo compare the incidence of C. difficile colonization and diarrhoea in elderly patients treated for presumed infection with either empirical cefotaxime (CTX) or piperacillin–tazobactam (PT).MethodsA prospective, ward‐based, crossover study was carried out on two well‐matched care of the elderly wards at a UK tertiary care hospital, in patients requiring empirical broad‐spectrum antibiotic treatment.ResultsThere was a highly significant increased incidence of C. difficile colonization (26/34 vs. 3/14, P = 0.001) and diarrhoea (18/34 vs. 1/14, P = 0.006) in patients who received CTX as opposed to PT. DNA fingerprinting suggested that most infections arose from strains acquired from the hospital environment.ConclusionsElderly patients are significantly less likely to develop C. difficile diarrhoea after treatment with PT than after CTX. The source of C. difficile appears to be predominantly from the ward environment.
Treatment of ulcerative colitis with germinated barley foodstuff feeding: a pilot study
Authors: Mitsuyama  , Saiki  , Kanauchi  , Iwanaga  , Tomiyasu  , Nishiyama  , Tateishi  , Shirachi  , Ide  , Suzuki  , Noguchi  , Ikeda  , Toyonaga  , Sata  
Published: March 2003

BackgroundGerminated barley foodstuff (GBF) has been shown to attenuate intestinal injury in animal models, largely by increasing luminal short‐chain fatty acid production.AimTo investigate the safety and efficacy of GBF in the treatment of ulcerative colitis (UC).MethodsTen patients with active UC received 30 g of GBF daily for 4 weeks in an open‐label treatment protocol while the baseline anti‐inflammatory therapy was continued. The response to treatment was evaluated clinically and endoscopically. Pre‐ and post‐treatment stool concentrations of short‐chain fatty acids were measured by gas‐liquid chromatography.ResultsPatients showed improvement in their clinical activity index scores, with a significant decrease in the score from 6.9 ± 1.4 to 2.8 ± 1.5 (mean ± S.E.M., P < 0.05). The endoscopic index score fell from 6.1 ± 2.3 to 3.8 ± 2.3 (P < 0.0001). Patients showed an increase in stool butyrate concentrations after GBF treatment (P < 0.05). No side‐effects were observed.ConclusionsOral GBF therapy may have a place in management of ulcerative colitis, but controlled studies are needed to demonstrate its efficacy in the treatment of this disorder.
Evaluation of omeprazole as a cost‐effective diagnostic test for gastro‐oesophageal reflux disease
Authors: BATE  , RILEY  , CHAPMAN  , DURNIN  , TAYLOR  
Published: March 2003

Background: There is a need for a simple, therapeutic test that is of diagnostic value and can also provide rapid symptom relief in patients who present with classic, mild symptoms suggestive of gastro‐oesophageal reflux disease (GERD), when the diagnosis is based on symptom assessment alone.Aim: To assess the diagnostic value of a therapeutic trial of omeprazole 40 mg in a dyspeptic population.Methods: A total of 90 patients with symptoms suggestive of GERD entered the study. Patients underwent endoscopy and ambulatory oesophageal pH monitoring for 18–24 h. Patients then received omeprazole 40 mg o.m. for 2 weeks.Results: There was a significant correlation between the diagnoses obtained from a trial of omeprazole and the diagnoses obtained from pH monitoring (P < 0.05). There was no significant correlation between the diagnoses obtained from endoscopy and those obtained from pH monitoring. Both omeprazole and endoscopy were compared to pH monitoring as the ‘gold standard’ for the diagnosis of GERD and the cost per correct diagnosis with omeprazole was £47 (95% CI: £40–£59) compared to £480 (95% CI: £396–£608) with endoscopy. There was a complete absence of acid‐related symptoms in the majority (59%) of patients after 3 days of omeprazole 40 mg therapy and, after 2 weeks, 82% of patients had experienced an improvement in overall symptoms ( 1 grade).Conclusions: We conclude that omeprazole can be used as a clinically effective tool in the initial management of GERD and that it is of diagnostic value in patients who present with typical symptoms, such as heartburn, when the diagnosis is based on symptom assessment alone.
Influence of the pharmacological modification of gastric emptying on lactose digestion and gastrointestinal symptoms
Authors: PEUHKURI  , VAPAATALO  , NEVALA  , KORPELA  
Published: March 2003

Background:In lactose maldigesters the ingestion of food which retards gastric emptying improves tolerance to lactose.Aim:To study the effects of the pharmacological modification of gastric emptying on the speed of development of lactose‐induced symptoms.Methods:After an overnight fast, 18 lactose maldigesters were given, in a randomized double‐blind study design at 1‐week intervals, either propantheline (as bromide 15 mg), metoclopramide (as hydrochloride 10 mg) or placebo, in identical capsules, 60 min before ingesting 50 g lactose coloured with 1 g carmine dye (to measure gastrointestinal transit time). Gastrointestinal symptoms, urinary galactose excretion, and breath hydrogen and blood glucose concentrations were recorded.Results:The propantheline‐induced prolongation of gastric emptying improved tolerance to lactose, as measured by reduced area under the gastrointestinal symptom score curve 0–12 h, compared to placebo (by 26%) (P < 0.05) or metoclopramide (by 30%) (P < 0.05). The total hydrogen excretion AUC (180 min follow‐up) increased by 15% after metoclopra‐ mide as compared with placebo (P = 0.18). Propantheline decreased this variable by 15% from placebo (P = 0.17). No significant differences in blood glucose, urinary galactose or gastrointestinal transit time were found.Conclusions:In an oral lactose tolerance test, delaying gastric emptying with propantheline improved tolerance in lactose maldigesters, as measured by diminished gastrointestinal symptoms and reduced breath hydrogen concentration.
Review article:Helicobacter pyloriand gastro‐oesophageal reflux disease—clinical implications and management
Authors: O’connor  
Published: March 2003

A significant proportion of patients with gastro‐oesophageal reflux disease (GERD) haveHelicobacter pyloriinfection, but it is unclear whether or notH. pylorishould be treated in this clinical setting. The aim of this review was to critically assess the relationship betweenH. pyloriand GERD and its potential implications for the management of GERD. Data for this review were gathered from the following sources up to April 1998—the biomedical database MEDLINE, a detailed review of medical journals, and a review of abstracts submitted to relevant international meetings.On average, 40% of GERD patients carryH. pyloriinfection, with a reported infection prevalence ranging from 16% to 88%. To date, there has been no reported controlled trial of effectiveH. pyloritherapy in GERD. GERD has been reported to developde novofollowing the cure ofH. pyloriin peptic ulcer disease.In the presence ofH. pylori, proton pump inhibitor therapy appears to accelerate the development of atrophic corpus gastritis, a potentially precancerous condition. Conversely, proton pump inhibitor therapy seems to become less effective after cure ofH. pylori. The mechanisms underlying these important contrasting phenomena are poorly understood.The relationship betweenH. pyloriand GERD is complex, and it is difficult to give definitive guidelines on the management ofH. pyloriinfection in GERD. Controlled trials ofH. pyloritherapy in GERD are urgently needed, as well as further long‐term data on both the natural history of gastric histopathological changes in theH. pylori‐positive GERD patient treated with proton pump inhibitors, and the impact ofH. pyloristatus on the clinical efficacy of antisecretory therapy. Pending these data, it is perhaps advisable to advocate cure ofH. pyloriin young patients with proton pump inhibitor‐dependent GERD who, in the absence of anti‐reflux surgery, are faced with the likelihood of long‐term medical therapy.
Effect of angiotensin II and telmisartan, an angiotensin1 receptor antagonist, on rat gastric mucosal blood flow
Authors: HEINEMANN  , SATTLER  , JOCIC  , WIENEN  , HOLZER  
Published: March 2003

Background:Angiotensin II (ATII) has been suggested to contribute to shock‐induced dysfunction of the gastric circulation.Aim:To substantiate this conjecture, the effects on gastric mucosal haemodynamics and the hyperaemic response to acid back‐diffusion of ATII and the angiotensin AT1 receptor antagonist, telmisartan, were examined in normal rats and in animals subjected to haemorrhage.Methods:Gastric mucosal blood flow in phenobarbital‐anaesthetized rats was recorded with the hydrogen clearance technique, and acid back‐diffusion was induced by perfusing the stomach with ethanol (25%) in HCl (0.05 M).Results:Intravenous infusion of ATII (0.3–10 nmol/min/kg) led to dose‐dependent hypertension and a reduction of blood flow and vascular conductance in the gastric mucosa. The gastric hyperaemia caused by acid back‐diffusion was attenuated by ATII (1 nmol/min/kg). These effects of ATII were antagonized by intravenous injection of telmisartan (1–10 mg/kg) which per se caused hypotension and dilated the gastric mucosal vasculature, but did not modify the gastric mucosal hyperaemia evoked by acid back‐diffusion. Hypotension induced by haemorrhage (1.3 mL blood per 100 g body weight) failed to alter the hyperaemia due to acid back‐diffusion, but caused gastric mucosal vasoconstriction, an effect that was left unaffected by telmisartan.Conclusions:ATII constricts the rat gastric microvasculature via an action involving AT1 receptors. The effects of telmisartan indicate that endogenous ATII contributes to the homeostatic regulation of gastric vascular tone but does not compromise the ability of the gastric microvasculature to react to influxing acid. These results negate the concept that ATII contributes to the␣gastric vascular perturbances in haemorrhagic shock.
Low‐dose ranitidine for the relief of heartburn
Authors: PAPPA  , GOOCH  , BUARON  , PAYNE  , GIEFER  , SIRGO  , CIOCIOLA  
Published: March 2003

Background: Approximately 30% of adults in the USA suffer from heartburn or related symptoms monthly; more than 20% of these sufferers experience heartburn at least once per day. Although many rely on self‐medication with antacids for the relief of their symptoms, treatments that decrease gastric volume as well as increase the pH of refluxed material should be more effective in relieving heartburn.Aim: To compare the safety and efficacy of low‐dose regimens of ranitidine for the relief of heartburn.Methods: Adults with at least a 3‐month history of heartburn were eligible for this randomized, double‐blind, parallel group, multicentre dose‐ranging study. Following a 1‐week open‐label run‐in phase to document baseline heartburn frequency, subjects were randomized to receive treatment with one tablet of either ranitidine 75 mg (n = 491), ranitidine 25 mg (n = 504), or placebo (n = 494), to be taken as needed up to four times daily for 2 weeks for the relief of heartburn.Results: The ranitidine 75 mg regimen was clinically (> 10 percentage points) and statistically (P < 0.05) significantly more effective than placebo for all measured efficacy end‐points in relieving heartburn and reducing antacid consumption. In addition, the ranitidine 75 mg regimen was superior to placebo in providing heartburn relief within 30 min of dosing that lasted for up to 12 h. Ranitidine 25 mg was observed to be statistically superior (P < 0.05) but not clinically different from placebo, as defined a priori, in providing heartburn relief. All treatments were well tolerated and adverse events occurred no more frequently with the ranitidine regimens than with placebo.Conclusions: Ranitidine 75 mg provides prompt relief of heartburn that lasts for up to 12 h and has a safety profile comparable to that of placebo.
Polaprezinc, a mucosal protective agent, in combination with lansoprazole, amoxycillin and clarithromycin increases the cure rate of Helicobacter pylori infection
Authors: KASHIMURA  , SUZUKI  , HASSAN  , IKEZAWA  , SAWAHATA  , WATANABE  , NAKAHARA  , MUTOH  , TANAKA  
Published: March 2003

Aim: To evaluate the efficacy of polaprezinc, a mucosal protective agent, in combination with a 7‐day triple therapy containing lansoprazole, amoxycillin and clarithromycin, as a treatment for Helicobacter pylori.Methods: Sixty‐six consecutive patients suffering from dyspeptic symptoms with H. pylori infection were randomly allocated to one of two regimens: one group (LAC; n = 31) received lansoprazole 30 mg b.d., amoxycillin 500 mg b.d. and clarithromycin 400 mg b.d. for 7 days. The other group (LACP; n = 35) received the LAC regimen plus polaprezinc 150 mg b.d. for 7 days. H. pylori status was evaluated by rapid urease test, histology and culture at entry and 4 weeks after treatment.Results: Five patients did not complete the treatment: no follow‐up endoscopy was performed on two patients in the LAC group; one patient in the LAC group and two in the LACP group had their treatment stopped due to severe diarrhoea. By per protocol analysis, H. pylori eradication was achieved in 24 of the 28 evaluable patients (86%; 95% CI: 72–100%) after LAC therapy, and in 33 of the 33 evaluable patients (100%) after LACP therapy (P < 0.05). On intention‐to‐treat analysis, the rates of eradication were 24 of 31 patients (77%; 95% CI: 62–93%) in the LAC group, and 33 of 35 patients (94%; 95% CI: 86–100%) in the LACP group (P < 0.05).Conclusion: A 7‐day triple therapy with lansoprazole, amoxycillin and clarithromycin is effective in H. pylori eradication, but this regimen is significantly improved by the addition of polaprezinc.
Altered oesophageal motility following the administration of the 5‐HT1 agonist, sumatriptan
Authors: Foster  , Houghton  , Whorwell  , Morris  
Published: March 2003

Background: The 5‐HT1 agonist sumatriptan, used in the treatment of migraine, can cause chest pain.Aim: To investigate the effect of a therapeutic dose of sumatriptan (6 mg s.c.) on oesophageal motility.Methods: In 16 normal healthy subjects aged 19–32 years (9 males), the manometric response of the lower oesophageal sphincter (sleeve sensor), oesophageal body (four sites), stomach and pharynx (to register swallows) to 5 mL water swallows was assessed before and after a subcutaneous injection of either sumatriptan (6 mg) or saline control. Symptoms and ECGs were also monitored.Results: Sumatriptan 6 mg s.c. altered oesophageal motility in all subjects. This was reflected by a significant increase in the amplitude of oesophageal body contractions (change from pre‐ to 1 h post‐injection: sumatriptan 9.9 (2.8, 17.1) mmHg vs. placebo – 0.8 (– 4.2, 2.6) mmHg, difference 10.8 (4.4, 17.1) mmHg; P=0.003) and a transient increase in lower oesophageal sphincter pressure (change from pre‐ to 5 min post‐injection: sumatriptan 10.9 (5.2, 16.6) mmHg vs. placebo 5.1 (1.8, 8.4) mmHg, difference 5.8 (– 0.7, 12.3) mmHg; P=0.08). Sumatriptan had no effect on the velocity of propagation of oesophageal contractions (change from pre‐ to 1 h post‐injection: sumatriptan – 0.1 (– 0.3, 0.1) cm/s vs. placebo – 0.1 (– 0.3, 0.0) cm/s, difference 0.1 (– 0.1, 0.2) cm/s; P = 0.40). One subject experienced chest symptoms following sumatriptan and, although motility was altered, this did not reach pathological levels. No ECG abnormalities were observed.Conclusion: Sumatriptan (6 mg s.c.) significantly alters oesophageal motor function without affecting the ECG. It is therefore possible that sumatriptan‐induced chest symptoms may have an oesophageal origin. The evaluation of similar therapeutic agents for migraine on oesophageal function may be justified.
Long‐term haemodynamic effects of octreotide on postprandial splanchnic hyperemia in humans: a placebo‐controlled echo–doppler study
Authors: Ludwig  , Terai  , Brüning  , Stange  
Published: March 2003

Background: Octreotide is a potent splanchnic hypotensive somatostatin analogue effective in the treatment of acute variceal bleeding.Aim: To study the effects of octreotide on basal and postprandial splanchnic and systemic haemodynamics, and hormonal changes in humans.Methods: Twenty‐four healthy volunteers were randomized to receive a liquid meal and either octreotide (OCT, 100 μg bolus) or placebo repeatedly every 4 h for 48 h. Splanchnic (Doppler ultrasound) and systemic haemodynamics (non‐invasive cardiac monitoring) were assessed for 2 h on four consecutive days: one control day and after doses 1 (0 h), 7 (24 h) and 13 (48 h).Results: The maximum postprandial increases in mean blood velocity of the superior mesenteric artery (SMA–Vmean + 72%), portal (PBF + 52%) and total hepatic blood flow (HBF + 50%) observed in the placebo group, were abolished after the first dose of octreotide (SMA–Vmean – 23%, P < 0.01; PBF – 22%, P < 0.01; HBF – 21%, P < 0.01). Postprandial hyperemia was restored at the end of the 48‐h study period, but baseline SMA–Vmean (placebo 40 ± 12, OCT 29 ± 11 cm/s, P < 0.05) and PBF (placebo 1200 ± 971, OCT 743 ± 449 mL/min, P < 0.05) remained significantly lower in the octreotide group. The postprandial decrease of systemic vascular resistance and increase of cardiac index were prevented by octreotide for 48 h.Conclusions: Repeated 4‐hourly bolus injections of octreotide reduce splanchnic blood flow for at least 48 h, but the prevention of food‐induced splanchnic hyperemia is short‐lasting.
Selective COX‐2 inhibitors and human inflammatory bowel disease
Authors: Mccartney  , Mitchell  , Fairclough  , Farthing  , Warner  
Published: March 2003

Background: Much recent effort has been made to produce selective inhibitors of cyclo‐oxygenase‐2 (COX‐2) in the belief that these will lack the gastrointestinal damaging effects of traditional non‐steroidal anti‐inflammatory drugs (NSAIDs). Inflammatory bowel disease is associated with increased local production of prostanoids. These prostanoids, particularly PGE2 and PGI2, may well be protective as inflammatory bowel disease is aggravated by NSAID use.Aim: To examine the effects of a traditional NSAID and a highly selective COX‐2 inhibitor on the production of these prostanoids in human inflammatory bowel disease.Methods: Colonic mucosal biopsies were obtained from patients undergoing routine colonoscopy and biopsy for diagnostic or surveillance purposes. Biopsies were incubated in culture medium containing 10% foetal calf serum and antibiotics, plus test drugs or vehicle for 24 h, after which time the medium was removed and the content of PGE2, PGI2 (measured as 6 keto‐PGF1α) and thromboxane (Tx) A2 (measured as TxB2) determined.Results: Biopsies obtained from diseased colonic mucosa produced significantly more PGE2, PGI2 and thromboxane A2 than did controls (for example, PGE2: ulcerative colitis, 4.17 ± 1.06; Crohn’s disease, 3.97 ± 1.66; control, 0.12 ± 0.13 ng/mL, n=8–12). These increases were inhibited to a similar extent by either a highly selective COX‐2 inhibitor (L‐745 337) or a traditional non‐selective NSAID (indomethacin).Conclusions: Until selective COX‐2 inhibitors have been assessed adequately in human inflammatory bowel disease, these compounds should not be assumed to be safe for the gastrointestinal tract in inflammatory bowel disease.