bluuebunny/crossref_metadata_2025_split huggingface dataset:
Randomized comparison of unfractionated heparin with corticosteroids in severe active inflammatory bowel disease
Authors: Ang Y. S. , Mahmud N. , White B. , Byrne M. , Kelly A. , Lawler M. , Mcdonald G. S. A. , Smith O. P. , Keeling P. W. N. 
Published: March 2003

Background:Heparin therapy may be effective in steroid resistant inflammatory bowel disease.Aim:A randomized pilot study, to compare unfractionated heparin as a first‐line therapy with corticosteroids in colonic inflammatory bowel disease.Methods:Twenty patients with severe inflammatory bowel disease (ulcerative colitis, n=17; Crohn’s colitis, n=3) were randomized to either intravenous heparin for 5 days, followed by subcutaneous heparin for 5 weeks (n=8), or high‐dose intravenous hydrocortisone for 5 days followed by oral prednisolone 40 mg daily, reducing by 5 mg per day each week (n=12). After 5 days, non‐responders in each treatment group were commenced on combination therapy. Response to therapy was monitored by: clinical disease activity (ulcerative colitis: Truelove and Witt Index; Crohn’s colitis: Harvey and Bradshaw Index), stool frequency, serum C‐reactive protein and α1 acid glycoprotein, endoscopic and histopathological grading.Results:The response rates were similar in both treatment groups: clinical activity index (heparin vs. steroid; 75% vs. 67%; P=0.23), stool frequency (75% vs. 67%; P=0.61), endoscopic (75% vs. 67%; P=0.4) and histopathological grading (63% vs. 50%; P=0.67). Both treatments were well‐tolerated with no serious adverse events.Conclusion:Heparin as a first line therapy is as effective as corticosteroids in the treatment of colonic inflammatory bowel disease. Large multicentre randomized comparative studies are required to determine the role of heparin in the management of inflammatory bowel disease.
Review article: the clinical influence of Helicobacter pylori in effective acid suppression—implications for the treatment of gastro‐oesophageal reflux disease
Authors: Martínek J. , Kužela L. , Špičák J. , Vavrečka A. 
Published: March 2003

The relationship between gastro‐oesophageal reflux disease (GERD) and Helicobacter pylori is unclear. Recent data indicate that H. pylori probably exerts a protective effect against GERD. In recent years, the interaction between H. pylori, proton pump inhibitors and GERD has been widely studied. Currently available proton pump inhibitors produce significantly higher intragastric pH in H. pylori‐positive patients than in those who are H. pylori negative, and this phenomenon may be clinically relevant.The mechanisms responsible for this difference in efficacy are not fully understood, although there are two major theories. Ammonia, produced by H. pylori, is able to neutralize gastric acid, and thus apparently increase the effect of acid suppressive agents (the ‘ammonia theory’). The other theory is that decrease in acid output is due to the development of corpus gastritis during treatment with a proton pump inhibitor (the ‘gastritis theory’).Treatment strategies to overcome this lowered sensitivity to acid suppression are to increase the frequency/dose of a proton pump inhibitor or to add an H2‐receptor antagonist in the evening—but both have pharmaco‐economic implications. An agent that could provide adequate pH control regardless of H. pylori status would be highly beneficial in the treatment of GERD, and may also lower treatment costs.
Pharmacodynamics and kinetics of omeprazole MUPS 20 mg and pantoprazole 40 mg during repeated oral administration in Helicobacter pylori‐negative subjects
Authors: Geus W. P. , Mathôt R. A. A. , Mulder P. G. H. , Lamers C. B. H. W. 
Published: March 2003

Background:Omeprazole has become available in a tablet formulation, a Multiple Unit Pellet System (MUPS) containing a large number of small individually enteric‐coated micropellets.Aim:To compare the acid‐inhibitory effect of omeprazole MUPS 20 mg with pantoprazole 40 mg and to describe the pharmacokinetics of both drugs following administration on day 1 and day 6.Methods:Randomized, two‐way crossover study. Sixteen Helicobacter pylori‐negative healthy subjects, whose gastric acidity fell below pH 4 for 70% of a 24‐h baseline period were included. Intragastric pH was measured continuously.Results:On day 1 both drugs significantly raised median 24‐h gastric pH compared to baseline. Median pH and percentages of time above pH 3 and 4 on day 1 and day 6 of administration were not significantly different, with the exception of median daytime pH on day 6, which was significantly higher with omeprazole (4.65 vs. 4.05). AUC and Cmax of omeprazole were significantly increased on day 6. AUC and Cmax of pantoprazole were not significantly increased.Conclusions:No significant difference in acid‐inhibitory effect on day 1. On day 6 median daytime pH was significantly higher with omeprazole MUPS, but the percentages of time spent above pH 3 and 4 were not significantly different. The significant increase in bioavailability of omeprazole may contribute to the increased effect on day 6.
Initial potency of lansoprazole and omeprazole tablets on pentagastrin‐stimulated gastric acid secretion—a placebo‐controlled study in healthy volunteers
Authors: Müller  , Göksu  , Fuchs  , Schlüter  , Simon  
Published: March 2003

Background:The new tablet formulation of omeprazole (Losec MUPS), is thought to have a stronger acid inhibition than the previously marketed capsules.Methods:The effects of the proton pump inhibitors lansoprazole and omeprazole tablets on pentagastrin‐stimulated acid secretion were compared in Helicobacter pylori‐negative healthy male volunteers (n=12). The study was placebo‐controlled, crossover matched and double‐blind for lansoprazole (Agopton) and placebo, and single‐blind for omeprazole tablets. Gastric acid response to sub‐maximal pentagastrin‐stimulation (0.6 μg · h/kg b.w.) was determined from 12.5 to 14.5 h after the first and second dose of the test drugs.Results:Lansoprazole 15 mg and 30 mg as well as omeprazole 20 mg tablets caused a marked decrease in gastric acid secretion, showing equipotency for 15 mg lansoprazole and 20 mg omeprazole tablets. Their efficacy, however, was lower than 30 mg lansoprazole. In addition, the inter‐individual variation after omeprazole tablets was higher than following lansoprazole. Neither 7.5 mg lansoprazole nor 10 mg omeprazole tablets were clearly different from placebo on the first 2 days.The drugs were well‐tolerated. No clinically relevant influence was found on either laboratory screen or cardiovascular parameters.Conclusion:Lansoprazole 15–30 mg shows a stronger acid inhibition and a lower inter‐individual variability than the new omeprazole 20 mg tablets on days 1 and 2 of dosing.
Gastric acid secretion in cyclooxygenase‐1 deficient mice
Authors: Borrelli F. , Welsh N. J. , Sigthorsson G. , Simpson R. , Palizban A. , Bjarnason I. , Tavares I. A. 
Published: March 2003

Background:Constitutive cyclooxygenase‐1 enzyme synthesizes prostaglandins which are thought to play an important role in the functional integrity of the stomach gastric mucosa. Recently, it was shown that cyclooxygenase‐1 deficient mutant mice did not develop spontaneous gastric pathology and appear less sensitive to indomethacin‐induced gastric damage.Aim:To investigate gastric acid secretion in cyclooxygenase‐1 deficient mutant mice.Methods:The basal and histamine or isobutyl methylxanthine‐stimulated acid secretion in stomachs of cyclooxygenase‐1 deficient homozygous mice and the effect of indomethacin was compared with that of heterozygous and wild‐type mice using isolated lumen perfused mouse stomachs, in organ baths, monitored by pH‐electrodes.Results:There was no significant difference in the basal or histamine stimulated gastric acid secretion between wild‐type or heterozygous or homozygous mice. However, isobutyl methylxanthine was more potent in the cyclooxygenase‐1 deficient and heterozygous mice than in wild‐type mice. Indomethacin, at concentrations below 1 mM, had no effect on either basal or histamine stimulated acid secretion in any of the mice populations.Conclusion:Gastric acid secretion is maintained without prostaglandin involvement in cyclooxygenase‐1 deficient mice. The finding that basal and histamine‐stimulated gastric acid secretion was similar in the cyclooxygenase‐1 deficient, compared to wild‐type mice is consistent with the lack of spontaneous gastric pathology in the cyclooxygenase‐1 deficient mice.
Helicobacter pylori‐positive duodenal ulcer: three‐day antibiotic eradication regimen
Authors: Catalano F. , Branciforte G. , Catanzaro R. , Cipolla R. , Bentivegna C. , Brogna A. 
Published: March 2003

Background:The most widely used treatments for ulcer healing and Helicobacter pylori eradication consist of a 1–2 week regimen of a proton pump inhibitor plus two or three antimicrobials.Aims:To evaluate the efficacy, safety, cost, and tolerance of a three‐day regimen with three antibiotics vs. a 10‐day treatment with a proton pump inhibitor or vs. a ranitidine bismuth citrate triple therapy.Methods:Two hundred and twenty‐one patients with endoscopically‐proven H. pylori‐positive duodenal ulcers were recruited to the study. Recruited patients were assigned to one of the following four regimens: (I) omeprazole 40 mg o.m. plus amoxycillin 1 g b.d. and clarithromycin 500 mg b.d. for 10 days (OAC: 55 patients); (ii) omeprazole 40 mg o.m. on days 1–5, plus amoxycillin 1 g b.d., clarithromycin 500 mg b.d. and metronidazole 500 mg b.d. on days 3–5 (OACM: 56 patients); (iii) ranitidine bismuth citrate 400 mg b.d. plus amoxycillin 1 g b.d. and clarithromycin 500 mg b.d. for 10 days (RAC: 54 patients); (iv) ranitidine bismuth citrate 400 mg b.d. on days 1–5, plus amoxycillin 1 g b.d., clarithromycin 500 mg b.d. and metronidazole 500 mg b.d. on days 3–5 (RACM: 56 patients). Fisher’s exact test was used to compare data regarding healing and eradication in the four groups.Results:The intention‐to‐treat eradication and ulcer healing rates for the RACM regimen were 95% and 98%, respectively. Statistically significant differences were observed, relating to the eradication and healing of ulcers, between RACM and either the RAC or OAC regimens.Conclusion:The three‐day antibiotic therapy with amoxycillin, clarithromycin and metronidazole in addition to ranitidine bismuth citrate is a very effective anti‐H. pylori regimen.
Review article: effect of bile salt pool composition on hepatic and biliary functions
Authors: Carulli N. , Bertolotti M. , Carubbi F. , Concari M. , Martella P. , Carulli L. , Loria P. 
Published: March 2003

SummaryThe enterohepatic recirculation of bile salts exerts important regulatory effects on many hepatic, biliary and intestinal functions; such regulation is likely to depend, to a large extent, on the physical–chemical property of hydrophobicity of the recirculating pool. The present review summarizes the main experimental evidence carried out by our research group over the past two decades, in the attempt to investigate systematically the relationships between structural properties and biological effects of bile acids in humans. Hydrophobic bile acids (chenodeoxycholic acid, deoxycholic acid), but not hydrophilic acids (ursodeoxycholic acid), significantly suppressed hepatic activity of HMG‐CoA reductase, the limiting step of cholesterol synthesis, and in vivo cholesterol 7α‐hydroxylation, the limiting step of bile acid synthesis. The output of biliary cholesterol and phospholipid was also directly related to the hydrophobicity of the bile acid pool. Finally, treatment with chenodeoxycholic acid, but not with ursodeoxycholic acid, significantly decreased gall‐bladder emptying rates. When turning to the in vitro model of HepG2 cells, hydrophobic bile acids were found to induce greater cytotoxic and pro‐apoptotic effects. From this series of studies, we conclude that the regulatory effects of bile acids on the liver and biliary tract are largely dependent on the hydrophobic–hydrophilic balance of the recirculating bile acid pool.
Walking and chewing reduce postprandial acid reflux
Authors: Avidan B. , Sonnenberg A. , Schnell T. G. , Sontag S. J. 
Published: March 2003

Background:Gastro‐oesophageal reflux is worse after meals, and antacids are usually consumed after dietary indiscretion.Aim:To investigate whether walking or gum chewing affect meal‐induced gastro‐oesophageal reflux.Methods:The study population comprised 12 case subjects with gastro‐oesophageal reflux disease and 24 healthy controls. Each subject was studied using pH‐metry for 5 h on 3 separate days. After baseline recording of pH for 1 h, all subjects were fed a standard breakfast over a 20‐min period. On one of the days, oesophageal pH was recorded after the 20‐min eating period for an additional 4 h in the sitting position. On another day, postprandial oesophageal pH was recorded for the first hour whilst walking, and for 3 subsequent hours whilst sitting. During a third day, oesophageal pH was recorded for the first postprandial hour whilst gum‐chewing, followed by 3 h of sitting.Results:Food intake promoted gastro‐oesophageal reflux in case subjects with GERD as well as in healthy controls, although postprandial reflux was more pronounced amongst the refluxers than amongst the controls. Chewing gum for 1 h after the meal reduced the acid contact time in both groups, with a more profound effect in refluxers than in controls. Whilst the beneficial effect of 1‐h of gum‐chewing lasted for up to 3 h in both groups, the beneficial effect of 1‐h of walking was apparent only in refluxers, only to a mild degree, and only for a short duration.Conclusions:Chewing gum after a meal helps to reduce postprandial oesophageal acid exposure.
Eradication of Helicobacter pylori prevents ulcer development in patients with ulcer‐like functional dyspepsia
Authors: Hsu P.‐I. , Lai K.‐H. , Tseng H.‐H. , Lo G.‐H. , Lo C.‐C. , Lin C.‐K. , Cheng J.‐S. , Chan H.‐H. , Ku M.‐K. , Peng N.‐J. , Chien E.‐J. , Chen W. , Hsu P.‐N. 
Published: March 2003

Background:Although the eradication of Helicobacter pylori infection benefits patients with gastric or duodenal ulcers, the value of eradicating the infection in the patients with functional dyspepsia (FD) remains controversial.Aims:To determine whether eradicating H. pylori can prevent the subsequent development of ulcers or relieve the symptoms of functional dyspepsia patients.Methods:In a double‐blind, placebo‐controlled trial, 161 patients infected with H. pylori who had functional dyspepsia were randomly assigned to 7 days of treatment with a lansoprazole‐based triple therapy or placebo and then followed for 1 year. The main outcome measures were the development of peptic ulcers and the resolution of symptoms.Results: H. pylori was eradicated in 63 out of 81 patients (78%) in the treatment group and none of the 80 patients (0%) in the placebo group. During the follow‐up period, two patients in the treatment group and six patients in the placebo group developed peptic ulcers at repeat endoscopy (2.5% vs. 7.5%; 95% CI: –12 to 2). The reduction in ulcer rates was statistically significant in the ‘ulcer‐like’ sub‐group (0% vs. 16.7%; 95% CI: –32 to –2), but not in the ‘dysmotility‐like’ and ‘unclassifiable’ sub‐groups. Regarding symptom response, the resolution rates of symptoms were similar between the treatment and placebo groups (58.0% vs. 55.0%, 95% CI: –12 to 18). Additionally, no significant differences existed in the symptom responses between the treatment and control arms in each of the dyspepsia sub‐groups.Conclusions:Eradicating H. pylori can prevent the subsequent development of peptic ulcers in the patients with ‘ulcer‐like’ functional dyspepsia. However, this approach does not significantly reduce the symptoms of functional dyspepsia patients.
Pain versus discomfort—is differentiation clinically useful?
Authors: Stanghellini V. 
Published: March 2003

Functional dyspepsia is highly variable in its clinical presentation and multifactorial in its underlying causes. Since many of the symptoms included in the definition of dyspepsia are intuitively suggestive of different pathogenic mechanisms, it has been proposed that patients with functional dyspepsia be divided into distinct dyspepsia sub‐groups according to symptom clusters. The goal was to classify patients more homogeneously for research purposes as well as to target treatment.However, recent epidemiological, pathophysiological, and clinical studies indicate that a priori definitions based on the presence/absence of symptoms or clusters of symptoms have no clinical utility due to the considerable overlap between symptoms, as well as the poor correlation between pathogenic factors and responses to treatment.Attention is now focused on identifying predominant symptoms. Recent studies suggest that the analysis of predominant symptoms, demographic features, and overlapping digestive syndromes can help to identify dyspepsia sub‐groups with different underlying pathophysiological features and aid in selecting appropriate treatment.The utility of this approach has been demonstrated in gastro‐oesophageal reflux disease, which can be reliably diagnosed and managed on the basis of the presence and severity of the predominant symptom, heartburn. It is likely that precise symptom definitions and history‐taking will be of pivotal importance in management strategies for functional dyspepsia.
Oral versus combination mesalazine therapy in active ulcerative colitis: a double‐blind, double‐dummy, randomized multicentre study
Authors: Vecchi M. , Meucci G. , Gionchetti P. , Beltrami M. , Di Maurizio P. , Beretta L. , Ganio E. , Usai P. , Campieri M. , Fornaciari G. , De Franchis R. 
Published: March 2003

Background:Oral and topical mesalazine formulations are effective in active ulcerative colitis, but little is known on the efficacy of combined treatment.Aim:To compare the efficacy of oral mesalazine vs. combined oral and topical mesalazine in mildly to moderately active ulcerative colitis.Methods:Patients with mildly to moderately active ulcerative colitis (Clinical Activity Index, CAI 4–12) were identified at 15 participating centres. They were randomized to receive either mesalazine 4 g orally plus placebo enema, or mesalazine 2 g orally plus mesalazine 2 g rectally as a liquid enema for 6 weeks. The rate of clinical remission (CAI < 4) or clinical remission/improvement (reduction of CAI of 50% from baseline) at 6 weeks and time to clinical remission/improvement were primary end‐points; the rate of endoscopic remission was a secondary end‐point.Results:67 patients were assigned to oral treatment and 63 to combined treatment. One patient in the oral group and 2 in the combined group discontinued the treatment due to adverse events. Following an intention‐to‐treat analysis, the rate of clinical remission was 82% for oral treatment and 87% for combined treatment (P=0.56); the mean time to remission 22.2 and 20.2 days, respectively (P=0.29); the rate of clinical remission/improvement and the rate of endoscopic remission were 85% and 91% (P=0.503) and 58% and 71% (P=0.21), respectively.Conclusions:In patients with mild active ulcerative colitis, mesalazine 4 g orally and 2 g orally plus 2 g enema are equally effective in inducing disease remission.
Meta‐analysis of smooth muscle relaxants in the treatment of irritable bowel syndrome
Authors: Poynard T. , Regimbeau C. , Benhamou Y. 
Published: March 2003

Aim:To update previous overviews of placebo‐controlled double‐blind trials assessing the efficacy and tolerance of smooth muscle relaxants in irritable bowel syndrome.Methods and trials:A total of 23 randomized clinical trials were selected for meta‐analyses of their efficacy and tolerance. Six drugs were analysed: cimetropium bromide (five trials), hyoscine butyl bromide (three trials), mebeverine (five trials), otilium bromide (four trials), pinaverium bromide (two trials) and trimebutine (four trials). The total number of patients included was 1888, of which 945 received an active drug and 943 a placebo.Results:The mean percentage of patients with global improvement was 38% in the placebo group (n=925) and 56% in the myorelaxant group (n=927), in favour of myorelaxants with a mean odds ratio of 2.13, P < 0.001 (95% CI: 1.77–2.58) and a mean risk difference of 22% P < 0.001 (95% CI: 13–32%). The percentage of patients with pain improvement was 41% in the placebo group (n=568) and 53% in the myorelaxant group (n=567): odds ratio 1.65, P < 0.001 (95% CI: 1.30–2.10) and risk difference 18%, P < 0.001 (95% CI: 7–28%). There was no significant difference for adverse events.Conclusion:Myorelaxants are superior to placebo in the management of irritable bowel syndrome.
Current endoscopic therapeutic options in the management of variceal bleeding
Authors: Helmy A. , Hayes P. C. 
Published: March 2003

Variceal bleeding is a frequent and life‐threatening complication of portal hypertension. The first episode of variceal bleeding is not only associated with a high mortality, but also with a high recurrence rate in those who survive. Therefore, many studies and randomized clinical trials have focused on different therapeutic strategies aiming to prevent the first episode of variceal bleeding (primary prophylaxis), to control haemorrhage during the acute bleeding episode (emergency treatment), and to prevent re‐bleeding (secondary prophylaxis). These strategies involve pharmacological, endoscopic, surgical, and interventional radiological modalities.This review concentrates on the clinical aspects of the endoscopic modalities used to treat oesophageal variceal haemorrhage, including variceal injection sclerotherapy, variceal band ligation, and the use of tissue adhesives (glue) and their substitutes. We also draw conclusions from the available literature regarding the use of endoscopic modalities in primary prophylaxis, emergency treatment, and secondary prophylaxis of variceal re‐bleeding. The management of gastric varices and variceal bleeding during pregnancy is also addressed.
Relationship between lactose digestion, gastrointestinal transit time and symptoms in lactose malabsorbers after dairy consumption
Authors: Labayen I. , Forga L. , González A. , Lenoir‐Wijnkoop I. , Nutr R. , Martínez J. A. 
Published: March 2003

Background:The relationship of symptoms with objective measurements, as well as some of the mechanisms involved in lactose tolerance after yoghurt consumption, remain unclear.Methods:The trial had a double‐blind design in which 22 lactose malabsorbers received 25 g daily lactose in fresh (living bacteria > 108 cfu/g) yoghurt or heated (< 102 cfu/g) yoghurt for 15 days, followed by a cross‐over (15 days) after a wash‐out period (14 days). The lactose digestion was determined by the breath H2 test, the gastric emptying (GE) with a 13C‐acetate breath test and the revealed transit time (OCTT) by 15N‐lactose‐ureide test. Subjects reported their gastrointestinal symptoms (GIS) in a validated questionnaire.Results:Breath H2 test indicated more effective lactose digestion after fresh yoghurt intake. The OCTT was shorter after heated yoghurt ingestion as compared with the fresh. There was lower severity of GIS (P < 0.05) after fresh yoghurt intake, and this showed an inverse correlation with OCTT (P < 0.05).Conclusions:Delayed orocoecal transit time was associated with fewer gastrointestinal symptoms. The improved lactose digestion and tolerance of fresh yoghurt should be mainly attributed to the presence of living bacteria.