bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of inhibition of gastric acid secretion on antropyloroduodenal motor activity and duodenal acid hypersensitivity in functional dyspepsia
Authors: Schwartz M. P. , Samsom M. , Van Berge Henegouwen G. P. , Smout A. J. P. M. 
Published: March 2003

Background:Heightened visceroperception and a decreased duodenal motor response to intraduodenal acid infusion have been reported in functional dyspepsia.Aim:To investigate the effect of treatment with a proton pump inhibitor on sensorimotor impairment in 19 patients with functional dyspepsia.Methods:Patients were assigned double‐blind to pantoprazole (n=10) or placebo (n=9) treatment for 2 weeks. Antropyloroduodenal manometry was performed before and after treatment, using a 21‐channel catheter, and the responses to intraduodenal infusion of 5 mL of saline and acid were assessed. Nausea, fullness and epigastric pain were scored before and after each infusion.Results:Acid induced a modest duodenal motor response and suppression of antral pressure waves, not altered by either treatment. However, acid evoked isolated pyloric pressure waves after pantoprazole treatment (P < 0.02), and not after placebo. Saline induced no motor response. Acid (not saline) induced nausea, both before and after treatment in both groups (all P < 0.05). Subgroup analysis of the seven acid‐hypersensitive patients (37%) showed a tendency towards a decrease in nausea in all four pantoprazole‐treated patients (P=0.07), in contrast to the three placebo‐treated patients (P=1.0).Conclusions:In functional dyspepsia, pantoprazole influenced the acid‐induced duodenogastric feedback mechanism, but not the impaired duodenal motor response. Duodenal acid hypersensitivity was decreased to some extent.
Efficacy of low‐dose clarithromycin triple therapy and tinidazole‐containing triple therapy for Helicobacter pylori eradication
Authors: Choi I. J. , Jung H. C. , Choi K. W. , Kim J. H. , Ahn D. S. , Yang U. S. , Rew J. S. , Lee S. I. , Rhee J. C. , Chung I. S. , Chung J. M. , Hong W.‐S. 
Published: March 2003

Background:Proton pump inhibitor‐based triple therapies are recommended as the first‐line treatment for Helicobacter pylori eradication.Aim:To evaluate the efficacies of low‐dose clarithromycin triple therapy and tinidazole‐containing triple therapy in a metronidazole resistance prevalent area and to compare the efficacies with standard triple therapy.Methods:In a randomized, multicentre, prospective study, a total of 352 patients with duodenal ulcer or non‐ulcer dyspepsia were randomly divided into three groups according to the administered regimen: OAC250 group (omeprazole, 20 mg, amoxicillin, 1000 mg, and clarithromycin, 250 mg), OAC500 group (omeprazole, 20 mg, amoxicillin, 1000 mg, and clarithromycin, 500 mg) and OTC group (omeprazole, 20 mg, tinidazole, 500 mg, and clarithromycin, 500 mg). The three groups received each regimen twice daily for 7 days. Upper gastrointestinal endoscopy was performed before and 4 weeks after treatment. H. pylori status was determined by rapid urease test and 13C urea breath test.Results:The eradication rates in the OAC250, OAC500 and OTC groups were 76.2%, 65.7% and 64.8% (95% confidence interval: 67.9–84.4%, 56.7–74.8% and 55.7–73.9%), respectively, by intention‐to‐treat analysis (P=0.149) and 92.8%, 87.2% and 84.1% (95% confidence interval: 84.4–97.3%, 77.9–93.8% and 73.9–91.2%), respectively, by per protocol analysis (P=0.088). All regimens were well tolerated and compliance was excellent.Conclusions:Both low‐dose clarithromycin triple therapy and tinidazole‐containing triple therapy are effective and safe regimens for H. pylori eradication.
The epidemiology and natural history of Crohn’s disease in population‐based patient cohorts from North America: a systematic review
Authors: Loftus E. V. , Schoenfeld P. , Sandborn W. J. 
Published: March 2003

Aim:To quantify, through systematic review, the epidemiology and natural history of Crohn’s disease in North America.Methods:The selected articles contained: (i) population‐based samples of patients followed from the time of diagnosis; and (ii) objective diagnostic criteria for disease. Studies on the natural history of Crohn’s disease also contained sufficient follow‐up.Data collection and analysis:For prevalence studies, data on the incidence, prevalence, gender and age at diagnosis were extracted. For natural history studies, data on the disease activity, use of medications and surgery were extracted.Main results:The prevalence of Crohn’s disease in North America ranges from 26.0 to 198.5 cases per 100 000 persons. The incidence rates range from 3.1 to 14.6 cases per 100 000 person‐years. Most patients have a chronic intermittent disease course, while 13% have an unremitting disease course and 10% have a prolonged remission. Less than half require corticosteroids at any point. During any given year, approximately 10% are treated with corticosteroids and 30% are treated with 5‐aminosalicylates. Up to 57% of patients require at least one surgical resection.Conclusions:Between 400 000 and 600 000 patients in North America have Crohn’s disease, and the natural history is marked by frequent exacerbations requiring treatment with corticosteroids, 5‐aminosalicylate products and surgery.
Topical mononitrate treatment in patients with anal fissure
Authors: Tankova L. , Yoncheva K. , Muhtarov M. , Kadyan H. , Draganov V. 
Published: March 2003

Aim:To assess the efficacy and patient compliance of topical mononitrate hydrogel for the treatment of anal fissure.Materials and methods:Nineteen patients with symptomatic chronic anal fissures were randomly allocated to receive either active (10 patients) or placebo (nine patients) gel treatment. Rectal administration of hydrogel containing 0.2% isosorbide‐5‐mononitrate was prescribed. Patients were instructed on its application to the anal canal twice daily for 3 weeks. A questionnaire was used to determine patient compliance with therapy. Anal manometry was performed before and after therapy.Results:At the end of therapy, the fissures were healed in 80% of actively treated patients compared with 22% of the control group. There was a mean reduction of 28% in mean resting anal pressure. Two actively treated patients (20%) suffered from mild headache relieved with oral analgesics and menthol lozenges. Faecal incontinence was not observed. There were no recurrences during at least 3 months of follow‐up.Conclusions:Topical mononitrate gel therapy of anal fissures is an effective and safe approach. In this study, the few cases of headache were rapidly relieved with oral analgesia and menthol lozenges.
Antioxidant effects of herbal therapies used by patients with inflammatory bowel disease: an in vitro study
Authors: Langmead L. , Dawson C. , Hawkins C. , Banna N. , Loo S. , Rampton D. S. 
Published: March 2003

Background:Herbal remedies used by patients for treatment of inflammatory bowel disease include slippery elm, fenugreek, devil’s claw, Mexican yam, tormentil and wei tong ning, a traditional Chinese medicine. Reactive oxygen metabolites produced by inflamed colonic mucosa may be pathogenic. Aminosalicylates (5‐ASA) are antioxidant and other such agents could be therapeutic.Aims:To assess the antioxidant effects of herbal remedies in cell‐free oxidant‐generating systems and inflamed human colorectal biopsies.Methods:Luminol‐enhanced chemiluminescence in a xanthine/xanthine oxidase cell‐free system was used to detect superoxide scavenging by herbs and 5‐ASA, and fluorimetry to define peroxyl radical scavenging using a phycoerythrin degradation assay. Chemiluminescence was used to detect herbal effects on generation of oxygen radicals by mucosal biopsies from patients with active ulcerative colitis.Results:Like 5‐ASA, all herbs, except fenugreek, scavenged superoxide dose‐dependently. All materials tested scavenged peroxyl dose‐dependently. Oxygen radical release from biopsies was reduced after incubation in all herbs except Mexican yam, and by 5‐ASA.Conclusions:All six herbal remedies have antioxidant effects. Fenugreek is not a superoxide scavenger, while Mexican yam did not inhibit radical generation by inflamed biopsies. Slippery elm, fenugreek, devil’s claw, tormentil and wei tong ning merit formal evaluation as novel therapies in inflammatory bowel disease.
Integrated acidity and rabeprazole pharmacology
Authors: Gardner J. D. , Perdomo C. , Sloan S. , Hahne W. F. , Barth J. A. , Rodriguez‐Stanley S. , Robinson M. 
Published: March 2003

Background:Integrated gastric and oesophageal acidity can be calculated from measurements of gastric and oesophageal pH and used to quantify gastric and oesophageal acidity over time. Rabeprazole is a new proton pump inhibitor that is effective in treating gastro‐oesophageal reflux disease (GERD).Aim:To use measurement of integrated gastric and oesophageal acidity to determine the onset, duration and overall effect of rabeprazole in subjects with GERD.Methods:Subjects with GERD were required to have oesophageal pH ≤ 4 for at least 10% of a 24‐h recording. Effects of 20 mg rabeprazole on 24‐h gastric and oesophageal pH were measured on days 1 and 7 of dosing. Integrated gastric and oesophageal acidity were calculated from time‐weighted average hydrogen ion concentrations at each second of the 24‐h record.Results:At steady‐state, 20 mg rabeprazole inhibited gastric acidity by 89% and oesophageal acidity by 95%. The first dose of rabeprazole inhibited gastric and oesophageal acidity by at least 70% of the steady‐state effect. Oesophageal acidity could be divided into monophasic and biphasic patterns, and rabeprazole had different effects on oesophageal and gastric acidity in these two GERD subpopulations. The onset of action of the first dose of rabeprazole on gastric acidity was 4 h and on oesophageal acidity was 4 h in monophasic subjects and 7 h in biphasic subjects. Integrated acidity was more sensitive than time pH ≤ 4 in measuring the inhibitory actions of rabeprazole.Conclusions:Integrated gastric and oesophageal acidity are quantitative measurements that provide useful and novel information regarding the pathophysiology of GERD as well as the impact of antisecretory agents such as rabeprazole.
Interferon‐α plus ribavirin for 12 months increases the sustained response rates in chronic hepatitis C relapsers
Authors: Moreno‐Monteagudo J. A. , Castro A. , De Pedro A. , Lorenzo J. A. , Fernández‐Bermejo M. , Lopez S. , García‐Buey L. , Borque M. J. , Pedreira J. D. , Moreno‐Otero R. 
Published: March 2003

Background:The effectiveness and tolerability of combination therapy for 12 months have not been evaluated sufficiently in chronic hepatitis C relapsers to interferon.Aims:To evaluate the sustained response to interferon plus ribavirin for 12 months in chronic hepatitis C relapsers.Methods:We included 55 chronic hepatitis C relapsers in a 12‐month treatment protocol with interferon (3 MU thrice weekly) plus ribavirin (1–1.2 g/day). The effectiveness was evaluated using serum aminotransferase and hepatitis C virus RNA levels, alanine aminotransferase normalization and viraemia clearance after 12 months, defining the end‐of‐treatment response, and 6 months after completion of therapy, defining the sustained response. Adverse effects were recorded.Results:End‐of‐treatment response and sustained response were achieved in 47 (85%) and 37 (67%) patients, respectively; there were 10 (21%) relapsers after combination therapy. Predictive factors of sustained response included the genotype (non‐1 95% vs. 1 48%; P < 0.001), lower viraemia (503 917 ± 553 230 vs. 901 393 ± 548 267 copies/mL; P < 0.005), higher alanine aminotransferase levels (137 ± 75 vs. 103 ± 41 IU/L; P < 0.05) and a lower γ‐glutamyl transpeptidase/alanine aminotransferase ratio (0.30 ± 0.23 vs. 0.49 ± 0.39; P < 0.05). Tolerance to therapy was good, with no withdrawals.Conclusions:Interferon plus ribavirin treatment for 12 months in chronic hepatitis C relapsers yields high sustained response rates and is well tolerated. The sustained response is related to a non‐1 genotype, lower baseline viraemia, higher alanine aminotransferase level and a lower γ‐glutamyl transpeptidase/alanine aminotransferase ratio.
Immunosuppressants in distal ulcerative colitis
Authors: Falasco G. , Zinicola R. , Forbes A. 
Published: March 2003

Background:Distal ulcerative colitis may prove to be resistant to steroids and aminosalicylates, but total colectomy is more difficult to justify than in severe extensive colitis. Immunosuppression is of established benefit in generalized colitis, but there are no data available specific to distal disease.Aim:To determine whether the protocol‐driven use of immunosuppressants in resistant distal ulcerative colitis is of similar efficacy and safety to that in extensive disease.Methods:Two hundred and twenty‐eight patients with distal ulcerative colitis seen in a 5‐year period were identified from a prospective database. Details of 52 who had received immunosuppression were analysed.Results:The 52 patients received 68 courses of therapy (53 azathioprine, five mercaptopurine, 10 ciclosporin). The thiopurines yielded clinically valuable responses in only 43% of courses, with failure of response in 16% and toxicity in 34%. Ciclosporin was helpful on only two of 10 occasions. Eight patients required total colectomy. Adverse events were typical of those normally associated with immunosuppressants, with potential risk to life in seven patients; treatment was discontinued because of toxicity on a total of 31% of occasions.Conclusions:Immunosuppression appears to be of lower efficacy and higher toxicity in resistant distal colitis than when used in more extensive colitis.
Primary resistance to antibiotics and its clinical impact on the efficacy of Helicobacter pylori lansoprazole‐based triple therapies
Authors: Poon S. K. , Chang C. S. , Su J. , Lai C. H. , Yang C. C. , Chen G. H. , Wang W. C. 
Published: March 2003

Aim:To evaluate Helicobacter pylori primary resistance and its clinical impact on the efficacy of two lansoprazole‐based eradication triple therapies.Methods: H. pylori‐positive patients (n=228) were randomized to receive one of the 1‐week regimens: lansoprazole 30 mg, clarithromycin 500 mg and amoxicillin 1 g (LAC), or lansoprazole 30 mg, clarithromycin 500 mg and metronidazole 500 mg (LMC), each given twice daily. H. pylori status was assessed by 13C‐urea breath test and culture at diagnosis and by 13C‐urea breath test 6 weeks after therapy. Antibiotic susceptibility was determined by E‐test (n=98).Results:The eradication rates with per protocol/ intention‐to‐treat analyses were: LAC (n=95/114) 83%/69% and LMC (n=96/114) 85%/72%. Primary resistance was 11% for clarithromycin, 41% for metronidazole and 0% for amoxicillin. Eradication in metronidazole‐susceptible/‐resistant strains was 85%/82% in LAC and 83%/63% in LMC. Significantly lower cure rates were observed in clarithromycin‐resistant patients treated with LAC (95% vs. 0%, P < 0.001) and LMC (86% vs. 0%, P < 0.001).Conclusions:One‐week LAC and LMC are similarly effective therapies. Clarithromycin resistance significantly affected H. pylori eradication in both regimens.
Effect of Helicobacter pylori eradication on oesophageal acid exposure in patients with reflux oesophagitis
Authors: Wu J. C. Y. , Chan F. K. L. , Wong S. K. H. , Lee Y. T. , Leung W. K. , Sung J. J. Y. 
Published: March 2003

Background:The effect of Helicobacter pylori eradication on reflux oesophagitis is unclear.Aim:To study the effect of H. pylori eradication on oesophageal acid exposure and disease severity in patients with reflux oesophagitis.Methods:Patients with reflux oesophagitis and H. pylori infection were recruited for 24‐h oesophageal pH‐metry. They were then randomly assigned to receive either treatment for H. pylori eradication (1‐week omeprazole‐based triple therapy, followed by 7‐week omeprazole) or omeprazole alone (8‐week omeprazole). Uninfected patients were recruited as controls. Endoscopy, pH monitoring and symptom assessment were repeated at 26 weeks.Results:Forty patients (25 H. pylori‐positive and 15 uninfected) with erosive oesophagitis were studied. Fourteen were randomized to receive treatment for H. pylori eradication and 11 to receive omeprazole alone. There was no difference in the percentage of time the oesophageal pH < 4 before and 26 weeks after treatment among the three groups. However, the percentage of time the oesophageal pH < 2 (P=0.01) and pH < 3 (P=0.02) was significantly increased in patients receiving treatment for H. pylori eradication. Three (21%) patients in the group receiving treatment for H. pylori eradication had worsening of reflux oesophagitis.Conclusions: H. pylori eradication increases oesophageal acid exposure and may adversely affect the clinical course of reflux disease in a subset of patients.
Interactions between Helicobacter pylori and other risk factors for peptic ulcer bleeding
Authors: Stack W. A. , Atherton J. C. , Hawkey G. M. , Logan R. F. A. , Hawkey C. J. 
Published: March 2003

Aim:To investigate the role of Helicobacter pylori, expressing the virulence marker CAGA (cytotoxin associated gene product A) in ulcer complications and its interaction with nonsteroidal anti‐inflammatory drugs (NSAIDs) and other risk factors.Design:Case control study using conditional logistic regression analysis.Setting:University and City Hospitals, Nottingham.Subjects:203 consecutive patients with ulcer bleeding and 203 age‐ and sex‐matched controls.Results:Ulcer bleeding was more likely with positive H. pylori serology (odds ratio = 3.3, 95% CI: 1.7–6.6 for CagA positive, but only OR = 1.6, 95% CI: 0.7–3.7 for CagA negative serology), current smoking (OR 2.2, 95% CI: 1.04–4.7), aspirin ≤ 300 mg daily (OR 7.7, 95% CI: 2.8–20.6), all other nonsteroidal anti‐inflammatory drugs (NSAIDs: OR 10.6, 95% CI: 3.1–35.7 for ≤ 1 defined daily dose lower and OR 22.6, 95% CI: 6.2–82.0 for higher doses) and past ulcer history (OR 5.6, 95% CI: 2.3–14.1). Aspirin ≤ 300 mg daily was used by 25.1% of patients vs. 7.4% of controls. Smoking only enhanced risk in the presence of H. pylori, with a synergistic interaction (interaction odds ratio = 4.9, 2.4–9.9, P=0.002). Conversely, risks with non‐aspirin NSAIDs were reduced in the presence of H. pylori, particularly if CagA‐positive (interaction odds ratio=0.21, 0.05–0.9, P=0.03).Conclusions:CagA positive H. pylori infection is associated with an increased risk of ulcer bleeding. The risk from non‐aspirin NSAIDs is even higher, but is less in H. pylori infected people. Low‐dose aspirin is now commonly associated with ulcer bleeding.
The concept of entero‐colonic encephalopathy, autism and opioid receptor ligands
Authors: Wakefield A. J. , Puleston J. M. , Montgomery S. M. , Anthony A. , O'Leary J. J. , Murch S. H. 
Published: March 2003

There is growing awareness that primary gastrointestinal pathology may play an important role in the inception and clinical expression of some childhood developmental disorders, including autism. In addition to frequent gastrointestinal symptoms, children with autism often manifest complex biochemical and immunological abnormalities. The gut–brain axis is central to certain encephalopathies of extra‐cranial origin, hepatic encephalopathy being the best characterized.Commonalities in the clinical characteristics of hepatic encephalopathy and a form of autism associated with developmental regression in an apparently previously normal child, accompanied by immune‐mediated gastrointestinal pathology, have led to the proposal that there may be analogous mechanisms of toxic encephalopathy in patients with liver failure and some children with autism. Aberrations in opioid biochemistry are common to these two conditions, and there is evidence that opioid peptides may mediate certain aspects of the respective syndromes. The generation of plausible and testable hypotheses in this area may help to identify new treatment options in encephalopathies of extra‐cranial origin.Therapeutic targets for this autistic phenotype may include: modification of diet and entero‐colonic microbial milieu in order to reduce toxin substrates, improve nutritional status and modify mucosal immunity; anti‐inflammatory/immunomodulatory therapy; and specific treatment of dysmotility, focusing, for example, on the pharmacology of local opioid activity in the gut.
Inhibition of Helicobacter pylori‐induced cyclo‐oxygenase‐2 aggravates NSAID‐caused gastric damage in Mongolian gerbils
Authors: Futagami S. , Hiratsuka T. , Wada K. , Tatsuguchi A. , Tsukui T. , Miyake K. , Akamatsu T. , Hosone M. , Sakamoto C. , Kobayashi M. 
Published: March 2003

Background:The effect of Helicobacter pylori infection on non‐steroidal anti‐inflammatory drug‐induced gastric mucosal injury is controversial.Aim:To examine the effect of the interaction between H. pylori and non‐steroidal anti‐inflammatory drugs on gastric mucosal injury.Methods:Mongolian gerbils infected with H. pylori were treated with indometacin at 8 mg/kg for 2 days or 7 days. Mucosal damage was assessed by macroscopic and histological examination, and myeloperoxidase activity was measured as an index of neutrophil infiltration. The expression levels of cyclo‐oxygenase proteins were determined by Western blot analysis and cyclo‐oxygenase activity.Results:A 2‐day course of indometacin did not cause an increase in gastric damage in H. pylori‐infected Mongolian gerbils compared to uninfected gerbils, while a 7‐day course of indometacin caused additive gastric damage in H. pylori‐infected animals. H. pylori infection induced cyclo‐oxygenase‐2 expression in the stomach. Treatment with indometacin for 2 days did not significantly affect cyclo‐oxygenase activity in H. pylori‐infected animals, while treatment for 7 days inhibited both cyclo‐oxygenase‐1 and cyclo‐oxygenase‐2 activities. Pre‐treatment with a selective cyclo‐oxygenase‐2 inhibitor aggravated mucosal injury in H. pylori‐infected animals treated or not treated with indometacin for 2 days.Conclusions:Our results suggest that cyclo‐oxygenase‐2 protein induced by H. pylori infection may be involved in the defence of the gastric mucosa against damage caused by non‐steroidal anti‐inflammatory drugs. Therefore, inhibition of cyclo‐oxygenase‐2 activity may enhance non‐steroidal anti‐inflammatory drug‐caused gastric damage in H. pylori‐infected animals.